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Cholera, Chloroform, and the Science of Medicine:

A Life of John Snow

Peter Vinten-Johansen, et al.

OXFORD UNIVERSITY PRESS

Cholera, Chloroform, and the Science of Medicine

ii

iii

Cholera, Chloroform,and the

Science of MedicineA Life of

Peter Vinten-JohansenHoward BrodyNigel Paneth

Stephen RachmanMichael Rip

with the assistance of David Zuck

1

2003

1

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Library of Congress Cataloging-in-Publication Data

Cholera, Chloroform, andthe Science of Medicine:

A Life of John SnowPeter Vinten-Johansen ... [et al].

p. cm.Includes bibliographical references and index.

ISBN 0-19-513544-X1. Snow, John, 1813—1858.

2. Epidemiologists—Great Britain—Biography.3. Anesthesiologists—Great Britain—Biography.

I. Vinten-Johansen, Peter.RA649.5.S66 S647 2003

617.9’6092–dc21[B] 2002030347

2 4 6 8 9 7 5 3 1

Printed in the United States of America on acid-free paper

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v

Preface

This book is the product of an ongoing scholarly collaboration among five profes-sors at Michigan State University who share an inordinate interest in the life andwork of an early Victorian physician, John Snow. Early on someone tagged us witha mildly embarrassing nickname, “The Snowflakes,” which stuck. Harmony does notalways reign among five men with varied training and scholarly expertise: a Euro-pean intellectual historian (Peter Vinten-Johansen), a philosopher–MD (HowardBrody), an epidemiologist–MD (Nigel Paneth), an American literary and culturalhistorian (Stephen Rachman), and a medical geographer–epidemiologist (MichaelRip). We began this project with very different views of Snow’s writings and his sig-nificance in the history of medicine. Because we all agreed that his investigationsduring the 1854 cholera epidemic in London constituted a singular achievement, ourinitial intent was to feature that incident in a relatively brief biographical study. Sev-eral jointly crafted articles and presentations shaped our collective sense of Snow. Inthe process, however, we came to believe that only an extensive, interdisciplinary bi-ography would do him justice.

In our view Snow’s accomplishments in anesthesia and epidemiology are inter-connected. His medical training occurred in the 1830s, when a new generation ofmedical men attempted to refashion medicine as a scientific discipline with linkagesto “the collateral sciences” such as chemistry and comparative anatomy. In this vi-sion of scientific medicine, the ultimate purposes of developing a solid groundingin the collateral sciences of medicine were to enhance one’s clinical acumen and toimprove the public health. Snow swallowed this intellectual regimen hook, line, andsinker and actualized the vision in his medical career.

Early on he took a special interest in respiratory cases among the patients he wastreating, devised animal experiments, and presented his findings and case reports atmedical society meetings and in the medical press. He was already a specialist, so tospeak, in respiratory physiology and clinical practice when news of inhalation etherreached London from the United States in 1846. Within two years he was arguablythe most accomplished anesthetist in the British isles—perhaps even farther afield.When the second pandemic of “Asiatic cholera” reached London in the fall of 1848,his understanding of gas law, respiratory physiology, and anesthetic agents led himto question the predominant theories about the nature and transmission of this dev-astating disease. The following year he published two essays that outlined his views

and offered preliminary substantiation. From then until his death, at the age of forty-five, in June 1858, his working days were spent administering anesthesia, conduct-ing laboratory and autoexperiments on new anesthetic agents, and tracking downinformation on outbreaks of cholera. Snow was a shoe-leather anesthetist and epi-demiologist par excellence.

It took us half a decade to develop this interpretation, but all along we were puz-zled by the fractured life and legacy depicted by other scholars. We mean no disre-spect. On the contrary, we acknowledge with admiration the devoted stewardship ofhis work undertaken by anesthesiologists and epidemiologists in Great Britain andthe United States; John Snow memorial lectures are given annually in both fields.Since the mid-1980s scholars have recast our understanding of Snow’s early life; ed-ited one of Snow’s major articles on narcotism and produced an annotated editionof his case books from the last decade of his life; self-published a biography; andwritten a dissertation from a historical–sociological perspective. In our view, it wastime for a synthetic study of Snow as an interdisciplinary thinker and medical prac-titioner that integrated this recent scholarship.

We wanted to produce a monograph, not an anthology, so we selected a teamleader–final reviser. For various reasons that role was given to Peter Vinten-Johansen;hence, he is listed as first author. Thereafter, the list is alphabetical because the bookis a collective product. We designated various members of the team “primary” writ-ers for particular chapters, but each chapter was subjected to rigorous group editingand revision. Two years into the project we made the acquaintance, first via the in-ternet, of David Zuck, a retired anesthesiologist but an active historian of medicine.His contributions as on-site researcher and in-house editor have been substantial,and he richly deserves the acknowledgment on the title page. However, it should besaid that we were sometimes unable to accept the Britishisms he strongly suggestedwould improve the readability of our book, or to include the detailed discussion ofanesthesia topics he recommended.

Please consult the following Web site for searchable transcriptions of John Snow’swritings (eventually, all of them), samples of word analysis and chronology com-parisons used in our research, as well as additional maps and images:http://www.msu.edu/unit/epi/johnsnow.

East Lansing, Michigan P.V.-J.H.B.N.P.S.R.

M.R.

vi Preface

http://www.msu.edu/unit/epi/johnsnow

vii

Acknowledgments

We have many people to thank for providing research assistance. At the Main Li-brary of Michigan State University: Peter Berg, Special Collections; Michael McSeoin,Inter-Library Loan borrowing coordinator; Ann Silverman, cataloger (retired); andAgnes H. Widder, humanities bibliographer. Professorial assistants assigned by theHonors College at Michigan State University: Joshua Courtade, Kristin Slattery, JerisStueland, and Damon Williams. Also at Michigan State University, research assis-tance was provided by Jennifer Beggs, Lyman Briggs School; Andrew Bielaczyc,College of Arts and Letters; Dan Hesse, the Honors College; Anne Forrester Barker,PhD candidate in history; Debra Mulrooney and Talmadge Holmes, the College ofHuman Medicine. At the University of Michigan Libraries: Shabbir Boxwalla, Taub-man Medical Library; Carol McKendry, coordinator of technical operations, BuhrShelving Facility; and Dawn Wallace, technical library assistant, Buhr Shelving Fa-cility. At the National Library of Medicine: Steve Greenberg and Betsy Tunis, His-tory of Medicine Division; and Ken Niles, Collection Access Section. In Canada: LeePerry, librarian, Woodward Biomedical Library, The University of British Columbia.In the United Kingdom: Dee Cook, archivist to the Society of Apothecaries, London;Kay Easson, librarian, Newcastle Literary and Philosophical Society; Stephen Freeth,keeper of manuscripts, Guildhall Library, London; Howard R. Hague, assistant li-brarian, Charing Cross Campus Library, London; Phoebe Harkins and Roy Porter(deceased), Wellcome Institute of Historical Research, London; Patricia Sheldon, as-sistant librarian, City Library, Newcastle upon Tyne; and Christopher Webb, archivist,The Borthwick Institute of Historical Research, University of York.

We are also grateful for the assistance provided by unnamed staff members at thefollowing institutions: the London Metropolitan Archives (formerly the Greater Lon-don Record Office); the Taubman Medical Center, University of Michigan; the Well-come Institute of Historical Research, London; and the Central Reference Library,York.

We discussed specific issues with many individuals, including Anthony Ashcroft,Frank A. Barrett, Charles Croner, Clive Davenhall, Andrew Dean, Andrew Dent, RustyDodson, Pamela Gilbert, Bill Henriques, William C. Hoffman, Joel Howell, DanielKarnes, David P. Lusch, Kari McLeod, Arthur Robinson, and Catherine Schenck-Yglesias.

Ralph R. Frerichs, DVM, DrPH, Department of Epidemiology, University of Cal-ifornia, Los Angeles, School of Public Health maintains an extensive Website on JohnSnow and consulted with us on issues related to mapping and the location of choleraoutbreaks that Snow investigated. H. Spence Galbraith, MD, an indefatigable re-searcher into Snow’s early life and extended family, read early drafts of several chap-ters and sent us manuscripts of prospective articles. Oxford University Press askedChristopher Hamlin, University of Notre Dame, to comment on a partial draft ofthe manuscript; he submitted an admirably detailed report that has proven helpfulin our revisions. David M. Morens, MD, National Institute of Allergy and InfectiousDiseases, read the drafts of several chapters and advised us on the history of cholerain the nineteenth century.

Throughout this long-term project, we received intellectual, emotional, technical,and financial support from faculty and staff at the Center for Ethics and Humani-ties in the Life Sciences, Michigan State University, and the Department of Epi-demiology, Michigan State University. An All-University Research Grant from Michi-gan State University in 1997–98 effectively launched our project. After two years asa research team, we were honored in 1999 with the Excellence in InterdisciplinaryScholarship Award from the Honor Society of Phi Kappa Phi at Michigan State Uni-versity; we used the monetary portion to cover research expenses and various pro-duction costs incurred in the preparation of this book. In addition, the Departmentof Epidemiology and the Mid-West Universities Consortium for International Activities covered a portion of Michael Rip’s travel expenses for a research trip toEngland.

viii Acknowledgments

ix

Contents

Abbreviations, xi

Introduction, 1

CHAPTER 1York and Newcastle, 1813–1833, 14

CHAPTER 2Senior Apprentice and Assistant, 1830–1836, 39

CHAPTER 3London Medical and Surgical Training, 1836–1838, 56

CHAPTER 4Forging a London Career, 1838–1846, 81

CHAPTER 5Ether, 110

CHAPTER 6Chloroform, 140

CHAPTER 7Cholera Theories: Controversy and Confusion, 165

CHAPTER 8Snow’s Cholera Theory, 199

CHAPTER 9Professional Success, 231

CHAPTER 10Cholera and Metropolitan Water Supply, 254

CHAPTER 11Broad Street, 283

CHAPTER 12Snow and the Mapping of Cholera Epidemics, 318

CHAPTER 13Snow and the Sanitarians, 340

CHAPTER 14Further Developments in Anesthesia, 359

CHAPTER 15Common Ground: Continuous Molecular Changes, 372

CHAPTER 16Snow’s Multiple Legacies, 388

Bibliography, 404

Index, 421

x Contents

xi

Abbreviations

AMJ Association Medical Journal.

ApothAct Holloway, Sydney W. F. “The Apothecaries’ Act, 1815: A reinterpreta-tion.” Medical History 10 (1966): 107–29, 221–36.

BF Galbraith N. Spence. “Dr John Watson (1790/91–1847) of Burnopfieldand his assistant Dr. John Snow.” Bulletin, Durham County Local His-tory Society 57 (1998): 32–50.

BIHR The Borthwick Institute of Historical Research, University of York,England.

BMJ British Medical Journal

CB Ellis, Richard H., ed. The Casebooks of Dr. John Snow. London: Well-come Institute for the History of Medicine, 1994.

CIC Cholera Inquiry Committee. Report on the Cholera Outbreak in theParish of St. James, Westminster during the Autumn of 1854. London:J. Churchill, 1855.

CMC Snow, John. On Continuous Molecular Changes, More Particularly intheir Relation to Epidemic Diseases. London: Churchill, 1853.

CSI Committee for Scientific Inquiries.

E Snow, John. On the Inhalation of the Vapour of Ether in Surgical Oper-ations: Containing a Description of the Various Stages of Etherization,and a Statement of the Results of Nearly Eighty Operations in WhichEther Has Been Employed. London: Churchill, 1847.

EMSJ Edinburgh Medical and Surgical Journal.

GBH General Board of Health.

GP Loudon, Irvine. Medical Care and the General Practitioner, 1750–1850.Oxford: Clarendon Press, 1986.

GPO Government Printing Office.

GRO General Register Office.

HMSO Her Majesty’s Stationery Office.

HoC House of Commons.

JPH&SR Journal of Public Health, and Sanitary Review. Continued as SanitaryReview and Journal of Public Health.

JS Shephard, David A. E. John Snow, Anaesthetist to a Queen and Epi-demiologist to a Nation: A Biography. Cornwall, Prince Edward Island:York Point, 1995.

JS-EMP Snow, Stephanie J. “John Snow 1813–1858: The emergence of the med-ical profession.” PhD diss, University of Keele, 1995.

JS-EY Galbraith, N. Spence. Dr John Snow (1813–1858). His early years. Lon-don: Royal Institute of Public Health, 2002.

L Richardson, Benjamin W. “The Life of John Snow.” Introduction toJohn Snow, On Chloroform and Other Anaesthetics. London: Churchill,1858.

LJM London Journal of Medicine.

LMG London Medical Gazette. (To avoid confusion, we cite volumes by theold series throughout.)

LRCP Licentiate of the Royal College of Physicians.

LSA Licentiate of the Society of Apothecaries.

MCC Snow, John. On the Mode of Communication of Cholera. London:Churchill, 1849.

xii Abbreviations

MCC2 Snow, John. On the Mode of Communication of Cholera, 2d ed. Lon-don: Churchill, 1855.

M-CJ Medico-Chirurgical Journal.

M-CR Medico-Chirurgical Review.

MCS Metropolitan Commission of Sewers.

M-CT Royal Medical and Chirurgical Society, Medico-Chirurgical Transac-tions.

MRCS Member, Royal College of Surgeons.

MSL Medical Society of London.

MT Medical Times.

MTG Medical Times and Gazette.

Newton Newton, John Frank. The Return to Nature, or, A Defence of the Veg-etable Regimen; With Some Account of an Experiment Made During theLast Three or Four Years in the Author’s Family. London: T. Cadell &W. Davies, 1811.

OC Snow, John. On Chloroform and Other Anaesthetics. London: Churchill,1858.

OED Oxford English Dictionary

ON Snow, John.“On narcotism by the inhalation of vapours.” London Med-ical Gazette (1848–51).

PB Galbraith, N. Spence. “Joseph Warburton (1786–1846) of PateleyBridge and his assistant Dr. John Snow.” Yorkshire Archaeological Jour-nal 71 (1999): 225–36.

PharJ The Pharmaceutical Journal.

PMCC Snow, John. “On the pathology and mode of communication ofcholera.” London Medical Gazette 44 (1849): 745–52, 923–29.

Abbreviations xiii

PMSJ Provincial Medical and Surgical Journal.

RM-CS Royal Medico-Chirurgical Society.

SCME Select Committee on Medical Education, House of Commons, 1834.

SR&JPH Sanitary Review and Journal of Public Health, Continuation of Journalof Public Health, and Sanitary Review.

S&V Southwark and Vauxhall Water Company.

VCH-Y Tillott, P. M. A History of Yorkshire. The City of York. Victoria Historyof the Counties of England, edited by R. B. Pugh. London: Oxford Uni-versity Press, 1961.

WH Galbraith, N. Spence. “William Hardcastle (1794–1860) of Newcastle-upon-Tyne and his pupil John Snow.” Archæologia Æliana (The Soci-ety of Antiquaries of Newcastle upon Tyne) 27 (1999): 155–70.

WMS Westminster Medical Society.

xiv Abbreviations

Cholera, Chloroform, and the Science of Medicine

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SOMETIME BETWEEN 1839 and 1841, John Snow drowned aguinea pig.1 It died in two minutes. An hour after its death, Snow

began dissecting. He observed that the heart was perfectly still and that the right sidewas swollen with blood while the left was nearly empty. As he proceeded he notedthat the surface of the lungs changed color when exposed to air. Then, much to hissurprise, the heart twitched in the form of “a slight vermicular motion in the rightauricle.” He opened the trachea and began artificial respiration. The heart’s ventri-cles began to move, and through the coats of the left atrium (the chamber that re-ceives blood from the lungs) he could see oxygen-rich, bright red blood. The heartcontinued to contract weakly, unable to expel blood from its chambers, but it keptbeating rhythmically for forty-five minutes.

What exactly was Snow up to in attempting to reactivate a guinea pigs’s dead tis-sue? This particular experiment took place in the course of his investigations intorespiration and asphyxia, undertaken with the desire to establish the physiologicalbasis for pulmonary resuscitation on infants. His efforts involved more unsettledquestions than would William Kouwenhoven’s when he developed his cardiopul-monary resuscitation (CPR) techniques in the 1950s. In the 1840s, according to thedata Snow cited, one in twenty births was stillborn, many of whom were asphyxi-ated at the very moment of birth. What method, based on principles rather thanhabit, he wondered, should be used to revive children “born in a state of suspended

1

Introduction

animation”?2 A number of practices were commonly used: dashing cold water in theinfant’s face; immersing it in warm water; performing mouth-to-mouth resuscita-tion; using a bellows (and extra oxygen) to inflate the lungs; and shocking it withelectricity. Snow acknowledged that each of these measures had merit, but all en-tailed considerable risks.

For Snow respiration—“essential to the life of the whole animal kingdom”—wasthe fundamental physiological principle at issue, so measures that directly restoredor established respiration would be most appropriate. Dashing cold water in a baby’sface, immersing it in warm water, or stimulating its skin with electroshocks mightwell rouse the nervous system and facilitate breathing, but these seemed indirect,risky methods compared with artificial respiration, which Snow reasoned “must behad recourse to as quickly as possible.”3 However, he worried that “breathing intothe lungs of the child” would be too unnatural to facilitate regular breathing andthat such air probably contained too much carbon dioxide gas to be effective, yet theordinary bellows frequently used could overinflate and damage the newborn’s lungs.

Snow delivered a paper at the Westminster Medical Society in October 1841 inwhich he proposed a resuscitating device constructed with newborn infants in mind.It consisted of two small syringes, one fitted over the mouth, the other fitted overthe nostrils. While the syringe over the mouth drew air from the lungs, the one overthe nostrils delivered fresh air. The device was as simple as a bellows but lacked itsdangers: “The two pistons are held in the same hand, and lifted up and pressed downtogether, the cylinders being fixed side by side, and each having two valves. Whenthe pistons are raised, one cylinder becomes filled with air from the lungs, and theother with fresh air from the atmosphere, which can be warmed on its way by pass-ing a tube and metal coil placed in hot water.” Snow had designed a hand-held re-suscitator, complete with a warmer to enhance the oxygenation of the blood.4 Snow’splan for an artificial respirator was a practical solution to a concrete and pervasivemedical and social problem, accomplished by a cogent application of physiologicalprinciples.

As an understanding of diseases reveals underlying patterns of normal functions,asphyxia was important to Snow because it revealed the underlying pattern of res-piration. Respiration was first and foremost a chemical exchange of gases—oxygenfrom the air for carbon dioxide from the blood—first shown by Lavoisier in the eigh-teenth century but most recently refined by the German physiologist Heinrich Mag-nus in 1837. Snow admired physiologists and chemists who were busy exploding theold vitalist doctrine that posited a peculiar lifeforce in living organisms, distinct fromgeneral physical and chemical forces. In Snow’s mind respiration disproved vitalismbecause, although crucial to life, it was based on the same principles that guided allphysicochemical forces: The exchange of gases “is not strictly a vital process, but onlyan operation of organic chemistry, since it continues after death as well as before,when the mechanical advantages for access of air remain the same.”5 There was gen-eral agreement that asphyxiation induced a distinct sequence of symptoms in adults

2 Cholera, Chloroform, and the Science of Medicine

as well as newborns, but there was considerable debate as to what caused it. Bichathad concluded that oxygen-depleted venous blood acted as a poison when it was re-circulated. Was he right? Or was asphyxia the result of “the poisonous effects of car-bonic acid detained in it”? If so, was carbon dioxide gas formed in the lungs or thecapillaries? There were other vexing questions, too: Was circulation primarily causedby the mechanical action of the heart or by the chemical exchanges in the blood?Was animal heat derived from this chemical exchange? Why did asphyxiation occurmore suddenly at higher temperatures?

Snow offered answers to all these questions in his paper on newborn resuscitationat the Westminster Medical Society, citing what he deemed the most reliable studiesand supplementing those findings with results from his own experiments. He thoughtBichat went “rather too far” in calling venous blood a poison, because if respirationis renewed in time, no ill effects remain from the circulation of dark blood. In a se-ries of eighteen experiments on small animals and birds, Snow had found that car-bon dioxide gas’s “injurious effects seem to depend rather on its physical properties,viz. its density and solubility in the blood than on any strictly poisonous qualities.”6

Asphyxiation was caused by the absence of oxygen, because experimental animalsbecame asphyxiated when placed in nitrogen and hydrogen gas. The bulk of evidencein experiments by Alison, Edwards, and Reid suggested, as well, that the exchange ofoxygen and carbon dioxide and the generation of heat and blood flow take place inthe capillaries and that higher temperatures accelerated such exchanges.

So what had Snow learned by performing artificial respiration on his suffocatedguinea pig? He surmised that the line between life and death was not fixed, and theheart retained its irritability (its ability to be stimulated by oxygen) beyond death.On this experimental and theoretical basis, Snow urged his colleagues to use his ar-tificial respirator on still-born infants. The new physiology had shown that respira-tion was the key to life, so oxygen was the appropriate stimulant for the asphyxiated.Other measures were indirect at best, harmful at worst. Above all, he urged the avoid-ance of the application of warmth, despite its time-honored use in medical circlesand endorsement by The Royal Humane Society. At higher temperatures and in theabsence of new incoming air (as when an infant is simply placed in a warm bath torevive it), the oxygen still present in the blood would be converted to carbon diox-ide more quickly, thereby accelerating the asphyxiation. In addition to questioningcontemporary clinical practice, Snow’s asphyxiation research allowed him to tracerespiration and its basic chemical exchanges into the womb and to the caudal brainstem.7

It also prepared him to manage clinical problems in a scientific manner. In the1841 presentation at the Westminster Medical Society, he noted “that even a strongchild does not always begin to breathe the minute when it is born; but if the um-bilical cord be pressed between the fingers it will instantly draw an inspiration.”8

Seven years later, on a Wednesday morning in November 1848, he was called in toadvise on a difficult delivery. Mrs. Strachan, a mother who had already given birth

Introduction 3

to several children in protracted, “very hard labors” was going through this ordealagain. She was distressed, tired, “out of patience,” and “wished to know if somethingcould not be done for her relief.” Snow administered moderate doses of chloroform.The patient experienced immediate relief and remained in a light state of uncon-sciousness for the duration of the labor (two-and-a-half hours) until a baby girl wasborn, but the infant was in “a state of asphyxia, fetching a breath only at intervals ofabout a minute. . . . Dashing cold water on the child sometimes caused it to breathea little sooner, & its lips remained black and limbs relaxed.” The umbilical cord, how-ever, pulsated as far as it was exposed, and shortly before the afterbirth was deliv-ered, Snow compressed the cord between his forefinger and his thumb; immediatelythe baby began breathing naturally. When he released the cord the breathing di-minished. On tying the cord the child breathed well and recovered quickly. He hadresolved the asphyxiation, as his physiological inquiries over the years had predicted,by stimulating the urge to breathe.9 In this way Snow’s research would become hispractice. He brought a knowledge of physiology and chemistry to bear on the taskof saving newborns that come into the world apparently dead.

In Snow’s day the scientific practice of medicine demanded the use of techniquesoften at odds with convention and established authorities. It also required a world-view in which humanity had to be understood as part of animal evolution ratherthan distinct from it. Perhaps drawing on the comparative anatomy and physiologyhe had learned at the Hunterian School of Medicine in London, he concluded his1841 presentation on asphyxia with a comparison: “Moralists have often assertedthat human beings come into the world in a more puny and helpless condition thanany other animals; but in this they are mistaken; for, without including marsupialanimals, the young of cats, and all those that are brought forth with their eyes closed,cannot maintain life without artificial heat, which they receive from lying close tothe mother: in fact they can scarcely be said to have a proper temperature of theirown. A child born at the full term, on the contrary, can maintain its temperature ifwell protected from cold.”10 In Snow’s vision of life, newborn infants were not as de-fenseless as convention would have it. Our animal heat at birth was a sign of ourrespiratory power, our resiliency, and, to the scientific medical practitioner, our ca-pacity for being restored to life from apparent death by the proper methods.

* * *

John Snow has been called a “compleat physician,” meaning exemplary in every way, but the basis for this exemplariness has remained suggestive until now.11 Qual-ifying as a surgeon-apothecary at the age of twenty-five in 1838, he had already hadeleven years of medical training and experience. He had served six years as an ap-prentice to a surgeon-apothecary who was attached to the Lying-in Hospital in New-castle, followed by three years as an assistant to two country apothecaries whose prac-tices also included midwifery. Then, while a medical student in London, he studied


medicine with a physician who had a particular interest in obstetrics, and he stud-ied midwifery and diseases of women and children with a physician who had a prac-tice at the Royal Lying-in Hospital. After qualifying he established a general practicein the Soho area of London that involved many deliveries. The young clinician, whoin 1841 “remarked that . . . if the umbilical cord will be pressed between the fin-gers it will instantly draw an inspiration” from a newborn who was not breathing,had probably already attended hundreds of deliveries.12 Others at the time couldequal or even surpass this clinical experience, but Snow belonged to a cadre of youngmedical men whose clinical practice was grounded in what was then called the col-lateral sciences of medicine. He chose to attend a London medical school renownedfor the teaching of anatomy and staffed by instructors all of whom were keenly in-terested in Continental developments in physiology and chemistry and several ofwhom had trained in Edinburgh, who taught their students the newest ideas in com-parative anatomy and Lamarckian evolutionary biology.

The antivitalist philosophy Snow confronted at the Hunterian School of Medicinewas cutting edge thought in the 1830s, and it contributed to his becoming an advo-cate of scientific medicine as distinct from a singularly experiential (bedside) med-icine that was dominant among many of his older colleagues. Snow’s approach wasto base clinical methods on the latest research in the sciences relevant to his chosenspecialty. When confronted by a pressing medical and social concern—newborn in-fants were dying of asphyxiation at an alarming rate—he surveyed the literature onrespiration, conducted experiments on a variety of animals, and designed a resusci-tation apparatus that would perform according to scientific principles. One sees inhis early research on asphyxiation the mind-set and process he would use in 1847 tobase the administration of ether and chloroform on medical scientific principlesrather than simple trial-and-error research. In some respects the ether inhaler he de-vised in 1847 permitted him to induce controlled “suspended animation” via the ad-ministration of anesthesia—in essence, the reverse of the resuscitation apparatus hedesigned in 1841. Like his colleagues in the Westminster Medical Society, Snow’s the-oretical and research interests were always stimulated by practical problems and di-rected to producing results with practical applications. There was no difference inEnglish medicine at this time between the medical researcher and the clinician.

In addition to being a conduit for Continental and Scottish ideas, Snow was anexemplar of moderate medical radicalism. This movement arose in conjunction withdebate on the First Reform Bill of 1831–1832, which eventuated in a modest ex-pansion of the franchise for elections to the House of Commons (including Snow’sfather, who had become a property owner by then). Medical radicals agitated to re-place the three medical orders of physician, surgeon, and apothecary, then under thecontrol of elite corporations, with a unified program of medical training, a singlequalification, and a democratic professional organization.13 The Hunterian Schoolof Medicine and the Westminster Medical Society were hotbeds for outspoken aswell as moderate radicals in the 1830s. Snow’s favorite teacher had earned his MD

Introduction 5

in Edinburgh but refused to take a license to practice as a physician in London inprotest of the power exerted by the Royal College of Physicians, but Snow was noagitator. Instead, he achieved three medical qualifications and then snubbed the cor-porate establishments for the rest of his career. The twenty-eight year old “Mr. Snow”who read a paper on resuscitating asphyxiated newborns at the Westminster Med-ical Society was a surgeon-apothecary, or general practitioner (GP) in emerging parl-ance, but within three years he would call himself Dr. Snow, having received the MDfrom the University of London. Certainly, he hoped to improve his prospects andexpand his practice by becoming a physician, but the medical colleagues with whomhe associated were medical radicals, and he occasionally found himself opposed tothe medical establishment.

Snow’s progression from animal experimentation to the invention of a device forthe resuscitation of newborns exemplifies his scientific modus operandi for the workthat made him famous in his lifetime—the development of scientific anesthesia. Inaddition, he was also profoundly interested in the public health questions of the day,and applied his scientific perspective to the major new epidemic disease of his time,cholera. Until his death in 1858 he would juggle a flourishing career as a premieranesthetist and new ventures in public health and epidemiology.

Testimony, 1855

For Snow 5 March 1855 was a typically busy Monday. His anesthesia practice broughthim to Hanover Square, a few blocks north of his residence in Sackville Street, to as-sist a dentist with a tooth extraction. There were complications, however. The at-tending physician was concerned that the administration of chloroform would placehis patient, a young man named Tudor with a “weak constitution,” at special risk.He reassured them both that everything would go smoothly, then took Tudor’s pulse.It was weak. When told that he would feel no pain and had nothing to fear, the youngman relaxed, and his pulse improved. Shortly thereafter Snow gave him chloroformwithout complications or subsequent depression of his pulse, and the dentist wasable to remove two teeth.14

Next he walked west toward Hyde Park but stopped in the Mayfair district to givechloroform to a middle-aged man from Staffordshire who was undergoing a secondoperation to remove dead bone tissue from the femur. A longtime colleague ofSnow’s, Mr. Bowman, was the surgeon. The outcome seemed successful, and, fromSnow’s perspective, the patient tolerated the anesthesia very well.15 His third anes-thesia case of the day was near Clapham Common in South London. To get therehe would have crossed the River Thames, then walked along the Wandsworth Road,where in 1849 he had investigated an epidemic outbreak featured in his first essay,On the Mode of Communication of Cholera. The uncle of yet another colleague, Dr.Spitta, was having lithotripsy, in which an instrument is inserted into the bladder to


crush stones. In the first decade of anesthesia use, only the number of dental ex-tractions exceeded lithotripsy in Snow’s caseload; third in frequency were lithotomies(surgical incision of the bladder to remove stones), followed by breast tumors, hem-orrhoids, anal fistulae, harelips, and childbirth.16 Anesthesia had become routine inmedical procedures, major and minor. Snow would log more than 5,000 cases in al-most a dozen years and in the process was exposed to every nook and cranny of Lon-don, every walk of life, and the widest imaginable array of diseases the metropolishad to offer.

Sandwiched among these visits, Snow found time on that Monday afternoon inMarch 1855 to testify at the Houses of Parliament, near Westminster Abbey, beforethe Select Committee on Public Health on the Nuisances Removal and Diseases Pre-vention Act. Parliamentary committees had been gathering data and hearing experttestimony for a quarter century on sanitary conditions throughout Britain, but es-pecially in the “towns and populous districts.” The sanitary reform movement wasdriven by the medical opinion that poisonous vapors, whether miasmas rising frommarshes or from decomposing organic matter near human dwellings, were the maincause of disease, including epidemic cholera, which had killed tens of thousands ofpeople in England since 1831. Much of the law resulting from this movement con-centrated on removing sources of filth and smoke from the environment, improv-ing sewage disposal, and forcing private water companies to provide purer drinkingwater. The bill then before the select committee would grant public officials the powerto regulate or eliminate the so-called offensive trades that released foul-smelling,noxious fumes: gasworks, bone boilers and merchants, soap manufacturers, tallowmelters, gut spinners, dye makers, market gardeners, and manufacturing chemistswho produced artificial manure for agricultural purposes. At the least, sanitation re-formers wanted to keep businesses from fouling up residential neighborhoods withpollutants viewed as pathogenic for a host of constitutional diseases and contribu-tory to the cause and spread of epidemic cholera. However, Henry Knight, a bonemerchant, and the consortium of “offensive trades” he represented believed the pro-posed act would, in effect, put them all out of business. He submitted Snow’s nameas an expert medical witness to plead their case, although he had never actually methim or discussed the matter with him.

The alliance between Snow and the “offensive trades” was entirely intellectual.Knight had read On the Mode of Communication of Cholera—the second, expandededition—in which Snow presented evidence drawn from three epidemics(1831–1832, 1848–1849, and 1853–1854) that cholera could be transmitted only byswallowing the “morbid matter” specific to that disease. He completely ruled out asa cause of cholera the inhalation of miasmas and effluvia, whether from the atmo-sphere or the bodies of the sick. His argument featured two landmark epidemiolog-ical studies of cholera that would secure his reputation into the twenty-first century:an analysis of the differential mortality in thirty-two London subdistricts suppliedby two companies drawing water from separate stretches of the Thames, and also

Introduction 7

the linkage of a lethal Golden Square outbreak to contamination of a popular pumpin Broad Street. Mr. Knight had been intrigued by Snow’s view “that measures nec-essary to protect the public health would not interfere with useful trades.”17 Manyof Snow’s contemporaries were unconvinced by his reasoning and practical recom-mendations, even though he was by then a forty-two-year-old physician of somegravitas (Fig. Intro.1): current president of the Medical Society of London and theleading authority on ether and chloroform in Britain, who, two years before, hadgiven chloroform to Queen Victoria when she was delivering Prince Leopold—anevent generally accepted as instigating the use of anesthesia in childbirth through-out the West.

In preliminary remarks Snow stated: “I have paid a great deal of attention to epi-demic diseases, more particularly to cholera, and in fact to the public health in gen-eral; and I have arrived at the conclusion with regard to what are called offensivetrades, that many of them really do not assist in the propagation of epidemic dis-eases, and that in fact they are not injurious to the public health. I consider that ifthey were injurious to the public health they would be extremely so to the workmen


Figure Intro.1. Photograph of John Snow, mid-1850s.

engaged in those trades, and as far as I have been able to learn, that is not the case;and from the law of the diffusion of gases, it follows, that if they are not injuriousto those actually upon the spot, where the trades are carried on, it is impossible theyshould be to persons further removed from the spot.”18 The crux of the matter forSnow was that “offensive trades,” much as they might offend our olfactory sensibil-ities, would not cause illness in the general population if the workers themselves wereuninjured. He knew from years of research, most recently on the properties of anes-thetic agents, that gases were “injurious” to health only at close range in very highconcentration, so if those closest to offensive smelling materials did not get sick, howcould such trades be spreading disease-causing vapors? While some people todaymight quarrel with Snow’s pollution-tolerant notion of public health, his conclusionwas sound: Carcass renderers and their ilk were not propagating cholera or otherepidemic diseases.19

But the chair, Sir Benjamin Hall, and twelve members of the Select Committee onNuisances Removal and Disease Prevention did not share Snow’s knowledge of gaslaws and were, not surprisingly, utterly astounded by his opening statement. “Are theCommittee to understand,” Hall inquired, “taking the case of bone-boilers, that nomatter how offensive to the sense of smell the effluvia that comes from the bone-boiling establishments may be, yet you consider that it is not prejudicial in any wayto the health of the inhabitants of the district?” Snow replied, “That is my opinion.”20

The committee seemed eager to probe him, to catch him in a contradiction. If itmade no difference living cheek by jowl to a knacker’s yard, were “all animal sub-stances” harmless to humans? “No,” Snow replied, “I believe that epidemic diseasesare propagated by special animal poisons coming from diseased persons, and caus-ing the same diseases to others, and that they are extremely injurious; but that sub-stances belonging to animals, that is to say, ordinary decomposing animal matter,will not produce disease in the human subject.”21 What about “decaying vegetablematter; do you consider that will not be productive of disease?” He did not, with thepossible exception of ague (recurring fevers such as malaria), about which there wasstill medical uncertainty; “but in London, in any trade I am acquainted with, I donot believe that any decomposing vegetable or animal matters produce disease.”22

Chairman Hall, however, remained in disbelief about Snow’s earlier commentabout the “knacker’s yard,” a slaughterhouse in which the animals are not fit for hu-man consumption. Would the “very offensive effluvia” from a pile of rotting horseflesh “not be prejudicial to the health of the inhabitants round”? “I believe not,” Snowfirst reiterated and then explained in reply to another questioner: “gases producedby decomposition when very concentrated, will produce sudden death; but wherethe person is not killed, if the person recovers, he has no fever or illness.”23 Anothermember wanted additional clarification of this point, and after two brief exchangeswith Snow asked him, “Do you mean to tell the Committee that when the effect isto produce violent sickness there is no injury produced to the constitution or healthof the individual?” Snow’s reply was careful and discriminating: “No fever or special

Introduction 9

disease.”24 But Mr. Greene did not catch his meaning: “Are you not aware that per-sons going into vaults where there are a number of dead bodies have suffered veryseverely, and that sometimes death has been produced by this cause?” “Yes, whenthose gases are extremely concentrated, they will actually poison and cause death.”However, the cause of death resulted from the laws of gases, not the local miasmatheory of disease, because the poisons in such gases do “not cause disease;” only poi-sons “that reproduce themselves in the constitution” can cause disease in that per-son and be transmitted to others to cause an identical disease.25 Nevertheless, Snow’sexplanation left yet another committee member confused: “You say that effluvia aris-ing from living subjects are dangerous?” He replied yes, “or even from certain per-sons who have died from disease,” Snow added. Another committee member asked,“But not from the mere decay of animal matter?” Snow responded that that was correct.26

At this point the committee moved on to other topics, but these parliamentaryexchanges offer a glimpse into Snow’s theory of disease transmission and the con-ceptual impasse that stood between him and those most influential in British gov-ernment at midcentury. The exchanges also reveal the differences between his think-ing and germ theory, which crystallized in the decades after Snow’s death in 1858.Snow’s theory of epidemic diseases was based on the communication of “special an-imal poisons.” As confusing as this notion was to the members of the parliamentarycommittee, he could not possibly have used a more precise term. In Snow’s day theagents (some called them “germs,” others an infectious “virus”) that caused cholera,typhus, and measles, for example, were unknown—unknown in the sense of not yetisolated, observed, or classified. Nevertheless, Snow believed, on medical and socialevidence, that cholera and other epidemic diseases were propagated from one dis-eased person to another, that like caused like, and that a particular disease-causingagent could not cause a different disease in someone else. Even though the agentswere unknown, the signatures of epidemic diseases were sufficiently apparent forhim to hypothesize how they were communicated from one person, household, town,city, nation, and continent to the next. Moreover, the pathways were sufficiently clearfor preventive public health measures to be enacted, whether or not the organizedlife forms that caused the disease in the human body were identified.

If the members of Parliament found Snow’s theory implausible, the Lancet, a lead-ing medical journal of the day, considered Snow a traitor to empirical medicine anda fellow-traveler with an “unsavory” consortium of profiteering businessmen. Histestimony lent support to the producers “of pestilent vapors, miasms, and loathsomeabominations of every kind” who fatten themselves “upon the injury of their neigh-bors.”27 Equally galling to the editors of the Lancet was Snow’s use of a public fo-rum to truck his unsubstantiated theories. “Is this evidence scientific?” Lancet askedrhetorically. “Is it consistent with itself? Is it in accordance with the experience ofmen who have studied the question without being blinded by theories?” There wasample evidence that fumes from gas-producing trades made local people ill.


And we presume that there is hardly a practitioner of experience and aver-age powers of observation who does not daily observe the same thing. Why isit then, that Dr. Snow is singular in his opinion? Has he any fact to show inproof? No! But he has a theory, to the effect that animal matters are only in-jurious when swallowed! The lungs are proof against animal poisons; but thealimentary canal affords a ready inlet. Dr. Snow is satisfied that every case ofcholera for instance, depends upon a previous case of cholera, and is causedby swallowing the excrementitious matter voided by cholera patients. Verygood! But if we admit this, how does it follow that the gases from decompos-ing animal matter are innocuous? . . . If this logic does not satisfy reason, itsatisfies a theory; and we all know that theory is often more despotic than rea-son. The fact is, that the well whence Dr. Snow draws all sanitary truth is themain sewer. His specus, or den, is a drain. In riding his hobby very hard, hehas fallen down through a gully-hole and has never since been able to get outagain. . . . And to Dr. Snow an impossible one: so there we leave him.28

The Lancet diatribe reverberates with the contumely that Snow’s ideas engenderedwhen they were first proposed. The most unpleasant aspect of Snow’s thesis—thatthe mass of cholera victims were swallowing other people’s fecal matter—made himappear to the Lancet to be like an offensive tradesman himself.29 We part companywith Snow when he argued that “ordinary decomposition” was not a source of dis-ease, because we associate decomposition and putrefaction with the bacteria andfungi that cause them, but the “germs” involved in bone-boiling and the other “of-fensive trades” that Snow considered harmless will not cause cholera or any otherepidemic disease. Snow was correct (or at least more correct than the Lancet) onthese matters.

* * *

These two snapshots of Snow—dissecting a guinea pig, then being dissected by Parliament—are illustrative of the medical road he traveled. He began his careerstudying the physiology of respiration and asphyxiation, which paved the way forhis approach to researching and administering anesthetic agents after 1846. When asecond cholera epidemic began in England in 1848, his understanding of gas law,the mechanism of respiration, and human physiology made him skeptical of the viewhe had once shared that this was fundamentally a febrile disease. These vignettes alsoshow the resistance Snow encountered when he sought to clarify his “special poi-sons” theory and its ramifications for public health.

The Lancet editorial considered his reliance on “theory” as suspect in itself, butthe fundamental disagreement was over which theory to trust and whose authorityto follow in the pre-germ theory era characterized by many informed and partiallyinformed opinions along with so many unknowns. Snow lived three more years

Introduction 11

after testifying before the parliamentary committee, during which time he contin-ued to defend his sanitary ideas in the London medical press and in the medical andsocial circles in which he traveled. He did not succeed in his lifetime, although hewould be vindicated after the fourth cholera epidemic of 1866. Even so, who couldpossibly have imagined that an impoverished Soho medical man and son of an un-skilled Yorkshire laborer would ever have achieved such notoriety?

Notes

1. Snow mentions this in “On asphyxia and the resuscitation of still-born children,” LMG29 (1841–42): 226. The exact date of the experiment is not known, but his interest in the sub-ject is easily traceable through his published writings on respiration and asphyxia dating fromJanuary 1839.

2. Snow, “On asphyxia,” 224.3. Ibid., 223, 225.4. Snow’s device was actually an adaptation of one designed for adults by a Mr. Read of

Regent Circus, who introduced the syringe method for artificial respiration at the Westmin-ster Medical Society in 1838, coinciding with Snow’s burgeoning interest in respiration. SeeSnow, “On asphyxia,” 225.

5. Ibid., 221–24. Other physiologists he cited over the years were William Frédéric Edwards,John Reid, Xavier Bichat, François Magendie, Collard de Martingny, Pierre Hubert Nysten,and William Alison.

6. On Bichat, see Ibid., 223. Snow performed these experiments in March 1839, but he de-scribed them several years later; see Snow, “On the pathological effects of atmospheres viti-ated with carbonic acid gas” (1846). In the same passage Snow added that “this view is sup-ported by Nysten’s experiments of injecting it [CO2 gas] into the blood-vessels” (55) and thenquotes Nysten’s article, in French.

7. In Snow’s mind there was nothing vital or special about the process: “Physiologists haveamused themselves in speculating on the cause of the first respiration; but doubtless it is thesame as the second and third, and all succeeding respirations; namely, a sensation or impres-sion arising from a want of oxygen in the system, and conveyed to the medulla oblongata,either by the blood circulating in it, by the nerves in connection with it, or by both causes”;“On asphyxia,” 227. He was referring to earlier generations of physiologists. For a parallel ar-gument that, “even a generation previously, Snow’s reasoning would have been improbable,if not impossible,” see Rosenberg, Explaining Epidemics, 118. Although Rosenberg was refer-ring to Snow’s reasoning about cholera, he goes on to mention “advances in chemistry, inpathology, in technology, and in public health practice”; Ibid.

8. Snow, “On asphyxia,” 227.9. Ellis, CB, 22 (1 November 1848).10. Snow, “On asphyxia,” 227.11. Shephard, JS, 279–94.12. Snow, “On asphyxia,” 227.13. Desmond, Politics of Evolution, 11–12, 102–04.14. Ellis, CB, 360.15. Ibid., 360, 356.16. Ibid., 360, 596–616. The contemporary term for lithotripsy was lithotrity.


Introduction 13

17. UK HoC, “Select committees on medical relief and public health,” par. 119, p. 328.18. Ibid., par. 120, p. 328.19. Lilienfeld, “John Snow: The first hired gun?” 8; Vandenbroucke, “Invited commentary:

The testimony of Dr. Snow,” 10, 12.20. UK HoC, “Select committees on medical relief and public health,” par. 121, p. 328. Hall

was also President of the Board of Health.21. Ibid., par. 122, p. 328.22. Ibid., par. 123, p. 328.23. Ibid., par. 124, 126, pp. 328–29.24. Ibid., par. 129, p. 329.25. Ibid., par. 130–32, p. 329.26. Ibid., par. 133–34, p. 329.27. Editorial, Lancet 1 (23 June 1855): 634.28. Ibid., 634–35.29. A fortnight later, a medical journal that had been receptive on past occasions to Snow’s

views and theories regretfully criticized his testimony before the Parliamentary Committee,albeit without the vituperative ad hominem tone used by its rival; “The Public Health Bill,”MTG 11 (1855): 12–13. A few days later, Snow published an open letter to the chairman ofthe committee in which he referred to the harsh criticism dished out by the newspaper andmedical press for his ostensible support of noxious trades, even though “I explained thegrounds of my opinions as well as the opportunity permitted”; Snow, [Open] Letter to theRight Hon. Sir Benjamin Hall (1855), 3. Snow continued, “The writers of these attacks haveassumed and asserted that the opinions I have expressed on the subject of offensive trades arealtogether new and peculiar”; Ibid., 4. Quite the contrary, Snow argued, and cited similar viewsof the non-danger attached to gases from decomposing organic matter published by Bancroft(1811) and Thomas Watson (1841–42). In mentioning Watson, Snow added that his attack-ers had assumed that he was drawn to his conclusions about offensive gases because of hispet theory of cholera transmission, whereas in actuality Snow had entertained his views ongases long before he began to study cholera; Ibid., 9. In an 1856 article published by the Lancethe marshaled statistics to show that workers in those trades seemed as healthy as other work-ers; Snow, “On the supposed influence of offensive trades on mortality” (1856).

14

A PICTURESQUE GRAVEYARD adjacent to the church of AllSaints North Street (Fig. 1.1) in the ancient English city of York

contains one of the few tangible traces of John Snow’s origins: the Snow family plotwith a gravestone for four members buried there just before city authorities out-lawed intramural interments. The church was one of six in Micklegate Ward, an areaof about forty acres south of the River Ouse. The ward included the northern partof North Street and contiguous courts, rows, and alleys, many named Tanner, in-dicative of a long-standing local industry, tanning (Fig. 1.2). The buildings were amixture of residential housing, craft shops, flour mills, and warehouses. Carts fromthe southern and western hinterlands carrying grain and produce, cattle bound forthe central market, and coaches all used the city portal at Micklegate Bar, where in-coming traffic was inspected and tolls assessed. Quays along the Ouse were the un-loading point for goods brought downstream by barges and small boats from thewest and the north via a tributary, the River Swale, as well as from London, New-castle, and elsewhere via the Humber inlet from the North Sea. The vessels were thenrefilled with cattle, agricultural produce from the Yorkshire countryside, and assortedcommercial goods. Large warehouses lined the riverbank and served double duty asdikes, protecting low-lying houses in North Street from periodic flooding of the slow-moving river. Laborers were in great demand, as were transport workers such as car-men. Alleys connected the quays with North Street, which intersected Micklegate

Chapter 1

York and Newcastle,1813–1833

near the Ouse Bridge, the only vehicular and pedestrian connection to the rest ofthe city lying north of the river.1

Early in the nineteenth century the city of York bore traces of a history spanningalmost two millennia. It was still a walled city. The foundations of some walls erectedduring the Roman era for a small military outpost of the empire were extended andrepaired over the centuries as York was transformed into an autonomous borough.Some street names still ended in “-gate,” medieval Danish for “street” and indicativeof a ninth-century occupation by Scandinavian invaders. By the late Middle Ages,however, York had risen in significance to become a cathedral town (York Minster)and the northern capital of England by virtue of its location at the junction of tworivers and at the confluence of roads from the hinterlands. Some of the medievalquays and market squares still hummed with activity at the turn of the nineteenthcentury, when almost 17,000 people inhabited a contained area intended for half thatmany. At a time when the Industrial Revolution was transforming economic life, roil-ing social relations, and altering the landscape elsewhere in England, York was dom-inated by artisan guilds, and the mayor annually rode ceremoniously across the im-

York and Newcastle, 1813–1833 15

Figure 1.1. Church of All Saints North Street, c. 1840

(F. Bedford, illustrator, from Booth, pl. 13).

mediate suburbs that were claimed by the four wards into which the city was dividedfor administrative purposes.2

Much of Micklegate Ward, particularly the streets near the river, was consideredunsanitary, even in Snow’s day. For centuries most of the parish had drawn waterfor household use from the Ouse near the North Street postern. In the 1670s the citycorporation commissioned the York Waterworks company to provide running wa-ter. For more than a century the company pulled relatively fresh water from the Ousenear the North Street postern, eventually serving many customers in the three north-ern wards with running water via taps to cisterns placed in backyards and court-


➅

① ➁

➂

➃

➄

Figure 1.2. Micklegate Ward: 1—All Saints North Street Church; 2—Possible location of Snow

family residence and John Snow’s birthplace; 3—North Street postern by Wellington Row, to

which the Snows moved in the early 1820s; 4—Micklegate Bar entrance; 5—Dodsworth School

that Snow may have attended from approximately 1819 to 1827; 6—Queen Street, where the

Snows moved in 1825 (adapted from Hargrove, vol. 2, between iv and 6).

yards. The water company found few customers in Micklegate Ward, however, be-cause of low pressure and intermittent supply; the hollow tree trunks that carriedwater under the Ouse Bridge frequently developed leaks because of the heavy traf-fic above. Consequently, many residents in the ward as a whole, All Saints NorthStreet parish in particular, drew water for drinking and washing either from shallowlocal wells or directly from the river. Neither source was particularly salubrious. Theriver water below the North Street postern was frequently polluted by discharges ofdung from livestock pens near the ferry crossing. Although most houses in the parishhad water closets connected to basement cesspits, which night soil men emptied pe-riodically for a fee, some householders ran drains directly into the river to avoid pay-ing sewage rates.3

Similar violations of city regulations for the disposal of human and industrialwastes occurred north of the river. The result was that water quality gradually dete-riorated as the river bisected the city and was foul when it reached the Skeldersgatepostern and the southern suburbs. All wells situated in the Ouse River floodplain re-ceived episodic overflows and became contaminated. Runoff from tanneries and mar-ket squares polluted springs that supplied wells or drained through cracks in liningsinto the wells themselves. Water tables within the city were also tainted by seepagefrom cemeteries and dunghills where night soil wagons dumped their loads for useas manure in the communal vegetable gardens. Conditions for residents near theRiver Ouse were often unsanitary, but they were much worse in the eastern andsoutheastern parishes of Walmgate and Monk Wards near the River Foss. A lock nearthe junction with the Ouse turned the Foss into a stagnant river, with an adjoiningbog into which “poured the fetid contents of the drains” from nearby houses. Cityauthorities in the eighteenth century considered such problems with water supplyand sanitation unavoidable annoyances, but they became a matter of increasing con-cern among the earliest sanitary reformers in the 1820s, when the population of Yorkexceeded 22,000—an increase of twenty-five percent since 1801.4 In such an unsan-itary environment, Frances Snow would give birth to seven healthy and long-livedchildren before the family moved to higher ground just outside the city walls in 1825,when their first-born, John, was twelve.5 Perhaps the unhealthy conditions duringthese formative years stimulated his later obsession with the purity of what peopleingest.

The Snows in York

Frances (Fanny) Askham was the “base born,” or illegitimate, daughter of John Emp-son and Mary Askham. Being illegitimate, she was assigned her mother’s surname.In 1792, three years after Fanny’s birth, her parents exchanged vows of marriage inthe parish church of the village of Acomb, two miles west of York (Fig. 1.3).6 Thecouple had another daughter and three sons in the following nine years, all sur-


named, unlike their elder sister, Empson (Fig. 1.4). During this period John Emp-son was a weaver, a “gentleman’s servant,” and a laborer—all “genteel occupations”in an era when self-reliance was the hallmark of respectability among the workingpoor and lower middle classes.7 Sometime after 1801 John and Mary Empson movedto Huntington, a farming parish on the northern outskirts of York.8

In 1812 Fanny Askham, aged 24, married William Snow, aged 29. Both were suf-ficiently literate to sign the marriage register, and both listed their residence as Hunt-ington. William Snow was a laborer.9 His parents, Hannah and William Snow, aremore mysterious than his in-laws. One view is that they were longtime residents ofYork, perhaps in the parish of All Saints North Street because their names are carvedon a family tombstone in that churchyard. It is more likely, however, that they owneda farm in Upper Poppleton a few miles east of the city.10 Shortly after their marriageWilliam and Fanny Snow moved into the city of York. They set up a household some-where in North Street, described in an 1818 guidebook as a “narrow” street with


Figure 1.3. Parishes and townships around York (adapted from Tillott, 312).

Hannah(1792-??)

Askhams are recorded in Ledsham andYork parish registers from 1300s.

William Askham = Mary Butler of Ledsham

Mary Askham (1769-??)

Empsons appear in Yorkshire parish records from 1500s.

Lancelot Empson = Hannah ? of Strensall

John Empson (?-1850)Weaver, gentleman’s servant, laborer, gardener, yeoman farmer

m., 1792; Acomb parish

Frances Askham of Fairburn(1789-1860)

Illegitimate; York

Mary Ann Empson(18??) Illegitimate

Elizabeth(1830-??)Illegitimate

Mary Ann(1838-??)Illegitimate

Andrew SimpsonNurseryman, York

??

Charles(1794-1861)Adventurer,

South America;in Newcastle,

bookseller & stationer;in Bath, bookseller

& antiquities

John(1799-??)Gardener

William = Elizabeth Cobb(1801-??) m., 1825

Figure 1.4. Askham–Empson genealogy.

John(1813-58)

Apothecary, Surgeon,Physician.

William (1815-??)Temperance Hotelier,tailor & hatter.Emigrated to Australia?

Charles(1817-??)

Occupations andresidence after 1841

unknown.

Robert(1819-85/86)Secretary, then

manager of GarforthColliery, Leeds.

Thomas(1821-93)

Teacher; thencurate, chaplain,and eventually

vicar of Underbarrow.

Mary(1823-1911)Schoolteacher;

Head, “The Mount”school for girls, York.

Hannah(1825-1904)Schoolteacher;

Head, “The Mount”school for girls, York.

Sarah = Matthew Collier,(1827-91) farmer,Homemaker Osbaldwick

George(1828-30)

Buried, All SaintsNorth Street, York.

William = Frances Askham (1783-1846) (1789-1860)laborer, carman,farmer

Joseph(1788-??)

George(??-??)

John Ripley = Hannah Buckle = William Snow of Whixley. (1744-1827) (1754-1815) of Poppleton, farmer.

m2m1

John Buckleof Stillingfleet,

farmer.

m. 1812, Huntington parish.

Figure 1.5. Askham–Snow genealogy.

“several good houses” remaining from the previous century, but most houses wereapparently in various stages of disrepair and occupied by renters.11 Their neighborswere also general laborers, as well as watermen, cowherds, tanners, skinners, sail andflag makers, weavers, joiners, bakers, painters, merchants, and small manufacturers.12

William and Fanny Snow began their married life as a laboring family with theadvantages of literacy and connections to extended families with modest resources.13

On 15 March 1813 Mr. G. Brown, the minister at All Saints North Street since 1798,baptized “John son of William & Frances Snow,” born the same day.14 John’s birthoccurred ten months after his parents’ marriage; they had eight more children, threedaughters and five sons, over the course of fifteen years (Fig. 1.5) and maintainedattachments to their home parish throughout. They had ambitions for all their chil-dren and would provide each child with basic schooling. How an unskilled laboreraccomplished this feat is unclear. They had no prospects of a substantial inheritancefrom the Empsons, although the Upper Poppleton farm that may have been ownedby William Snow’s father would likely pass to their eldest son, but the in-laws couldhave provided some financial assistance during hard times.

There were notable changes in the family’s circumstances by the early 1820s. Thefirst indication was a change in William Snow’s occupation from unskilled to semi-skilled laborer sometime after the birth of his third son; the baptismal registers listhim as a carman from 1819 until 1828 (Table 1.1). Precisely what this occupationinvolved other than driving a cart is unclear. He may have worked for someone else,hauling goods from the quays on North Street to other parts of the city. He may haveinvested in his own rig and could have owned several. If so, he needed access to astable for the horses. Regardless of whether he worked for someone else or was aproprietor himself, William Snow’s income increased sufficiently from 1821 to 1823to allow him to move his family several blocks into “a row of new houses” on Welling-ton Row, an extension of North Street to the postern by the western wall.15 In 1824a William Snow appears in a county property tax register for St. Mary Bishophill Ju-nior, the parish to which Upper Poppleton belonged, as owner of land valued at


Table 1.1. William Snow’s occupational history and changes in family residence

Dates Occupation Residence

1812–1819 laborer North Street (rental?)1819–1821/23 carman North Street (rental?)1821/23–1825 carman Wellington Row (rental?)1825–1830 carman Queen Street (property holder)1830–1832 farmer Queen Street (residence unclear)1832–1846 farmer/landlord Queen Street (property holder)a

1841–1846 farmer Rawcliffe (purchased farm in 1841)

aCollected rents on four properties in Queen Street during this period.

Source: BIHR, PR Y/ASN 4; S. Snow, JS-EMP, 37.

nearly thirty-eight pounds, a substantial holding at the time.16 The likelihood isstrong that this person was John Snow’s father because the following year WilliamSnow purchased a home with some adjacent land on Queen Street, just outside thewall but still on the southwestern side of the Ouse. That is, the property in UpperPoppleton was apparently transferred to William Snow, which he used to purchasea house on Queen Street rather than move his family to the farm. His listed voca-tion remained carman until 1832, when he registered himself as a farmer when vot-ing in the first reform Parliament. He continued to live in Queen Street and collectedrent on four properties. In 1841 he purchased a farm in Rawcliffe that he workeduntil his death in 1846, aged 66.17

However, if William Snow hankered to farm while he was still a carman in the1820s, he might have done so long before he formally registered himself as a farmer.All inhabitants of Micklegate Ward had access to the ward’s “stray,” approximately500 acres of unenclosed pasturage southwest of the city. In addition, all residents ofYork could apply for the privilege of grazing cattle and horses throughout the yearon various moors and commons surrounding the city.18 It is entirely possible undersuch circumstances that before he bought property of his own on Queen Street,William Snow grazed the horses he used (or perhaps owned) as a carman on therough pasturage in Micklegate Stray and the encircling average grounds of Nun Ings,Campleshon, and York Fields. Such an arrangement would explain an otherwise puz-zling statement that John Snow, as a boy, “occasionally assisted his father in agricul-tural pursuits . . . [on] early winter mornings.”19

Snow’s Elementary School

William Snow’s vocation changed from general laborer to carman about the time hiseldest son was ready to enter an elementary school. State-subsidized, universal edu-cation did not begin in England until the 1880s, but York in 1819 had many peda-gogical institutions, public and private, that catered to the poor and laboring classes.20

Public meant that a school received substantial funding and direction from externalsources such as religious organizations, local government authorities, and philan-thropies. In York, for example, there were day schools administered by the Churchof England and a Blue Coat Charity School. Students attended such public schoolseither free of charge or for a very modest “school-pence.”21 There were also aboutfifty for-profit preparatory academies and at least thirty “private schools for the ed-ucation of the poor” (common day schools) operating in York between 1819 and1823, including two common day schools in the parish of All Saints North Street,which charged parents about six pence per week for each child enrolled.22 John Snowmight have attended one of these day schools.23 However, because there were alreadythree boys in the family queue behind John Snow and his parents were dedicated togiving all their children primary education, we think it likely that they would have


preferred to send him to a less expensive alternative, the Dodsworth School in a near-by parish.24

John Dodsworth, an ironmonger, founded three schools in York and establishedendowments that paid a teacher to instruct poor boys in reading and writing free ofcharge. In this respect Dodsworth Schools were philanthropic charities, but becauseparents paid fees for their children to be taught some subjects as well as the fact thatthe schools were administered locally by parish officials rather than centrally by theAnglican Church, Dodsworth Schools were private schools by contemporary stan-dards. In short, Dodsworth Schools were curricular equivalents to common dayschools, just less expensive.25 The charter for the school that had operated since 1803in a house adjacent to the Church of St. Mary, Bishophill Junior, required “that twentypoor children from the six parishes on . . . [the Micklegate Ward] side of the river,in proportion to their sizes, should be educated therein, free of expense.”26 The al-lotment for All Saints North Street was three. The Snow family’s long-standing con-nection with the parish church would have made their eldest son a suitable candi-date for admission. From 1824 to 1832 William Snow did a variety of odd jobs forthe church, and he became a warden in 1836.27 Therefore, if a space was availablearound 1819 and the vestry recommended him for it, we believe that the “privateschool in York” Snow attended was the Dodsworth School at Bishophill.28

On the assumption that Snow attended this elementary school, he would have tra-versed the heart of the ward twice every schoolday for eight years. A short walk fromhome along North Street lay the Ouse Bridge at the intersection with Briggate. Acrossthis major thoroughfare lay Skeldergate, a “narrow, and disagreeable street” alongwhich he would have continued east for one block. At the Elephant and Castle, a“commodious and respectable inn,” he would have turned south into “a narrow dirtystreet” called Fetter Lane. About 150 meters west, Fetter Lane intersected Bishophill.The Dodsworth School was sixty meters straight ahead, occupying the ground floorroom of a small house; the master lived above the school-room.29 The curriculum—”reading, writing, arithmetic, and the Scriptures, Church Catechism, and the use ofthe Prayer Book”—was similar to that offered by the private schools in the ward,with the possible exception of the absence of Latin.30 Every pupil was required to at-tend Sunday school in his home parish. The rector at All Saints North Street ran “aSunday School, supported by voluntary subscription, in which about forty-five boysare instructed,”31 so Snow’s Sunday school was independent of the Church ofEngland.32

Apprenticeship in Newcastle-upon-Tyne

As Snow approached his fourteenth birthday his parents began looking for a suit-able apprenticeship for him. It is unclear who suggested the unusual route of a med-ical career. In Suffolk, for example, about half the apprentices came from medical


families, while the remainder were sons of clergymen, farmers, gentlemen, and a scat-tering of artisans and tradesmen. Not a single apprentice was the son of a generallaborer or carman. In Bristol the distribution was similar to that in Suffolk, althoughthere were fewer sons of surgeon–apothecaries and more whose fathers were arti-sans; only one listed his father as a carrier.33 Similar studies do not exist for York,but by 1827 William Snow’s listed vocation no longer reflected his financial situa-tion as a property holder.34 The Snows could probably have afforded the indenturefee required for a medical apprenticeship in a provincial town.35

William Snow reached an agreement with William Hardcastle, a surgeon–apothecaryin Newcastle upon Tyne and close friend of Snow’s maternal uncle, Charles Emp-son. A native of York born in Micklegate Ward in 1794, Hardcastle was the son of acobbler. In 1808, aged 14, Hardcastle had been apprenticed to a licensed surgeon,William Stephenson Clark, who expanded his premises on Micklegate, the thor-oughfare that bisected the ward, to include an apothecary shop.36 When Hardcastlecompleted his indenture in 1814, he joined the practice of an established apothecaryin Newcastle upon Tyne. Two years later he traveled to London to take the lecturecourses and practical medical training necessary to become a Licentiate of the Soci-ety of Apothecaries. He continued his training for an additional six months with lec-tures in surgery and midwifery, as well as participating in surgical rounds at a Lon-don hospital, and then passed the examination that gave him membership to theRoyal College of Surgeons of London. Dual qualification as a surgeon–apothecarymade Hardcastle a general practitioner. He returned to Newcastle in the spring of1818 and purchased the practice of his former principal. Within a few years he wasappointed surgeon–apothecary to the Newcastle Lying-in Hospital, where he and twocolleagues shared duties as male midwives.37

Changing Medical Orders in England

Snow began his apprenticeship during a period of transition from local to nationalregulation of medical corporations. Medicine as a profession had been “incorporated”in England since the sixteenth century, when local authorities began delegating con-trol of occupational training and practice to guilds, or companies. The result in Lon-don and large towns was a tripartite division of medical activities similar to, if lessrigidly enforced than, many Continental versions. University-trained physicians diag-nosed and prescribed for “internal” complaints (medicine, or physic). Barbers and bar-ber–chirurgeons (surgeons) were considered the manual workers who performed ve-nesection and treated a variety of “external” conditions. Apothecaries—originallygeneral merchants and retailers in spices, drugs, and medicinal compounds who hadbecome specialty shopkeepers selling medicines and filling prescriptions written byphysicians—were considered tradesmen and the lowest of the three medical orders bypeople who believed the professions should be gentlemanly occupations.38


Local authorities of the City of London had given physicians and barber–surgeonscharters of incorporation to control their own affairs.39 Henry VIII created the Col-lege of Physicians of London, which gave its members independence from local au-thorities, but he refused their request for nationwide jurisdiction (Table 1.2). TheBarber-Surgeons of London remained a city company after unsuccessful lobbyingfor parity with the College of Physicians. In the next century the apothecaries wereseparated from the Grocers’ Company when James I chartered the Worshipful Soci-ety of Apothecaries of London, but independence came with a proviso: Londonapothecaries could fill prescriptions written only by physicians licensed by the Col-lege of Physicians.40

Surgeons did not extract themselves from their corporate affiliation with barbersuntil the mid-eighteenth century. Their practice premises became “surgeries” to dis-tinguish them from barber shops. They gradually replaced another corporate ves-tige, the apprenticeship, with formal schooling including anatomy lectures and dis-sections. In 1800 London surgeons shed their company status for good, becoming aroyal college with authority to establish requirements for anyone who sought itsdiploma and a license to practice in the City of London. The college had no juris-diction in the provinces, however, where competition with apothecaries and irregu-lar practitioners of all types remained the norm.

Surprisingly, the Worshipful Society of Apothecaries was the first of the Londonmedical orders to achieve nationwide authority. As late as the mid-eighteenth cen-tury, the apothecary’s vocation was considered an intellectually undemanding, albeitoften prosperous, trade.41 The Apothecaries’ Act of 1815 empowered a reorganizedsociety to establish licensing requirements for all apothecaries in England and Wales,to conduct examinations, and to monitor the behavior and services of its member-ship. Henceforth the apothecary’s duties were legally limited to compounding med-icines prescribed by a licensed physician. In the words of one angry critic, the apothe-cary was reduced to “the phisician’s cooke,”42 but compounding and dispensingbecame the exclusive purview of apothecaries under the act, which expanded pre-rogative distinctions among the three medical orders in London to all of Englandand Wales. As such, the 1815 act affirmed the physicians’ long-standing claim to ex-clusive treatment of internal (“constitutional”) diseases, and only licensed surgeonswere supposed to treat external diseases and perform surgical procedures.43

However, the Apothecaries’ Act of 1815 was a jerry-built dike, unable to containthe tides of medical convergence that had begun a century earlier. Part of the prob-lem was that licensed physicians, who constituted less than five percent of medicalpractitioners at the turn of the nineteenth century, were concentrated in London andthe larger provincial towns. Apothecaries continued to advise patients on how totreat internal complaints and to charge for such advice, either separately or absorbedin the cost of the medicines they dispensed. Among the middle and upper middleclasses, surgeons served similar functions. They attended patients presenting inter-nal and external complaints alike, they occasionally cut into bodies, and increasingly


Table 1.2. English medical orders: from London medical corporations to unified medical register

Physicians Surgeons Apothecaries

1518

College of Physicians of London (by charterfrom Henry VIII). Removed physicians fromcontrol by church authorities. Privilege togive licenses and right to suppress unli-censed practitioners of physic (medicine) inLondon and within 7 miles of the City.

1523

Royal charter reconfirmed. Authority overLondon apothecaries established.

1300–1540

Company of barbers (incorporated 1462) andGuild of Surgeons (not incorporated), Cityof London

1540

Company of Barber-Surgeons, City of London(no authority beyond City). Barbers andsurgeons maintained distinct functions; sur-geons could operate and treat external in-juries/complaints. Apprenticeship required.

1745

Company of Surgeons, City of London. Anat-omy schools evolved in response to theemergence of new hospitals in London.Apprenticeships gradually fell out of favor.

1800–1843

Royal College of Surgeons of London, Lin-coln’s Inn Fields. Apprenticeships not re-quired. Minimal formal training untilApothecaries’ Act of 1815, after which RCS developed parallel requirements forprospective members. Lectures must becompleted in London; hospital training inspecified metropolitan hospitals.

Medieval Times

Apothecarius (Spicer or Pepperer) became partof monarch’s retinue.

13th/14th centuries

Apothecaries joined Company of Grocers,City of London. Joint responsibilities forregulating the importation and sale ofdrugs, spices, and medicinal compounds.Apothecaries gradually specialized inpreparing medicinal compounds.

1523

Apothecaries in London and within 7 miles ofthe City permitted to fill only prescriptionswritten by licensed physicians.

1617

Worshipful Society of Apothecaries, City ofLondon (and 7-mile radius) (by charterfrom James I). Restrictions from 1523 re-mained in force.

Source: Adapted from Cope, Royal College of Surgeons; Copeman, Worshipful Society; Holloway, ApothAct; Porter, Greatest Benefit; SCME; Wall, London Apothecaries; Wall,Cameron, and Underwood, Worshipful Society of Apothecaries.

Anatomy Act of 1832

Medical profession permitted to use “un-claimed bodies” in dissecting rooms ofmedical schools.

1832

RCS recognized provincial medical schoolsthat offered curricula similar to what wasavailable in London, but at least six monthshospital training had to be completed inspecified metropolitan hospitals.

1843

Royal College of Surgeons of England.

1858

Medical Act established a unified register oflicensed practitioners, specified requirementsfor qualification, and created the GeneralMedical Council to investigate charges ofmalpractice and improper conduct.

1703

House of Lords ruled that apothecaries couldgive advice on internal complaints but couldnot charge for it.

1815

An Act for better regulating the Practice ofApothecaries throughout England and Wales(Apothecaries’ Act).

1834

In Woodward v. Ball apothecaries could mixmedicines prescribed by themselves. InApothecaries’ Co. v. Lotinga the apothecarywas defined as “one who professes to judgeof internal disease by its symptoms and applies himself to cure that disease by medicine.”

they advertised as male midwives. Surgeons who wished to augment their practiceswith the sale of medicines continued to do so after 1815 with little fear of prosecu-tion. Despite the provisions for distinct functions, the 1815 act actually furthered theemergence of the general practitioner by permitting dual qualification as surgeon andapothecary. When the Society of Apothecaries upgraded its curriculum for prospec-tive licentiates in the decades after the 1815 act, the Royal College of Surgeons of Lon-don was spurred to raise its standards for membership and, eventually, work with thesociety in developing a complementary training scheme. By the mid-1820s there wasa noticeable increase in the number of licensed surgeon–apothecaries such as Hard-castle—medical men who were Members of the Royal College of Surgeons (MRCS)as well as Licentiates of the Society of Apothecaries (LSA).44 Legal barriers to generalpractice in the 1815 act were eliminated by a series of judgments. By the mid-1830ssurgeon–apothecaries were essentially unrestricted in their practice opportunities, ful-minations from the Royal College of Physicians notwithstanding.45

However, when John Snow finished elementary school, the separation into threemedical orders mandated by the 1815 act was still in force. Dispensing drugs pro-vided the bulk of a practitioner’s income, so the prospective medical man in En-gland and Wales normally completed the requirements for a license from the Soci-ety of Apothecaries. The Society required a five-year apprenticeship, which Snowbegan under Hardcastle’s tutelage in June 1827.

Life as an Apprentice

It was some eighty miles from York to Newcastle, a journey of five or six days byfoot, or a day by coach, in 1827. Mail coaches were the safest mode of travel avail-able, because they carried armed guards to discourage highway robbers.46 A smoothturnpike linked York to Northallerton, a rough road traversed County Durham toGateshead, and then a short bridge took the traveler over the River Tyne to New-castle (Fig. 1.6). Like York, Newcastle was a walled town but had twice as many in-habitants. Hardcastle lived in a house at 52 Westgate Street, next to the Spital fieldby the western wall and directly opposite St. John’s Church. The accommodationswere spacious, including a personal apartment, surgery, and shop and a stable offthe courtyard behind the house.47

We have not located Snow’s actual indenture, but we assume it was similar to thestandard version used during the reign of George IV.48 By law, all masters were re-quired to feed their charges, while lodging, laundry, and tools of the trade were ne-gotiable. In turn, the medical apprentice was expected to serve his master “well andfaithfully,” to follow all “lawful Commandments,” to stay clear of alehouses, and toabjure from playing “Dice, Cards, [gambling] Tables, Bowls or any other unlawfulGames.”48a In addition, the apprentice was expected to accommodate to his master’sdomestic routine and remain a bachelor for the duration of his contract.


Typically, apprentices rose early enough to sweep the shop floor and set up forbusiness and were already washed and dressed for the day before eating breakfast.Shop tasks included much drudgery, such as washing bottles, maintaining an in-ventory of drugs, “dispensing” (filling prescriptions and running them to patients’houses), and keeping accurate ledgers. It was not uncommon for apprentices to di-agnose and dispense for anyone who could not pay for the master’s attendance. Suchpatients received medical advice for the cost of drugs alone. Many masters dictatedinformation about each patient’s age, occupation, constitution, living conditions, andpresenting symptoms that apprentices wrote in ledger books.49 Apprentices were alsoresponsible for delivering drugs to patients at all hours of the day and night.50 Afterseveral years apprentices often served as unsupervised assistants, making house calls,handling emergencies, and riding to mining villages if their masters were retainedby one of the local collieries. Thomas Giordani Wright, a senior apprentice from1826 to 1829 to the surgeon James McIntyre, with premises in nearby Newgate Street,recorded in his diary that he had set fractures, lanced abscesses, undertaken post-mortem dissections when the relatives would approve it, handled a bewildering ar-ray of accident injuries, pulled the occasional rotten tooth, and used a stethoscopefor auscultation. Such clinical encounters were over and above his usual routine ofcompounding medicines, treating childhood diseases, confronting the occasionalmeasles epidemic, and dealing with recurring bilious disorders.51


Figure 1.6. Newcastle upon Tyne from the south, 1827 (Wright, 16).

Snow left no first-hand account of his life as an apprentice, but there is evidencethat Hardcastle was a “progressive thinking” master rather than an exploiter of hisyoung charge.52 Progressive masters permitted their apprentices access to medicalbooks, made certain they observed and eventually treated a variety of clinical com-plaints, and released them from shop duties and rounds in order to receive formaltraining when possible. Thomas Wright’s master sent him to Edinburgh for somelecture courses, but McIntyre had a virtual stable of other apprentices to take up theslack. Hardcastle, it appears, had no apprentice other than Snow, which may explainwhy he did not send him to the nearest provincial medical school in Hull and Leeds,roughly 100 miles from Newcastle.53

In 1832 several Newcastle physicians and surgeons founded a medical schoolthat eventually was accredited by the Society of Apothecaries. The founders se-cured the use of “a large room over the entrance of Bell’s Court, Pilgrim Street,”above the consulting rooms and surgeries of three participating practitioners.They printed a prospectus of five courses for the forthcoming winter session tobegin on 1 October. Although nearly forty general practitioners worked in greaterNewcastle, only eight students enrolled, Snow among them. He was a senior ap-prentice with five years of experience, during which he had accumulated suffi-cient knowledge of Latin and Greek to begin formal training. Dr. George Fifeprobably had the best facilities for his course on materia medica and therapeu-tics, because Snow and his seven classmates had access to “a large physic garden.”The other instructors were Mr. H. G. Potter, who taught chemistry; Dr. SamuelKnott, who lectured on the theory and practice of medicine; Mr. John Fife, wholectured on surgery; and Mr. Alexander Fraser, who gave lectures on anatomyand physiology. The educational premises were less than ideal; there was no li-brary, the pathology museum contained few specimens, and there was no dis-secting room. Anatomical material was, in any case, hard to come by, despite theAnatomy Act of 1832, which had “awarded the medical profession rights to ‘unclaimed bodies,’ ” usually from workhouses and hospitals. When anatomical material did become available, public lectures and demonstrations were held in Surgeons’ Hall.54

As a complement to lectures, and for an additional fee, Snow attended clinical pre-sentations and “walked the wards” of the Newcastle Infirmary.55 In 1832–1833 thishospital contained 150 beds in renovated premises. Only patients with acute med-ical complaints or those requiring surgical treatment were admitted. The senior sur-geon was Thomas Michael Greenhow (1792–1881), a graduate of the University ofEdinburgh. He was also surgeon–apothecary at the Lying-in Hospital, where Hard-castle was on the staff. Hardcastle’s willingness to have Snow attend lectures at a nas-cent school of medicine and observe cases at the respected Newcastle Infirmary af-firm his progressive vision of what an apprenticeship should be and his confidencein Snow’s abilities.56


Uncle Charles Empson in Newcastle

Hardcastle’s practice extended beyond the town walls to include the mining villageof Killingworth connected to the West Moor colliery. For several years he was gen-eral practitioner for the family of George Stephenson, the pioneering mining andrailway engineer who invented the first steam locomotive, “The Rocket.” Hardcastledeveloped a close friendship with Stephenson’s son, Robert, and introduced him toCharles Empson, Fanny Snow’s half-brother. The three men were urbane, cosmo-politan, and pragmatic. All were members of the Newcastle Literary and Philosoph-ical Society.57

In 1824 a London firm asked Robert Stephenson to travel to Colombia to deter-mine if it was feasible to reopen several derelict gold and silver mines. He, in turn,engaged Empson, who was fluent in Spanish, to serve as translator, secretary, andadministrator for this exploratory venture.58 In the free time available during hisSouth American stay, Empson observed, collected many specimens of native floraand fauna, and made notes for a comprehensive journal of his researches. On the re-turn voyage in the summer of 1827, the ship was supposed to make a short stop inNew York but capsized on the shoals off Sandy Hook, New Jersey. All hands wererescued and deposited in New York City, but Empson lost most of his naturalist col-lection. Because no alternative conveyance was immediately available, he andStephenson walked to Montreal but found no ship bound for England there, either.Returning to New York, they found a packet ship bound for Liverpool, whereStephenson’s parents had moved in the interim so his father could supervise con-struction of the Liverpool–Manchester Railway.59

Robert Stephenson decided to return to Newcastle, and Empson also settled in thetown in which his nephew had lived for half a year as an apprentice. In 1830 he be-came a dealer in antiques, old books, and paintings, opening a shop on CollingwoodStreet, just a few blocks from Hardcastle’s home. He advertised as a bookseller andstationer, and within months his shop became a virtual museum of fine art and nat-ural history collections (Empson’s speciality was shellfish), as well as a meeting placefor local literati, naturalists, gentry, professionals, and commercial folk. A dapperdresser,“He usually wore full dress-black cloth and ruffled shirt, and in warm weatherhe wore a white waistcoat, white trousers and a white hat” (Fig. 1.7) He was an en-gaging conversationalist. He actively promoted the artistic interests of local youthsand offered tuition-free drawing lessons to some poor students and modest schol-arships to others. Meanwhile, he prepared a series of colored sketches of Colombianlife and an accompanying travel narrative.60

It is unclear how often Snow joined his uncle and two friends on social occasionsduring his six years as an apprentice, or how his elders responded to his increasinglyindependent thinking about medicine, health, and life, but it seems certain thatCharles Empson provided Snow access to higher social circles than he might have


expected given his mother’s illegitimacy and father’s early laboring-class occupations.Like York itself, the Snow family was in social flux in the early nineteenth century.Uncle Charles was a mysterious figure but central in expanding the Snow family’sconnections, establishing them in the middle class, and facilitating his nephew’s ap-prenticeship with Hardcastle. In many ways, then and later, Empson may have madeSnow’s medical career possible.

Notes

1. Armstrong, Stability and Change, 16–36; G. Benson, City and County of York, 88–91, 101.Hargrove, York, 2: 197–206; Tillott, VCH-Y, 256–62, 517, and S. Snow, JS-EMP, 20–21, 24.

2. The Industrial Revolution would not envelop York and the surrounding region until the1840s, when the city became an important railway hub. Rail service to London did not com-mence until 1840. For administrative purposes, the city lumped parishes into four wards:Monk, Walmgate, Bootham, and Micklegate. The wards were responsible for paving, sanita-tion, and resolving interparochial disputes; wards were also the basic administrative unit inYork’s civil government. The lord mayor regularly perambulated all lands outside the walled


Figure 1.7. Charles Empson (courtesy of Anthony Snow;

black and white reproduction supplied by David Zuck).

city on which York’s citizens enjoyed rights of pasturage to reconfirm the city’s “ridden bound-aries”; see Tillott, VCH-Y, 315–18. On the administrative structure of York, see Tillott, VCH-Y, 311–15; and Hargrove, York, 1: 308–36.

3. Tillott, VCH-Y, 210–11, 281–82, and Armstrong, Stability and Change, 117–23.4. Armstrong, Stability and Change, 117–18; Tillott, VCH-Y, 254. Information about pub-

lic health and sanitation problems in York is impressionistic until the cholera epidemic of1832, when residents of North Street were among those first affected. The earliest systematicsurvey of sanitary arrangements, housing, and water supply in York was undertaken by ThomasLaycock for the Commissioners Inquiring into the State of Large Towns and Populous Districts; his report was included in the Commission’s First Report (1844). See also S. Snow,JS-EMP, 22–23.

5. She gave birth to two more children, although the last died as a toddler. The survival ofeight children to adult life in the first half of the nineteenth century is remarkable by any mea-sure, but especially so in light of Laycock’s estimate that until 1831 the mortality rate for chil-dren aged 5 and under in the parish of All Saints North Street was 44%; UK Parliament, FirstReport 1: 106 (Table 17). In 1813 the mean age of death in York was 32 years. Mean age ofdeath was slightly lower (29 years) in the parish of All Saints North Street. The Snows’ suc-cess in child rearing suggests a home in which breastfeeding was prolonged, postweaning nu-trition more than adequate, and standards of personal hygiene exceptional.

6. We follow family custom by referring to John Snow’s mother as Fanny Snow. Her homeparish of Ledsham lay twenty miles south of York. The baptismal entry for 15 February 1789reads, “Fanny, daughter of Mary Askham of Fairbourn, base born”; cited in Galbraith, JS-EY,8. Fairburn lies just south of Ledsham village. For the marriage entry of John Empson andMary Acomb, a variant spelling of Askham, see H. Richardson, Parish Register of Acomb, 85.We thank Spence Galbraith for alerting us to this source. John Empson noted in his will thatFanny was “my natural daughter”; BIHR, “Last Will and Testament.”

7. Thompson, Rise of Respectable Society, 199–200.8. For genealogical details, see Zuck, “Charles Empson,” 3; Galbraith, JS-EY, 8–9;

H. Richardson, Acomb, 101, 104, 122, and 124.9. BIHR, PR HUN 6, cited in Galbraith, JS-EY, 18. A signature is a vague indicator of lit-

eracy, but “it is usually taken to show the ability to read fluently and to write laboriously”;Digby and Searby, Children, School and Society, 3.

10. Sims, “Family history”; Leaman, “John Snow MD,” 803; S. Snow, JS-EMP, 23. However,a search of the marriage register covering 1750 to 1812 for All Saints North Street by Ms.Davison of BIHR found no entry for William and Hannah Snow; BIHR, PR Y/ASN 6. In ad-dition, the surname Snow does not appear in All Saints North Street baptismal registers; BIHR,PR Y/ASN 2 and 3. Galbraith may have solved the mystery when he located a baptismal en-try from 1788 in the register for St. Mary’s, Bishophill Junior, that listed William Snow, farmerof Upper Poppleton, and Hannah (Buckle) Snow, daughter of a farmer in Stillingfleet, as par-ents of Joseph Snow; JS-EY, 7; William Snow, the younger, born in 1783 (according to hisgravestone), apparently had a brother named Joseph. Although S. Snow states (JS-EMP, 23)that William Snow, the younger, was baptized at All Saints North Street in 1783, neither Gal-braith nor the staff at BIHR could locate such an entry in that register (PR Y/ASN 2).

11. The 1818 description of North Street is from Hargrove, York, 2: 186–87. The exact lo-cation of the Snow residence in North Street is unknown; see Galbraith, JS-EY, 22–24. For aview that it was a house by a coal yard near the present position of the Viking Hotel, see A.Leaman, “John Snow MD,” 803; and Galbraith, JS-EY, 24.

12. The baptismal register suggests that occupations associated with the respectable poorpredominated in the parish; BIHR, PR Y/ASN 4. See also Ashcroft, “John Snow,” 246. How-


ever, Baines’ Directory & Gazetteer for 1823 lists more than a score of artisans, merchants, andsmall manufacturers on North Street; see Galbraith, JS-EY, 61.

13. John Empson’s estate was settled in 1850 for less than £100; BIHR, “Last Will and Tes-tament”.

14. BIHR, PR Y/ASN 4. The first page of this parish register lists eight infants born be-tween late January and mid-March 1813; all but one were baptized on the day of or within aday of birth. No street numbers are given.

15. At Thomas’ baptism on 25 February 1821, the Snows resided on North Street; at Mary’sbaptism on 2 March 1823, they resided on Wellington Row; Ibid., entries 261 and 339. Thedescription of Wellington Row is from Hargrove, York, 2:186.

16. Galbraith, JS-EY, 24.17. S. Snow, JS-EMP, 25.18. There were also fields with “average,” or half-year, rights of pasturage between Michael-

mas (in October) and the Annunciation (usually in late March); the rest of the time, thesefields were used for crops. The York corporation administered commons and average landsthrough the four wards. Aldermen hired pasture-masters and set limits on “rights of stray”—whose stock, which kinds, and how many could graze in each field and moor, including thoseareas specifically designated as ‘strays’; Tillott, VCH-Y, 498–504; and Richardson, L, ii.

19. Richardson, L, ii, and Thompson, Rise of Respectable Society, 131.20. In 1818 approximately one-quarter of English children were receiving some form of el-

ementary education, and most of that was vocationally oriented; see K. Evans, English SchoolSystem, 24. The percentage seems to have been higher in York, in which charitable and pri-vate institutes can be traced to the late eighteenth century and a limited manufacturing sec-tor kept child labor to a minimum; see E. Benson, “Education in York,” 22. In 1819–1820 about1,300 children attended day schools, whether public or private, in York; E. Benson, “Educa-tion in York,” 134–35.

21. Pedagogy in day schools administered by the Church of England National Society forPromoting the Education of the Poor (the National Schools) was based on the monitorial sys-tem, under which older pupils led younger pupils in group reading and recitation as well ascirculating among the desks as “monitors” when their charges practiced penmanship andmathematics. To support National Schools throughout the country, local congregations heldsubscription drives, donating the proceeds to the parent societies, which in turn sponsoredlocal schools offering basic instruction in the three Rs and religion for children from the work-ing and lower middle classes. Because subscriptions were theoretically voluntary, recipient in-stitutions were frequently referred to as “voluntary” schools. When imposed, the “schoolpence,”a certain amount of money per child payable in weekly or quarterly installments, was a pre-servative against the taint of charity; see Hurt, Education in Evolution, 14–17, and Thompson,Rise of Respectable Society, 143. In York about 440 pupils were enrolled in the Manor NationalSchool “for the education of the poor, in the principles of the church of England”; see Tillott,VCH-Y, 449, and Hargrove, York, 2: 581–82.

Other schools under denominational control, such as cathedral and grammar schools, werealso considered public. In York Haughton’s School was available only to pupils who residedin St. Croix parish; see E. Benson, “Education in York,” 40, and Hargrove, York, 2: 664–65. Agrammar school on St. Andrew Gate, descended from the cathedral school founded in theseventh century and known today as St. Peter’s, had twenty boys enrolled in 1818 who re-ceived instruction in “‘the realm in knowledge of letters and integrity of manners’”; quotedin E. Benson, “Education in York,” 39. See also Hargrove, York, 2: 362–64. Archbishop Hol-gate’s grammar school had free places for some “foundation scholars,” while others paid fees;see Hargrove, York, 2: 135–36. “These two free grammar schools, which drew their pupils al-


most entirely from within the city, were the sole representative at that time of the higherschools that taught the classics and prepared students for residence at Oxford and Cambridge”;E. Benson, “Education in York,” 40.

Charity schools were financed by subscription and administered by leading men and womenof a town or county. York in1818 had at least two such schools: the Blue Coat Charity School,with places for fifty-six boys, and Wilson’s Green Coat Boy’s Charity School, which boardedtwenty pupils from the parish of St. Denis; see Tillott, VCH-Y, 443 and 458. See also Har-grove, York, 2: 350–54 and 289–90, and E. Benson “Education in York,” 41–49, 97–106.

22. Only one of the private academies and institutes in York, most geared for middle andupper classes, was located in Micklegate Ward; see E. Benson, “Education in York,” 107–25.The number and nature of common day schools is based on reports by parish rectors in 1818;UK House of Commons, “Digest of Parochial Returns,” Sessional Papers, 1819, vol. 9, no. 2,County of York, East Riding. Average enrollment in each school was between twenty and thirtypupils. The typical school consisted of a single room in a private house. Most offered in-struction to boys and girls of varying ages, without sex segregation; only two were limited togirls. The two common day schools in the parish of All Saints North Street served a total ofsixty children.

23. According to Richardson, Snow was “sent to a private school at York”; L, ii. To date noone has located his name on any list of pupils in the city. Ellis was the first to suggest that itwas a “private school for the education of the poor,” otherwise known as a “common dayschool”; CB, xii.

24. For the alternative suggestion that Snow may have attended a Quaker school, see A.Leaman, “John Snow,” 803–04, and Shephard, JS, 17. The first Quaker school for boys in Yorkwas a private school, but it did not open until October 1822 and appears to have been lim-ited to sons of affluent Friends. The (public) Friends’ Bootham school for boys was not foundeduntil 1828; see E. Benson, “Education in York,” 114, 126–28. For the possibility that Snow waseducated at St. Peter’s grammar school, see Ashcroft, “John Snow,” 247. But Benson states thatpupils at this school were being groomed for Oxford and Cambridge; “Education in York,”40. According to Ellis, Richardson’s assertion that Snow was privately educated “has, erro-neously, been taken by some commentators to imply that Snow received an expensive educa-tion at an institution analogous to a present-day British public school”; CB, xii.

25. Lawson, Education in East Yorkshire, 9, states that contemporaries did not make sharpdistinctions among endowed and private schools when the former required modest fees; seealso P. Gardner, Lost Elementary Schools, 15–16. Fees at common day schools varied from 3 to9 pence per week (1–3 shillings per month, because 12 pence � 1 shilling, 20 shillings � 1pound); see P. Gardner, Lost Elementary Schools, 12, 16. If Snow attended the DodsworthSchool, his parents paid only 2 shillings per year for instruction in mathematics plus extrafees for rudimentary training in Latin, at least. The difference was considerable, especially bythe mid-1820s, when the Snows had four school-age boys. All received primary schooling.William Snow (born 1815) became a hotel keeper and a tailor/hatter, Thomas Snow (born1817) a vicar, and Robert Snow (born 1819) a secretary/manager of a colliery. Two daughtersalso received an education adequate for them eventually to become heads of their own sem-inary for girls. S. Snow, JS-EMP, 50–58, discusses Snow’s brothers and sisters in detail. Thewillingness of the working poor to pay for the education of their children is also noted byDigby and Searby, Children, School and Society, 5, and is discussed in detail by Laquer, “Work-ing-class demand and the growth of English elementary education.”

26. Hargrove, York, 2: 157. See also Tillott, VCH-Y, 445–46.27. Churchwarden’s Accounts, All Saints North Street, 1818–45 (PR Y/ASN 12), BIHR, cited

in S. Snow, JS-EMP, 48, 27.


28. Hargrove, York, 2: 157; Lawson, Education In East Yorkshire, 12; and E. Benson, “Edu-cation in York,” 69, 93–95. There is a family story that William Snow worked in Dodsworth’scoal yard as a young man, and on this basis S. Snow thinks it possible that Snow attended aDodsworth School, although she does not specify which one; see JS-EMP, 32.

29. Hargrove, York, 2: 186 (North Street), 168 (Skeldergate), 172 (Elephant and Castle), 172(Fetter Lane).

30. E. Benson, “Education in York,” 94.31. UK House of Commons, “Digest of parochial returns,” Sessional Papers, 1819, vol. 9,

no. 2, 1075.32. On the attraction of schooling in general, Sunday schools in particular, for working-

class parents “dedicated to self-respect and respectability,” see Thompson, Rise of RespectableSociety, 139–41.

33. Van Zwanenberg, “Apothecaries in Suffolk,” 141, 149; Loudon, GP, 29–31.34. S. Snow, JS-EMP, 37, 71–72. For typical occupations of the fathers of medical appren-

tices, see Loudon, GP, 256–59.35. In the early nineteenth century medical indentures outside London generally cost be-

tween £100 and £200; see Loudon, GP, 41–42; Peterson, Medical Profession, 69–70; and Digby,General Practice, 43. S. Snow states that the Snows paid £100 for their son’s indenture, but thesource she cites does not give a fee; JS-EMP, 72.

36. Clark had attended medical school in London and qualified as a Member of the RoyalCollege of Surgeons in 1804; see Galbraith, WH, 155–57.

37. Galbraith, WH, 157; Society of Apothecaries, Records, Ms 8241/1, 213.38. In the eighteenth century some provincial apothecaries were still members of mercers’

guilds (dealers in textiles); Burnby, English Apothecary, 14–15.39. The City of London occupies about one square mile, largely within the area encom-

passed by the original Roman walls, including the Tower of London and St. Paul’s Cathedral.Beyond the City lay various “liberties,” such as Westminster, considered part of the metropo-lis.

40. Background on medical organization and care in England is derived from Webster, Car-ing for Health, 25–32; Clark, Royal College of Physicians, 2: 476–79; Cope, College of Surgeons;Copeman, Worshipful Society; Wall, London Apothecaries; Wall, Cameron, and Underwood,History of the Worshipful Society; Waddington, Medical Profession, 1–4; Newman, Evolution ofMedical Education, 1–21; Peterson, Medical Profession, 5–21.

41. A mid-eighteenth century-commentator offered a deprecating description: “His Knowl-edge, by his Profession, is confined to the Names of Drugs, of which he is not so much as tounderstand the Etymology; he must only know that Rhubarb is not Jesuit’s Bark, that Oil isnot Salt, and that Vinegar is not Spirit: He must be able to call all the Army of Poisons bytheir proper Heathenish Names, and to pound them, boil them, and mix them into theirproper Companies; such as Pills, Bolus’s, Linctus’s, Electuaries, Syrups, Emulsions, Juleps, &c.&c. He must understand the Physical Cabala, the mysterious Character of an unintelligibleDoctor’s Scrawl”; Campbell, London Tradesman, 64. The apothecary’s “profits are unconceiv-able; Five Hundred per Cent. is the least he receives”; Ibid., 64.

42. J. Cordy Jeaffreson, A Book about Doctors (1851), 70, quoted by Holloway, ApothAct,127.

43. Holloway, ApothAct, 124–25. See also Newman, Evolution of Medical Education, 58–79;and Peterson, Medical Profession, 20–23.

44. Waddington, Medical Profession, 2; Loudon, GP, 13–28. Loudon also argues that sur-geon–apothecaries normally served a wide range of social classes wherever physicians werenot plentiful and therefore enjoyed greater incomes than pure apothecaries; GP, 114. See also


Bishop, “Evolution of the general practitioner,” in Underwood, Science and Medicine in His-tory, 2: 350–54; Reader, Professional Men, 1–58; and Peterson, Medical Profession, 10–11, 60–61.Apothecaries practicing before the 1815 act were exempted from qualifying examinations andcalled “pre-1815 medical men.”

45. Loudon, GP, 189–94; Holloway, ApothAct, 221–23; in Apothecaries Co. v. Lotinga(1834), “Justice Cresswell felt justified in defining an apothecary as ‘one who professes to judgeof internal disease by its symptoms and applies himself to cure that disease by medicine’”(222).

46. In York the Wellington departed the Black Swan General Coach Office on Coney Streetevery evening at 9:30. A Royal Mail stage coach departed from the tavern on St. Helen’s Squareevery midnight. In Newcastle the private and postal coaches stopped at Loftus’ Turf Hotel andthe Queen’s Head Inn, respectively. See Hargrove, York, 2: 671–74; Dyos and Aldcroft, BritishTransport, 76; Simmons, Transport, 38–41; Tillott, VCH-Y, 475–77.

47. Galbraith, WH, 157–60.48. His apprenticeship began on 22 June 1827; Society of Apothecaries, Court of Examin-

ers’ Entry Book, Ms 8241/10, 61. The standard indenture was a printed form that listed ex-pected duties and obligations, with spaces to enter names and particular details; see Walker,“Surgical apprentice,” 68–70, and Digby, General Practice, 43.

48a. Walker, “Surgical Apprentice,” 68.49. Loudon, GP, 39, 46–47, has generalizations about the daily routines of apprentices dur-

ing this period. S. Snow, JS-EMP, 78–91, contains examples of the apprenticeship experiencefrom several contemporaries, including James Paget. Paget’s recollections in their entirety arein S. Paget, Memoirs and Letters, 19–30.

50. Gas lamps were installed within the town walls of Newcastle in the mid-1820s, but sub-urban roads remained unlit; Charleton, Newcastle Town, 427.

51. See also Wright, Diary of a Doctor, containing excerpts from records kept by a seniorapprentice in Newcastle from 1826 to 1829.

52. The phrase is taken from Ellis, CB, xv. See also Loudon, GP, 45. Nothing indicates thatSnow fit the image of “a downtrodden, aproned lad whose life was spent behind the counterof the shop or in a backroom, washing bottles and making up the stocks of medicine, work-ing late into the night” because his master was “selfish and negligent in the performance” ofhis responsibilities; Loudon, GP, 44.

53. For a contemporary view of what a progressive master would teach his charges, see T.Turner, Outlines of Medico-Chirurgical Science, 4, 10. See also Reader, Professional Men, 119.In 1815 there were no authorized provincial medical schools in England; in 1832 there wereeight. See UK House of Commons, SCME (1834) 602-III, appendixes 27 and 23, and Anning,“Provincial medical schools,” in Poynter, Evolution of Medical Education, 124.

54. Turner and Arnison, Newcastle School, 13–20; SCME (1834) 602-III, appendix 27. In 1834the medical college secured better quarters and officially inaugurated itself as a teaching insti-tution, enrolling twenty-six students and adding lectures in midwifery, medical jurisprudence,and botany. The school continued to flourish, survived a schism among its faculty between 1851and 1857 (when there were two rival medical schools in town), and affiliated with the Univer-sity of Durham, after which it could bestow the degree of MD. Quotation about Anatomy Actfrom Porter, Greatest Benefit, 318. Thomas Wright attended a series of lectures at Surgeons’ Hallin March 1829 when John Fife was demonstrating “on the brain of the criminal” hung after be-ing found guilty of murder; Wright, Diary of a Doctor, 69–70.

55. Richardson, L, vii.56. Greenhow did not join the faculty of the new medical school in Newcastle until after

its merger with Durham University in 1852, when the institution could confer the MD


degree. On Greenhow’s futile attempts to set up a university in Newcastle, see Turner and Ar-nison, Newcastle School, 14–16.

57. Galbraith, WH, 161; memberships in Literature and Philosophical Society confirmedby Zuck. Thomas Wright was also a member of the Literary and Philosophical Society, somedical apprentices and assistants could join; Wright, Diary of a Doctor, 84–86. According toKay Easson, librarian to the society, Snow does not appear among the new members addedbetween 1827 and 1833; electronic communication to David Zuck, 20 May 2002.

58. Zuck, “Charles Empson”, and Galbraith, WH, 161.59. Zuck discusses Robert Stephenson and Empson’s fascinating voyage to Colombia in

“Charles Empson.” George Stephenson had also served as the railway engineer during con-struction of the Stockton–Darlington Railway while his son and Empson were in SouthAmerica.

60. R. W. Heatherington, “Newcastle fifty years ago,” Newcastle Weekly Chronicle (17 No-vember 1883), reprinted in Galbraith, JS-EY, 62–63; quotation from 62. See also WH, 162.The most complete scholarly study of Empson is Zuck, “Charles Empson.” See also Empson,Narratives, 1836 and the accompanying Portfolio. Empson was and remained a bachelor.Stephenson married after his return from South America. In 1830 Hardcastle married AnnPhilipson; Empson appears to have been one of the witnesses.


SNOW WAS SEVENTEEN WHEN he read John Frank Newton’sessay The Return to Nature: A Defence of the Vegetable Regimen. The

argument convinced him that a vegetarian diet would reduce irritation of the intes-tines and promote personal health. Newton’s form of vegetarianism included a fas-tidious attention to drinking water, purifying it by distillation and testing its puritychemically. Newton’s essay convinced Snow that diet, pure water, and a healthy colonwere essential to one’s well-being.1

Newton wrote Return to Nature to popularize an “important discovery” by thephysician William Lambe. Newton, a lawyer, believed that Lambe had shown that allmedical and social problems result from “the dire effects on the human frame of an-imal food, cooperating with that baneful habit, the use of water, or of somethingmore pernicious [fermented drinks], to allay the thirst which that food occasions.”When Newton shifted to a “regimen of distilled water and vegetable diet,” his chronicintestinal distress disappeared within two years. In gratitude he wrote Return to Na-ture to make Lambe’s hypothesis known to a wide audience.2

The unifying assumption in Newton’s essay is that an Edenic fare of fruits andvegetables was created for human consumption and is essential for a full and healthylife span. After the Fall and the discovery of fire, however, humans increasingly par-took of cooked meat. The die was cast: “Thirst, the necessary concomitant of a fleshdiet, ensued; water [often polluted] was resorted to, and man forfeited the inestimable

39

Chapter 2

Senior Apprentice andAssistant, 1830-1836

gift of health which he had received from heaven: he became diseased, the partakerof a precarious existence, and no longer descended slowly to the grave.” Newton thenoffered additional evidence to substantiate his scriptural premise that vegetables (ashe called all plant products) are our only natural food, whereas animal flesh is un-natural and unhealthy.3

One who consumes a healthy plant diet needs only an occasional drink of water,but if the water is impure the vegetable diet is undermined. Modern humans hadfouled the natural world to such a degree that “common water” near large settle-ments was invariably impure. In large metropolises like London and Paris, only dis-tillation was foolproof. “Our own Thames water,” said Newton (who lived in ChesterStreet, Belgravia, London), was so polluted by “animal oil” and “septic matter” thatevery household should use a distillation apparatus such as he had constructed andplaced in his own kitchen. Newton discarded the first three gallons of distillate, keptthe next ten to twelve gallons of “almost imputrescible” water, and stopped the pro-cess when three or four gallons remained at the bottom of the still because of the“residuary filth” it contained. Before drinking he undertook “a test of the purity ofwater, familiar to every chymist. Drop into a glass of water a few drops of nitrate oflead.”4 If properly distilled, the fluid should remain clear; if it turned cloudy, he re-peated the distillation.

The recommended breakfast consisted of “dried fruits, whether raisins, figs, orplums, with toasted bread or biscuits [preferably without butter], and weak tea, al-ways made of distilled water, with a moderate portion of milk in it.”5 For childrenthe tea was replaced by diluted milk. A typical dinner was “potatoes, with some othervegetables, according as they happen to be in season [in a sauce of Portuguese onionsand walnut pickle]; macaroni; a tart, or a pudding, with as few eggs in it as possi-ble: to this is sometimes added a dessert. . . . As to drinking,” Newton cautionedthat “we are scarcely inclined on this cooling regimen to drink at all; but when it sohappens, we take distilled water.”6 At the time (1811) twenty-five people were ac-tively practicing this regimen, including seven in Newton’s own household. The re-sults were promising: All were in good health, use of medicines was rare, and indis-positions, if any, were trifling. Because he had tested the vegetable and distilled waterregimen on himself, his family, and several friends, he claimed that it “rests on theonly firm basis of philosophical conclusions, on Experiment.”7

It took Snow several years to find a situation in which he could fully imple-ment Newton’s regimen, but then he adhered to it rigidly for nearly a decade andin a modified form for the rest of his life. Obtaining pure water became a dom-inant element in his personal life and affected his view of public water supplies.Perhaps the prevalence of impure drinking water in his childhood town primedhim as a teenager for Newton’s alternative. Certainly, when in 1848 he altered hisviews on the pathology of cholera, he was intellectually predisposed by Newton’sideas to consider the intestines a primary site of infection and impure water a po-tential source of morbid poisons. Nevertheless, when epidemic cholera first


reached England in 1831, he assumed, like everyone else, that it was contractedby inhalation or contact.

Snow and Cholera, 1831–32

As the familiar adage emphasizes, Newcastle was a coal town. Hardcastle’s practiceincluded people whose livelihood depended on the extraction, transport, and tradeof this fuel, essential for the industrial revolution that had been changing the land-scape and social structure in Northumberland county for half a century. He was themine doctor at Killingworth, a company village owned by the “Grand Allies”—threewealthy families who also had extensive mineral holdings in County Durham southof the River Tyne. When Snow moved to Newcastle in 1827, the coalfield close totown was largely depleted, but it was still in full production beyond a three-mile arcnorth of the Tyne, including the mines near Killingworth, which lay five miles northof central Newcastle.

Except for those who had had military or administrative service in India and thosewho had recently traveled to eastern Europe or Scandinavia, no English medical manhad seen a case of Asiatic cholera until 1831. When several people became ill in theport of Sunderland early that fall, observers from the local board of health were un-sure whether the disease was the endemic English, bilious, or summer cholera (in-terchangeable names for common diarrheal diseases) or the feared Asiatic cholerafrom abroad. However, as a precautionary measure against noxious vapors, or mi-asmas, lime was spread on the streets. When a Newcastle man died early in Novem-ber 1831, three surgeons, including Mr. Greenhow of the infirmary, assured the mayorthat there was no cause for alarm, because the “efficient cause” of cholera (presumedto be a miasma in the atmosphere) settled only in low-lying areas and was not con-tagious. Most of Newcastle was situated at an altitude considered safe. Consequently,Greenhow assumed the man who died must have contracted cholera elsewhere andwould remain an isolated case.8

However, on 7 December 1831 Newcastle’s medical men officially confirmed thatAsiatic cholera was indeed present in the town. Thereafter, the disease appeared invillages and towns throughout Northumberland and the adjacent county of Durham.The colliery villages were especially hard hit: “The majority of the houses were twoor three roomed, terraced and built in rows. They were cluttered with sheds for pigsand poultry.” It was generally thought that overcrowding and manure produced anunwholesome air that facilitated the transport of the morbid poison of cholera, aswell as other epidemic diseases, to its victims. Newburn, a mining village of 131houses with 550 inhabitants, was decimated by fifty-five deaths among 320 choleracases in the middle of January 1832. On Christmas day in Gateshead, across the Tynebridge from Newcastle, “nearly fifty different cases occurred almost at the same in-stant.” When word of outbreaks in the collieries, river ports, and Gateshead reached

Senior Apprentice and Assistant, 1830–1836 41

London, the Central Board of Health sent medical agents to the Tyne region. Theyfound walls placarded with a variety of handbills. Some implored people to reportall suspicious illnesses; others suggested preventive potions and measures, soundedalarms, or appealed for calm in the midst of chaos. The medical men from Londonhad no authority to intervene in local affairs, so they left the town to its own de-vices. Those who believed a mild winter had caused such a rapid diffusion of thedisease felt vindicated when, early in February, the temperature dropped and the epi-demic seemed to be over.9 Even so, new cases popped up early in the summer, andit was soon apparent that the epidemic had temporarily abated rather than ended.According to the Poor Law in place since the sixteenth century, parish authoritieswere responsible for sanitary measures related to the epidemic and for medical treat-ment for the destitute. On 7 August 1832 the vestry of St. John’s appointed Hard-castle and another surgeon as Poor Law medical officers for the duration of the cri-sis. Shortly thereafter, cholera was reported in another part of Hardcastle’s bailiwick,the mining village of Killingworth, which had been spared a “visitation of cholera”in 1831. Because he could not be in two places at once, he sent Snow to Killingworthas his unsupervised assistant.10 Snow was responsible for medical treatment for every-one in the village, but he appears to have remained on the surface and never ven-tured below ground.11

Burnop Field

Crossing the bridge over the River Tyne between Newcastle and Gateshead, Snowturned southwest into the road to Stanhope in County Durham. After seven mileshe reached Burnop Field, a village of about 100 houses. It was early April 1833 andSnow was about to become the assistant to a rural apothecary.12 A few years as anassistant would permit him to save money toward the two years of schooling in Lon-don he needed to become a licensed practitioner in his own right.13 He could prob-ably have found a position in Newcastle, but the town may have held little attrac-tion for him once his uncle moved to Bath early in 1833.14 Snow’s new employerwas John Watson, a “pre-1815 medical man” without formal training who had es-tablished his practice before the Apothecaries’ Act became law. He lived in Burnop-field Hall, a spacious house on Front Street in the center of the village. Snow’s po-sition included a room in the house and board. Mr. Watson and his wife, Jane(Toward) Watson, had five children ranging in age from one to thirteen.15 Watsonwas in his mid-forties, and Snow now probably met him for the first time. It wasnot uncommon for rural practitioners in Northumberland and Durham to adver-tise for an assistant in Newcastle newspaper, after which an agreement could bereached by post.

Watson had very different attitudes about managing a practice than Hardcastle.Snow was in for a shock:


I found his surgery in a very disorderly state, and thinking on my first day withhim that I would enhance myself in his opinion by my industry, I set to work,as soon as his back was turned, to cleanse the Augean stable. I took off mycoat, cleared out every drawer, relieved the counter of its unnecessary cover-ing, relabelled the bottles, and got everything as clean as a new pin. When thedoctor returned, he was quite taken by storm with the change, and commencedto prescribe in his day book. There was a patient who required a blister, andthe worthy doctor, to make dispensing short, put his hand into a drawer toproduce one. To his horror, the drawer was cleansed. Goodness! cried he, whywhere are all the blisters? The blisters, I replied, the blisters in that drawer? Iburnt them all; they were old ones. Nay, my good fellow, was the answer, thatis the most extravagant act I ever heard of; such proceedings would ruin aparish doctor. Why, I make all my parochial people return their blisters whenthey have done with them. One good blister is enough for at least half a dozenpatients. You must never do such a thing again, indeed you must not.

L, xxxiv

This anecdote shows that Snow was organized, energetic, and impetuous. His de-sire to bring order to a chaotic shop obscured the diplomatic nicety that it wouldhave been appropriate to consult his principal first and to follow his instructions.16

The purpose of counterirritation, whether via blistering, cupping, or the insertionof setons (usually threads or horse hairs placed under the skin) was to concentratewhatever irritation was causing a local inflammation or mild fever, then draw it fromthe body.17 When the blister had accomplished its intended purpose, the doctorlanced the swollen skin and judged by the appearance of the discharge whether theapplication had diverted the humor from the worrisome inflammation.18 In short,Snow as an assistant seems to have considered blisters an acceptable therapy undercertain circumstances. His Case Books show he prescribed blisters, liniments, and setons in the 1850s.19

The blister anecdote reveals that Watson was a “parish doctor,” which in 1833meant that a significant percentage of his practice included people too poor to payhim directly for treatment. The Parish of Tanfield paid him a retainer to care for“parochial people”—“the destitute, aged, infirm or sick . . . supported by a poorrate levied on householders in each parish.”20 Like most general practitioners at thetime, Watson probably counted on trade in drugs for much of his income. It wasusual to send fee-paying patients itemized bills of attendances and therapeutics everyquarter, and Watson must have had a substantial number because the nearby Burnop-field Colliery employed many of the men in the village. Receiving no compensationfor medications prescribed and prepared for patients covered by the poor rate, Wat-son cut his losses on the parish poor by demanding that they return the gauze so hecould reuse it, but only on other parochial patients. He probably expected Snow todo the same, although Snow noted only that he never burned used blisters there-


after. He had no choice. Being in “charge of a gentleman’s practice” meant followingorders and doing most of the work.21 Two decades after his first day in Watson’spractice, Snow recalled that he and “the worthy doctor . . . never had any more serious misunderstanding” (L, xxxiv–xxxv).

Watson soon summoned Snow from the erstwhile Augean stable to help him treatan unusual influx of patients with influenza. Years later Snow’s recollection was thatthe epidemic commenced shortly after a “sudden and considerable increase of tem-perature” in the region. After an extended period of “cold wet weather” earlier inApril 1833, it had suddenly turned “warm and dry,” followed by the outbreak of in-fluenza. “The complaint appeared to attack the coalminers in greater numbers thanthe agricultural and other people; now the coalminers . . . often had to work atnight, and they were always deprived of day-light whilst at their work.” Night work-ers seemed predisposed to other epidemic diseases as well, such as erysipelas, whichhe characterized as “an asthenic inflammation, in some respects resembling influenza;so that it seemed probable that night occupations rendered persons more liable todiseases of this class.”22 These remarks contain parallel terminology to that used bythree British medical theorists commonly cited in the 1830s and 1840s.

The first was Thomas Sydenham (1624–1689), an English physician whose ideaswere still influential in the nineteenth century. His concept of the “epidemic consti-tution” had become generic. “The core of this theory was the conviction that the sea-sons of the year and the atmosphere were the main determinants of the nature of adisease. While these determinants caused a particular atmospheric condition suit-able to the spread of a particular disease,” whether an individual was susceptible de-pended on various predisposing factors such as humoral imbalance.23 Sydenham’sapproach to “bedside medicine” was also widespread in Snow’s day. According toSydenham, all diseases had distinguishing symptoms to the observant physician, sohe recommended observation at the bedside with explicit purposes: to establish whatdisease the patient presented, determine the species of disease by association withthe parts of the body it affected, decide whether to let nature take its course or ad-minister therapeutics, and monitor the patient’s progress for the duration of the disease.24

Snow’s expression “diseases of this class” may signify familiarity with the nosol-ogy devised by William Cullen (1710–1790), a celebrated Scottish physician andteacher, but Cullen’s disease classification was so commonplace as to render a searchfor influence superfluous. A medical naturalist like Sydenham, Cullen also believedthat a proper classification of diseases was essential to appropriate and standardizedtreatment.25 He reduced all diseases to four kinds, or classes, of physiological dis-ruption, all caused by nervous dysfunction. The most inclusive of Cullen’s classeswere the pyrexia, or febrile diseases.26 He considered most epidemic diseases to befevers in which “some matter floating in the atmosphere, and applied to the bodiesof men, ought to be considered as the remote cause. . . .”27 Many fevers were of un-certain origin, although he believed that there was probably a common origin that


manifested itself differently, depending on predisposing factors such as vocation andthe state of the nervous system.28 Snow’s suggestion that “night occupations” mightpredispose such workers to influenza and erysipelas more so than people on a “nat-ural” diurnal schedule could be considered a susceptibility to a first-stage fever inCullen’s system of classification.

Snow’s comment that erysipelas was “an asthenic inflammation” could be inter-preted as Brunonian. John Brown (1735–1788) diverged from the theory of histeacher, William Cullen, by asserting that all human diseases are reducible to insuf-ficient or excessive “excitability.” Too little excitement produced “asthenia” (equiva-lent to Cullen’s stage of debility). Too much excitement, and the bodily reaction was“sthenic.” The appropriate medical response in the Brunonian system was coun-tertreatment: stimulants (such as alcohol) to raise the level of excitability, sedatives(opium, for example) to reduce excitability to the desired midpoint, or health. Brownquantified the range between mortal asthenia (zero) and mortal sthenia (eighty).Brunonian practitioners prescribed therapeutics that were supposed to return thepatient to the desirable midpoint of excitability—forty on Brown’s health and illnessscheme,29 but we do not know what medical texts Snow was exposed to under Hard-castle’s tutelage or during his year of formal training in Newcastle. He may have readSydenham, Cullen, and Brown, or he may have indirectly absorbed conventionalmedical theories at his master’s elbow in the early years of his apprenticeship andvia lectures in his last year. Clinical experience was desirable in an assistant, not booklearning.

Pateley Bridge

Snow left Burnop Field in April 1834. Besides having little in common with Watson,Snow felt he had to “work too hard for his money.”30 He was now twenty-one andapparently still short of the funds required to complete his medical training. Un-certain about what to do next, he visited his family in York. A few things had changed,but much remained the same as it was when he had left York for Newcastle in June1827. His parents were still alive, as were the seven siblings he had known before hisdeparture. His three sisters were still living at home: Mary was eleven, Hannah nine,and Sarah seven. Of his brothers, William at nineteen was training to be a tailor,Charles at seventeen was helping his father with farm work, and Robert at fifteenand Thomas at thirteen were in school and still living at home. However, George,born in 1828, had died in infancy; it is unclear if Snow ever saw him. The familyhome was still on Queen Street, but in a different house. The move had been unex-pectedly propitious: there had been many cases of cholera in North Street in 1832,but none in Queen Street.31 In compliance with the First Reform Bill, William Snowwas registered in the York Poll as a property-owning farmer, and he had begun topurchase additional properties on Queen Street that he rented out.32


After a short stay in York, John Snow traveled to Pateley Bridge, a small markettown on the River Nidd in one of the dales of West Yorkshire. He signed on as as-sistant to Joseph Warburton, a licensed apothecary with an extensive practice in thetown and the four rural parishes of upper Nidderdale. Warburton was nearing fiftyand had lived in Pateley Bridge since 1807, apart from a six-month interlude at theLondon Hospital in 1816 while qualifying for the LSA. By one estimate, seventy-eightpercent of general practitioners (GPs) who set up a practice in the north of Englandbetween 1820 and 1879 did so near their birthplaces. Warburton fit this pattern, eventhough he was only an apothecary and settled in Pateley Bridge a few years beforethe GPs covered in this sample.33 He married Harriet Thackery of Pateley Bridge,and by 1822 was the father of three children and had purchased Fog Close House,which served as home and practice premises.34

Snow joined the household on his arrival in 1834 and immediately became partof the medical team that sallied into the surrounding parishes. Warburton tookcharge of patients in town and supervised Joseph, Jr., his son and apprentice. Snowwas responsible for patients in the rural parishes. As in Burnop Field, medical careduring his second assistantship involved “many rough rides, [and] a fair share ofnight work”—but now in terrain that was stunningly beautiful and dangerouslyrough rather than dingy with mining hamlets. He continued to accumulate experi-ence in bedside medicine as a provincial GP: diagnosing and prescribing for inter-nal complaints, treating external lesions, setting fractures, performing minor surgery,and compounding his own prescriptions. Contrary to his experiences with Watson,Snow thought he was fairly treated during his eighteen months in Pateley Bridge.Afterward, he “spoke of Mr. Warburton, his ‘old master,’ in terms of sincere respect,and depicted his own life there with great liveliness.”35

The Warburtons also tolerated his “culinary peculiarities” as a vegetarian andshared his commitment to temperance reform. According to Richardson,“At or aboutthe same time that he [Snow] adopted his vegetarian views, he also took the ex-tremity of view and of action, in reference to the temperance cause.”36 Temperancewas central to John Newton’s belief in a natural regimen: in his words, “the tutelargoddess of health and universal medicine of life.”37 It could be coincidental thatSnow’s conversion to Newton’s vegetarianism and interest in immoderate alcoholconsumption as a health problem occurred the same year, 1830, that a temperancesociety was founded in Newcastle. It is possible that Snow was introduced to New-ton’s ideas at this society and then read his essay, but it is unlikely that we will everknow for sure how it came about.

However, it is certain that near the end of his stay in Pateley Bridge he publicallyadvocated vegetarianism and had moved beyond Newton in his opposition to alco-hol. In 1836 he justified vegetarianism on medical grounds: “That diet is most con-ducive to strength which keeps the body in the most healthy and natural state, thatfood and drink which affords the necessary quantity of nutrition, and is at the sametime least heating and stimulating.”38 He borrowed the words “heating and stimu-


lating” from Newton, but the context suggests Snow believed that a vegetarian dietwas as close as humans could come to a natural regimen. In addition, he followedNewton’s recommendation to avoid alcoholic beverages because they, too, are heat-ing and stimulating. Snow preferred “cold water . . . I can drink it [in] modera-tion when I am thirsty, and I never tire of it.” This “limpid element” had great healthbenefits, but the drinking water available where humans lived often contained “im-purities.” Because Snow considered pure water an ideal beverage, “The way to getwater pure is to distil [sic] it. Those huge stills in different parts of the country thatpour forth evils amongst mankind in greater proportion than the fabled Pandora’sbox, may, by distilling water instead of spirit, be made to be the fountains of health;and wherever there is a steam engine, a very trifling expense in a few additional pipeswould condense the steam that now flies away into the air, or is otherwise wasted,and supply plenty of the purest water to the whole neighbourhood.”39 Thus, purewater joined nonstimulating, vegetarian food in Snow’s ideal regimen for health. Histhird prescription was “exercise”; like his uncle, he had become an inveterate walker.With the Warburtons he was able to actualize his ideals. They permitted him to con-struct a simple still for producing pure water, and the cook provided him with veg-etarian meals: fruits and vegetables but no butter, milk, or eggs. Warburton was ac-tive in local temperance activities and established a cocoa house as an alternative tothe ubiquitous public houses (pubs).40

Toward the end of his contract as Warburton’s assistant, Snow converted fromtemperance to teetotalism—the latter distinctly more secular and radical–demo-cratic compared to the evangelical and republican-minded moderationists.41 Thisshift occurred late in 1835 or early in 1836, after he met John Andrew, Jr. Andrewwas the son of a corn-miller and maltster who forsook the latter after signing a“moderation pledge.” Young Andrew spent little time in the family business afterhe took a total abstinence pledge in 1834. Using Leeds as base, Andrew and a smallband of campaigners visited villages and market towns throughout Yorkshire wherelike-minded persons had arranged meetings.42 After speeches extolling the bene-fits of abstinence, he would urge his listeners to show their commitment to “theteetotal principle” by signing a pledge book. Snow attended one such meeting and“became an abstainer.” The pledge he took was probably similar to the one adoptedat Preston in 1832: “We agree to abstain from all liquors of an intoxicating qual-ity, whether ale, porter, wine, or ardent spirits, except as medicine.”43 Andrew andhis colleague, W. A. Pallister, visited Pateley Bridge in the spring of 1836. They con-tacted Snow, who assisted them in organizing a public meeting. “In addition to thestirring addresses of the zealous young advocates from Leeds, Mr. Snow read a pa-per on the physiological action of alcohol.”44 The next morning Andrew returnedto Leeds, but Pallister “remained to the end of the week, holding meetings at someof the neighbouring villages, with enduring results.”45 When he had time, Snowparticipated with these itinerant abstinence missionaries at public debates andmeetings.46


In the summer of 1836 he returned to York for an extended visit with his family.By then temperance had become a family affair. Thomas Snow had joined the YorkModeration Society in 1835 at the age of fifteen. Another brother, William, two yearsyounger than Snow, was also a temperance advocate in York.47 On Snow’s “first walkinto the heart of the city” in almost two years, he was struck by the conjunction ofpoverty and intemperance all around him. As he considered possible “means of in-troducing teetotalism” to the residents of York, someone told him about “anotheryoung man who was on a visit to his friends, and was also bent on the same errand”—William Laycock, a schoolteacher. Snow sought him out, and the two then met ateetotaling Methodist minister, who assisted them in organizing a meeting at theMethodist chapel on the last day of June 1836. Snow and Laycock spoke convinc-ingly enough to garner seven pledges. “Several of the members of Mr. Snow’s fam-ily were present at this meeting, his mother taking an active interest in the arrange-ments for the comfort of those present.” Fanny Snow apparently served tea and anonmalt beverage at the first meeting of what soon became the York TemperanceSociety (of the teetotal faction). Pleased with their success, Snow and Laycock ad-vertised a public meeting for 6 July in Merchants’ Hall, at which John Andrew wasthe principal speaker. “Fifteen pledges were taken, making a total membership oftwenty-two,” including, apparently, Thomas Snow, who could not attend the firstmeeting. Laycock had to leave town, “but Mr. Snow remained until September, con-tinuing his efforts for the promotion of the cause” in weekly meetings in York andreform crusades into neighboring villages. He “secured the use of the Bilton Streetschoolroom, Layerthrope, where a meeting was held, and another at Acomb [Emp-son’s native village], under the presidency of the clergyman. . . .”48

Snow’s Teetotal Address

Like J. F. Newton, Snow made temperance a corollary of vegetarianism and pure wa-ter. In June 1836 he delivered a “teetotal address” in Pateley Bridge, which shows himto have been psychologically astute in assessing his audience, judgmental and deci-sive in his opinions, yet tolerant of people whose habits he might abhor.49

The address is the only direct source of Snow’s medical worldview after nine yearsas an apprentice and assistant. He objective was to give a medical explanation of thedeleterious effects of alcohol. Physiologically, he asserted that the consumption ofalcohol resulted in overheating and overexcitement, both of which caused “seriousderangement in the [bodily] economy.” There were instances when alcohol had me-dicinal value, such as in “some case[s] of spasmodic pain,” but these were uncom-mon. The terminology may reflect Cullen’s influence, but it was in generic use bythe 1830s.50 With respect to cholera, Snow believed the reliance on “the brandy treat-ment” early in the 1831–1832 epidemic tailed off as practitioners realized that ad-ministration of the liquor only “hurries on and makes more violent that reaction,


that secondary fever which is most to be dreaded, and increases the tendency whichthere is to inflammation in the head and elsewhere.” Once again, Snow employedlanguage that originated with Cullen and Brown but was so common by the 1830sthat one should not connect him to them specifically.51

Nevertheless, Snow’s teetotal address is unambiguous in one respect: In the wakeof the first cholera epidemic, he was (theoretically, at least) a therapeutic skeptic likemany other medical men.52 “Medicines,” he told his audience in 1836, “are indeed agreat blessing, but at the same time, their use is generally the substitution of a lesserevil for a greater”—death. Snow believed “the unassisted powers of nature inherentin the body” were usually superior to what medicines could accomplish.53 This per-spective associates him with therapeutic skepticism, a notion that the healing powerof nature (vis medicatrix naturae) rarely needed a helping hand. The skeptical med-ical man patiently monitored the patient’s struggle with disease, trusting in the in-ner strength of the mysterious life force and administering medicines only if the dis-ease appeared to gain an edge. Despite “all our progress in natural history and thephysical sciences,” he asserted, “we are far behind some of the civilized nations ofantiquity in knowledge of the things most nearly connected with our health andwell-being.”54 His admonitions against overdependence on medicines in combina-tion with his preference for doctrines from antiquity that stressed diet and exerciseecho John Newton and are remindful of Sydenham’s revival of the Hippocratic reg-imen. So while therapeutic skepticism likened him to Newton and Sydenham, it dis-tanced him from Cullen and Brown.55 His early obsessions with pure drinking wa-ter and the diseases carried by impure water were unusual and indicative of an earlyinterest in public health that he maintained when he moved to London for the restof his life.

Notes

1. Newton, Return to Nature. When Richardson composed his biographical sketch of Snow’slife in 1858, he discovered a copy of Return to Nature in Snow’s personal library. It appearedto him that annotations in it had been made in 1833, but Snow told him that he had “formedan idea that the vegetarian body-feeding faith was the true and the old” as early as 1830 (L, ii).

2. Newton, Return to Nature, 2, 66. He based his argument for a natural diet on passagesextracted from literature, examples from comparative anatomy, analogical reasoning, and whathe termed “experiment.” Newton cites two works by Lambe: “Reports on Cancer” and “Con-stitutional Diseases.” The former is either Lambe, Reports on the Effects of a Peculiar Regimen,or Additional Reports; the latter is A Medical and Experimental Inquiry into Constitutional Dis-eases. Newton may also have consulted Lambe, Researches into the Properties of Spring Water.

3. Newton, Return to Nature, 9. Newton’s assumption about the basics of a healthy diet isbased on Genesis: “Man is created and placed in a garden abounding with fruits and vegeta-bles, with which he is commanded to sustain himself” (4). Newton used fables and recentstudies in comparative anatomy to construct physiognomic and anatomical descriptions of


ideal humans. Again, he drew on Lambe: There are remarkable parallels in “the form and dis-position of the intestines” in humans and orangutans. So, Newton reasoned syllogistically, be-cause the orangutan “lives on fruits and vegetable in so vigorous [a] state” [and] the intes-tines are similar in both “tribes” of animals, that “man is wholly adapted to vegetable sustenanceis evident from his anatomy” (17–19).

4. Ibid., 43. Newton entreated “earnestly that those who may be influenced by our reason-ing, will not adopt this system by halves, since a small portion of fish or meat, taken daily,will maintain irritation [of the bowels], and vegetable diet, without quitting the use of com-mon water, whether drank alone, or in tea, coffee, beer, &c will by no means insure health”(37–38).

5. Ibid., 113–14.6. Ibid., 114–15.7. Ibid., 71. Newton’s medical framework was humoral. Health existed when the body’s in-

ternal secretions were in balance, illness when the balance was disturbed. He assumed healthwas the natural order of things: “If we reason analogously, and consider how measured, howdefinitive nature is in her operations, . . . [then the only reasonable explanation] for the as-tonishing deviation from such laws of which human diseases are an instance, must be attrib-uted to some extraneous cause, acting powerfully in contravention of the order of nature”(116–17). Although we do not have an “exact description of that morbid humour” that pro-duces disease, “the investigation of the chymist or the physician” will discover it eventually.Regardless of what they find, we should immediately adopt the “regimen of distilled waterand vegetable diet” (66) because it has indisputable benefits. Those who do will find “the stom-ach is so fortified by the general increase of health, that a person thus nourished is enabledto bear what one whose humours are less pure may sink under” (80). Distilled water and veg-etables is the only diet “that secures and perfects digestion, and therefore avoids the fumesand winds to which we owe the cholic and the spleen; those crudities and sharp humours thatfeed the scurvy and the gout, and those slimy dregs out of which the gravel and stone areformed within us” (105). Everyone who has followed it to date reports “the secretions dulyregulated, and the strength and health completely re-established” (70).

8. For a map of the first European pandemic, see Bonderup, “Cholera- Morbro’er”, 17, andMorris, Cholera 1832, 60–61. For Greenhow’s explanation of the lessons from the 1831–32epidemic, see Lancet 2 (1848): 452. Durey, Return of the Plague, 101–18, discusses contempo-rary views of the cause of cholera; we defer an extensive discussion of this topic to later chapters.

9. Descriptions of housing in the colliery villages and the action of the board of health isfrom Morris, Cholera 1832, 61–63, and Creighton, Epidemics in Britain, 2: 802–05; on theChristmas day outbreak, see Greenhow, Cholera as It Has Recently Appeared, cited in Creighton,803.

10. Morris, Cholera 1832, 59; Creighton, Epidemics in Britain, 803.11. More than twenty years later Snow recalled “having seen [miners] brought up from

some of the coal-pits in Northumberland, in the winter of 1831–32, after having had profusedischarges from the stomach and bowels, and when fast approaching to a state of collapse”;MCC2, 20. His use of plurals—“coal-pits in Northumberland” and “1831–32”—suggests thathe may have observed cholera victims at collieries during the initial Tyne outbreak in the fallof 1831 as well as at Killingworth in 1832. Snow had no personal knowledge of conditions inthe pits because later references are to published reports and information derived from abrother. Richardson did not explain why he thought Snow’s “exertions [at Killingworth] werecrowned with great success”; L, iv.

12. We date Snow’s arrival in Burnop Field from remarks he made at a meeting of the West-minster Medical Society, Lancet 1 (1841–42): 598.


13. Medical assistants in provincial towns earned £80–90 per year, the equivalent of a cu-rate at a parish church. The salary in rural areas was usually less; see Loudon, GP, 258–60. Thedata base of GPs used by Digby generated few patterns about assistants in the early part ofthe nineteenth century, but it was apparently common after mid-century to interrupt one’straining with assistantships if one needed the funds; British General Practice, 46–47. In 1833it cost £150–200 for two years of medical training in London; see Loudon, GP, 230, and S. Snow, JS-EMP, 146–48. Ellis suggested additional considerations behind Snow’s decision todelay schooling, including a realization that his grasp of Latin and Greek was inadequate forformal training; CB, xvi.

14. Empson “became the victim of a cruel, malicious, and slanderous report” by a formeremployee; see R. W. Heatherington, Newcastle Weekly Chronicle, 17 November 1883, quotedin Galbraith, WH, 162; Galbraith has reproduced the entire newspaper article; JS-EY, 62–63.We agree with Zuck that Empson probably left Newcastle in the spring of 1833, shortly afterhe auctioned “a large collection of Pictures and Prints, some of them well-known originals. . .”; Newcastle Chronicle, 23 March 1833, quoted in “Charles Empson,” 24. Robert Stephen-son moved to London in 1833; see Galbraith, WH, 161. Galbraith found the following entryunder the “Newcastle Police” column of the Newcastle Courant of 15 January 1831: “On Mon-day last, John Snow, an apprentice to a surgeon in the town, was brought before the Mayor,charged with having on the Sunday evening preceding, wilfully disturbed the congregation inthe meeting house of the Rev. Mr. Syme . . . while they were assembled for religious worship,by letting off a [fire]cracker within the porch.” “Two friends” posted bail of £50 to assure “hisappearance at the next sessions to answer the charge. . . .” The punishment for this misde-meanor was £60 or imprisonment in default of payment; JS-EY, 32. We do not know the out-come of this case, but lingering repercussions from this bit of mischief-making may have con-tributed to Snow’s decision to leave Newcastle as soon as he had fulfilled his contractualobligation as an apprentice.

15. The description of Burnop Field is from Surtees, History and Antiquities of Durham, 2:219. The population was about 500. It is unlikely that Snow had visited the village while anapprentice. Hardcastle’s practice area did not include Burnop Field in County Durham. Alsoliving at Burnopfield Hall were the house servants, including the family cook and her illegit-imate infant son, reputedly fathered by Watson. For a description and illustration of the house,as well as particulars on the Watson family, see Galbraith, BF, 33–35. According to Galbraith,John Watson (1790/91–1847) was a practicing apothecary before the 1815 act and exemptedfrom the licentiate examination; BF, 32.

16. The anecdote also gives us some hint of Snow’s medical philosophy at what would proveto be roughly the midpoint of his training. He did not dismiss Watson’s assessment that the“patient required a blister.” A blister was an irritating medicament applied to the skin on apiece of muslin or gauze with the object of raising a pustule that could be lanced to draw offthe accumulated fluid. The standard application for nearly two centuries had been a paste orointment containing powdered cantharides, derived from the green blister beetle, Spanish fly.But cantharides had an unpleasant side effect—irritation of the urinary tract and bladder. Bythe 1820s it was common for medical practitioners to use active ingredients that did not causethis complication, such as savine cerate (mixed with lard and wax), mustard, or capsicum;David Zuck, mail message, 4 July 2000. Blisters, including cantharides, continued as a stan-dard method of treatment for various inflammatory and painful conditions until the end ofthe nineteenth century.

17. Some healers still believed that the offending irritation was cause by humoral imbal-ance. Three of the primary humors (black bile, yellow bile, and blood) were associated withdry and hot qualities that, in combination, produced the greatest amount of “sharpness” andconsequent irritation in the body. The signature diagnostic signs were bitter taste and odor.


The sharpness in yellow bile was particularly irritating, although the liver was less susceptibleto surpluses because it was the source of that humor. Individuals whose normal constitutionincluded a predominance of yellow bile were prone to overheating—their temperament wascholeric, their physical disposition bilious—without, however, becoming ill, but if predispos-ing factors such as aging, improper diet, debilitating habits, or unusually hot weather gener-ated too much yellow bile in the liver, a fluxion (flow) of irritating sharpness could cause lo-cal sites or the entire body to become overheated. See Porter, Greatest Benefit, 55–61; and King,Medical Thinking, 21–23.

18. Caustic blisters were sometimes applied to unaffected parts of the body “on the as-sumption that the excoriation of one area and consequent suppuration could ‘attract’ the mor-bid excitement from another site to the newly excoriated one, while the exudate was signifi-cant in possibly allowing the body an opportunity to rid itself of morbid matter, of rightingthe disease-producing internal imbalance”; see Rosenberg, “Therapeutic revolution,” 23 (end-note 8). On counterirritation as treatment until well into the twentieth century, see Brock-bank, Ancient Therapeutic Arts, 105–34.

19. Snow prescribed “a large blister” (Ellis, CB, 107) in 1850 for a patient with pleurisy, fol-lowed a week later by cupping six ounces from “the right suprascapular space” (109). The nextday, he wrote, the patient’s “pains removed by cupping” (109). Eventually the consulting sur-geon tapped large quantities of fluid from the chest cavity and the patient recovered fully.Snow visited this patient on sixteen different days, often several times a day. In general, heemployed cantharides such as plaster of lyttae and plaster of antimony potassium tartrate inhis practice well into the 1850s; Earles, “Glossary of Latin abbreviations,” in CB, liii–lvii.

20. Porter, Greatest Benefit, 239. “Out-door” relief based on the English Poor Law of 1601(sometimes referred to as the Elizabethan Poor Law) was still in effect in 1833. The New PoorLaw, which consolidated 15,000 parishes into less than 600 Poor Law Unions and recom-mended institutional (“in-door”) relief in the form of workhouses, was enacted in 1834; seeWebster, Caring for Health, 31, 41. Implementation varied by regions, with some parishes inLondon, for example, not incorporated into Poor Law Unions until well after midcentury.

21. “Westminster Medical Society,” Lancet 1 (1841–42): 598.22. Ibid.23. Durey, Return of the Plague, 105. See also Roy Porter, Greatest Benefit, 230, and Seale

and Pattison, Medical Knowledge, 41, 33.24. Sydenham classified diseases by analogy with current naturalistic approaches to plants:

“It is necessary that all diseases be reduced to definite and certain species, and that, with thesame care which we see exhibited by botanists in their phytologies; since it happens, at pre-sent [1676], that many diseases, although included in the same genus, mentioned with a com-mon nomenclature, and resembling one another in several symptoms, are, notwithstanding,different in their natures, and require a different medical treatment”; Sydenham, Works, 1: 13.See also King, Medical Thinking, 112. Although Sydenham’s goal was to find a specific rem-edy for every specific disease, he was able to “reduce” only smallpox and ague (intermittentfever) to specific entities. The popular use of cinchona bark for the treatment of ague is at-tributable to him; see Porter, Greatest Benefit, 229–30.

25. “In the English-speaking world, the most influential attempt to set disease in a coher-ent framework lay in the teachings of William Cullen”; Porter, Greatest Benefit, 260. Cullen’srecommended therapeutics differed little from those advocated by humoral doctors—blistersto counter local irritations and venesection to reduce fever and an overly rapid pulse; see King,Medical Thinking, 197–98, 229–31.

26. Specific fevers were distinguished by variations in local inflammation and by whichstage predominated: atony, an excessive relaxation of arterial walls that produced debility; ir-ritation, caused by a buildup of acrimonious elements in the blood if the atony stage were


not corrected; if irritation was unrelieved, arterial spasms set in, followed by heat and end-stage fever. The three other classes of disease in Cullen’s nosology were neuroses (affectionsof sense and motion, without fever, caused by external stimuli); cachexia (wasting diseasessuch as consumption or the results of malnourishment); and local diseases (diseases that couldnot be classified in the other three classes, attributed to local conditions and not discussed inFirst Lines); see King, Medical World, 215–18; and Porter, Greatest Benefit, 261–62.

27. Cullen, First Lines, 1: 133–34, quoted in King, Medical World, 141.28. Porter, Greatest Benefit, 261–62.29. Porter, Greatest Benefit, 262; King, Medical Thinking, 232–33, and Medical World,

143–47; Risse, “Brownian system.”30. Richardson, L, xxxiv.31. Barnet, “1832 cholera epidemic in York,” 30.32. S. Snow, JS-EMP, 37, 45. On Snow’s siblings, see Galbraith, JS-EY, 14–16.33. Digby, British General Practice, 72, 74.34. It was thirty-two miles from York to Pateley Bridge, a collection of houses along two

roads meeting at a T-junction. A Black Swan coach to Harrogate departed York every Tues-day, Thursday, and Saturday at 7:00 in in the morning. Snow could have taken it as far asKnaresbrough, then walked fourteen miles to Pateley Bridge. Hargrove, York, 1: 410–11, 2: 674.

35. Joseph Warburton, Jr., was indentured from 1831 to 1836, took lecture courses in 1833(probably in Leeds), served fifteen months at Leeds General Infirmary, and qualified for theLSA in December 1837; Galbraith, PB, 229, 233–34. On the multifarious activities of the ru-ral general practitioner, see Loudon, GP, 54–99, 257–58. Snow’s comments about Warburtonand life in Pateley Bridge were made to Richardson in the 1850s; L, iv. When Snow noted someyears afterward that his work in Pateley Bridge had involved negotiating difficult terrain, of-ten at night, he may have had the senior Warburton’s fate in mind: he died in 1841 after be-ing thrown from his horse outside Pateley Bridge.

36. Richardson, L, iii. Richardson was also a temperance reformer, eventually president ofthe British Medical Temperance Association; Winskill, Temperance Movement, 1: v; 4: 241. Onthe first temperance society in Newcastle, see Galbraith, WH, 162. The Newcastle-upon-TyneTotal Abstinence Society was founded on 3 December 1835; Winskill, Temperance Movement,1: 138.

37. Newton, Return to Nature, 105. Dietary autoexperiments in connection to temperanceand teetotalism had been conducted since the seventeenth century; see Harrison, Drink andthe Victorians, 111–12, although he does not discuss Lambe or Newton.

38. Snow, “Teetotal address,” (1836), 20.39. Ibid.40. Galbraith, BP, 231–32.41. Harrison, Drink and the Victorians, 127–30.42. Of the 261 teetotal leaders identified by Harrison, Yorkshire contributed thirty-five, just

behind Lancashire (with forty); Ibid., 140. Other leaders beside Andrew abandoned the tradeof a corn-dealer; Ibid., 147.

43. Winskill, Temperance Movement, 1: 89, 168. The abstinence pledge that Andrew usedwas “similar to the Preston one” (1: 164). Both distinguished teetotalers from the temperanceadvocates, who took a “great moderation” pledge such as the following: “We, the undersigned,believe that the prevailing practice of using intoxicating liquors is most injurious both to thetemporal and spiritual interest of the people, by producing crime, poverty, and distress. Webelieve, also, that decisive means of reformation, including example as well as precept, are im-peratively called for. We do, therefore, voluntarily agree that we will abstain from the use ofardent spirits ourselves, and will not give nor offer them to others, except as medicine. Andif we use any other liquors, it shall at all times be with great moderation, and we will, to the


utmost of our power, discountenance all the causes and practices of intemperance” (1: 87;pledge of the Preston Temperance Society, adopted 22 March 1832). It is possible that the ab-stinence pledge Snow signed in Yorkshire replaced a “great moderation” pledge that he hadsigned earlier in Newcastle. The origins of “teetotal” are unclear. Winskill attributes it toRichard (“Dickie”) Turner, who in a speech at a temperance meeting in Preston in Septem-ber 1833 allegedly said, “I’ll have nowt to do wi’ this moderation, botheration pledge; I’ll bereet down and out and out tee-te-total for ever and ever” (1: 103). For a slightly different ver-sion of Turner’s assertion, see Harrison, Drink and the Victorians, 120.

44. Winskill, Temperance Movement, 1: 168. No copy of this paper is extant. Speeches onthe physiological dangers of drink, especially on nutritional grounds, were common featuresof teetotal meetings; Harrison, Drink and the Victorians, 115–19, which includes an analysisof Joseph Livesey’s Malt Lecture, first delivered in Preston in 1833.

45. Winskill, Temperance Movement, 1: 168, 176–77. W. A. Pallister of Leeds was the sameage as Snow; both were slightly younger than John Andrew, Jr. Pallister founded the YorkshirePioneer; Andrew eventually became secretary of the British Temperance League; Ibid., 1: v.

46. Galbraith, PB, 231; Winskill, Temperance Movement, 1: 165, 168.47. William Snow eventually managed the City Temperance Hotel in York.48. British Temperance Advocate (December 1886), 196–97, in Winskill, Temperance Move-

ment, 1: 177–79. Winskill considered Snow “one of the pioneers of temperance in the York-shire districts” (Ibid., 2:174). In Harrison’s “occupational analysis of prominent teetotalers:1833–1872,” there are nine doctors (sixth on the list); Drink and the Victorians, 144. He doesnot discuss Snow as a teetotaler, however.

49. Snow, “Teetotal address” (1836). After delivering the address, he read it to his brotherThomas, who said it converted him “to teetotalism from that day”; Winskill, Temperance Move-ment, 1: 179. In the 1880s Thomas Snow found a copy of the address “in some papers sent tohim by his sisters from York,” and he published it in a temperance journal; British Temper-ance Advocate (1888): 182.

50. Snow, “Teetotal address” (1836), 182, 20. According to Cullen, the essence of this lifeforce was nervous excitement, which produced sensation (irritation) in the body. A healthystate required a moderate amount of irritation, but normal organ functioning was disruptedby environmental stimuli that produced “spasms” in the nervous system. The exciting stimu-lus could be any external substance with an irritating “acrimony”: excessive heat or cold,trauma, or even the force of the circulating blood itself. Such nervous spasms could result in“increased action of the [blood] vessels,” reduced blood flow, spastic capillaries, and excessivefluid accumulation; Cullen, First Lines, 1: 276, cited by King, Medical Thinking, 231. See alsoKing, Medical World, 139–43, and Porter, Greatest Benefit, 260.

51. Snow, “Teetotal address” (1836), 20. Thomas Snow believed his brother’s opposition tobrandy treatment was connected to his temperance beliefs: “Having for two years been anearnest abstainer from alcoholics on hygienic grounds, and having no faith in the curativeproperties of brandy in cases of cholera, [Snow] objected to take it [to Killingworth], but wasoverruled. . . . On his return to Newcastle Mr. Hardcastle said: “Well, Snow, you’ve done ex-ceedingly well.” And he promptly replied: “No thanks to the brandy, for the bottles were neveruncorked” ”; cited in Winskill, Temperance Movement, 1: 176. By then temperance as an anti-dote to cholera was not limited to some medical men. For example, Directions to Plain Peo-ple recommended that everyone during the epidemic “use wine in moderation, but drink nospirituous liquors, and indulge in no irregular and vicious habits, for these materially increasethe virulence of cholera”; cited in Morris, Cholera 1832, 137. For additional discussion of tee-total opposition to alcohol as a medicinal restorative, see Harrison, Drink and the Victorians,298–99. Such opposition could also be mounted on purely therapeutic grounds.


52. On the conceptual basis for therapeutic skepticism, see Rosenberg, “Therapeutic revo-lution,” 14–21. Snow’s skepticism may antedate the cholera epidemic. According to a familystory, Hardcastle had “complained he lost good patients because he [Snow] told them theyhad no illness”; Andrew L. Simpson, Snow Collection, VIII.3.iii.

53. Snow, “Teetotal address” (1836), 20.54. Ibid.55. On the concept of the healing power of nature and Sydenham, see Porter, Greatest

Benefit, 58–59, 229–31. On the continuing influence of Sydenham into the 1840s, see GavinMilroy, “On the writings of Sydenham,” Lancet 1 (1847): 60–65; 375–78, 400–03, and Lancet2 (1847): 152–56, 673–77.


56

IN AUGUST 1836 Snow left behind his family and his temperance ac-tivities in York to continue his medical training in London. He took a cir-

cuitous route, however, traveling first to Liverpool, perhaps to visit teetotal acquaintances.Thereafter, according to Richardson, he “trudg[ed] it afoot from Liverpool through thewhole of North and South Wales, turned London-ward, calling at Bath on the way, ona visit to his uncle, Mr. Empson.” Like his uncle, who had hiked from New York to Mon-treal and back a few years earlier, Snow enjoyed walking. This tour from Liverpool toLondon covered almost 400 miles and probably took four or five weeks (Fig. 3.1).1

It is likely that Snow’s visit with Uncle Charles had a purpose beyond familial dutyand personal friendship. Snow intended to be a full-time student, and it is improb-able that he could have saved enough during his three years as an apothecary assis-tant to cover fees, books, and room and board for as much as two years of medicaltraining. He probably received financial help from Uncle Charles and perhaps fromhis parents as well.2

Requirements for Certification

Dual qualification necessitated that candidates complete the requirements of boththe Royal College of Surgeons in London and the Worshipful Society of Apothe-

Chapter 3

London Medical andSurgical Training,

1836–1838

caries. The Lancet, a London medical journal published every Saturday, listed cur-rent requirements in an issue each fall before the beginning of the academic year.There were two sessions for lectures—a winter session from 1 October to mid-April,with a two-week break around Christmas, and a session from 1 May to the end of July.Hospital attendance was available the entire year. The examiners in Apothecaries’Hall specified the lectures they expected students to take in each session and whento begin and end medical practice. The Royal College of Surgeons, however, listedonly the numbers of courses and length of surgical practice expected of studentswho wanted to take the qualifying examination. Some lecture courses and hospitalrotations satisfied both college and hall (the monikers for these two medical corpo-rations). Table 3.1 suggests how medical students might have planned their semes-

London Medical and Surgical Training, 1836–1838 57

Figure 3.1. Place-names, towns, and cities of significance to Snow.

Table 3.1. Schedule of lecture courses and hospital attendance for dual qualification for students in London beginning in October 1835

1st Winter Session 1st Summer Session 2nd Winter Session 2nd Summer Session 3rd Winter Session(Oct. ‘36–Apr ‘37) (May ‘37–July ‘37) (Oct. ‘37–Apr ‘38) (May ‘38–July ‘38) (Oct. ‘38–Apr ‘39)

Chemistry Botany Anatomy and Physiology Forensic Medicine Dissections

Anatomy and Physiology Electives Anatomical Demonstrations Midwifery and Diseases of Midwifery with

Anatomical Demonstrations DissectionsWomen and Children attendance on cases

Dissections Midwifery (lectures) Medicine (physic)

Materia Medica and Medicine (physic, lectures)Therapeuticsa

Surgery (lectures)

Surgery (lectures) Hospital attendance Hospital attendanceb Hospital attendance c

(through September)

Key: Italics—Required by Apothecaries Hall (AH) only.

Bold—Required by College of Surgeons (CoS) only.

Normal—Required by both college and hall.a Pharmacology, including identification and compounding, preservation, and administration of mineral and vegetable drugs. The CoS required only a three month ses-sion.b CoS required twelve months of surgical attendance at an approved hospital in London, Dublin, Edinburgh, Glasgow, or Aberdeen; or six months in one such hospitalplus twelve months in an approved provincial hospital (such as the Newcastle Infirmary).c AH required a total of eighteen months of medical practice, which could overlap with surgical practice, at a recognized hospital or dispensary.

Source: Lancet 1 (1836–37): 6–7.

ters if they hoped to qualify in the shortest time: twenty-two months to become aMember of the Royal College of Surgeons (MRCS) in London, thirty-one monthsfor a prospective Licentiate of the Society of Apothecaries (LSA).3

Snow took his surgical examination in May 1838 after eighteen months of train-ing in London and the apothecary examination the following October. Therefore,both college and hall must have accepted some of his certificates of attendance fromlecture courses at the uncertified medical school in Newcastle.4 In addition, the RoyalCollege of Surgeons in London credited him with the full twelve months he hadspent at the Newcastle Infirmary; to fulfill the remainder of its hospital requirementhe needed only six months at a London hospital, but the examiners at Apothecaries’Hall would only accept half of Snow’s clinical training at the Newcastle Infirmary.They insisted he spend a full year in hospital practice before qualifying.5

The London Medical Schools

When Snow arrived in metropolitan London twenty-one schools of varying size andcurricular range competed for students of medicine and surgery, who had to amassthe required certificates of attendance at lectures, anatomical demonstrations, anddissecting (Fig. 3.2). Some of these schools were attached to hospitals where a stu-dent could also satisfy clinical requirements. Most were proprietary schools that of-fered a full complement of lecture courses, although a few advertised only a limitednumber of subjects. Two institutions of higher learning—King’s College and the newLondon University—had affiliated medical schools that offered all the required lec-ture courses, demonstrations, and dissecting opportunities.

London proprietary schools of anatomy, medicine, and surgery traced their ori-gins to the mid-eighteenth century and emerging doubts about the value of indi-vidual apprenticeships. It was more efficient for a few surgeons and apothecaries tooffer formal instruction to a large assemblage of apprentices than for each master toteach his own. A number of committed and enterprising practitioners had renovatedand extended buildings in the metropolis to provide amphitheaters for lectures,rooms for anatomical demonstrations and dissecting, surgical museums, and occa-sionally herb gardens and garrets for the study of botany and materia medica. Whenthe London Corporation of Surgeons was reconstituted as the Royal College of Sur-geons, the availability of institutional training was so extensive that the new medicalcorporation eliminated the apprenticeship as a requirement for membership. Thatmeant a loss of income for hospital surgeons in the metropolis, but some soon of-fered lecture courses, students paid for tickets to attend, and hospital-based medicalschools were in competition with the proprietary schools.6 There were advantagesin attending an institution where lecture halls and wards were in close proximity, es-pecially because after the first winter session theoretical and clinical instruction be-came more integrated.


Figure 3.2. Hospitals and medical schools of London, 1836–1837 (adapted from Lancet, 24 September 1836).

When Snow reached London in 1836, medical education was still part of a bour-geoning market economy. Every school distributed a prospectus of the courses it in-tended to mount in the coming session, the names of the lecturers it had retained,the facilities it provided, and the perquisites that students received if they purchased“perpetual” tickets of admission, that is, took all courses at one school for a reducedfee compared to purchasing tickets for individual courses at several.7 Newspaper ad-vertisements trumpeted the star quality of a school’s faculty and the success rate ofits students in qualifying examinations. However, the editorial staff at the Lancet wasgenerally unimpressed with what the schools actually delivered:

The puffs and pretensions are innumerable, whereas the claims of the differ-ent teachers and establishments to distinction, where, indeed, any exist, areeasily enumerated. The whole system . . . is the prolific source of extortionand fraud. . . . [It requires] from the students the outlay of such enormoussums of money in the purchase of “tickets” [of admission] and “certificates”[of having attended the expected number], under the colour of enforcing at-tendance on lectures not one-fourth of which, from their multiplicity, can everbe heard. . . .8

Nevertheless, if one hoped to practice general medicine in England and Wales, therewas really no alternative to accumulating all the certificates expected by the exam-iners at college and hall.

Snow, like hundreds of other incoming medical students in London in October1836, had to decide where to take courses in the forthcoming session. Lectures dur-ing the first ten days were open to the public free of charge, with the expectationthat students would shop for bargains (Table 3.2).9 Snow became a perpetual stu-dent at the Hunterian School of Medicine at 16 Great Windmill Street, near Hay-market in Westminster (an incorporated city in West London). The Hunterian, acontinuation of the first school of anatomy in London, was renowned for havingdedicated instructors. Among them in the fall of 1836 was John Epps—physician,phrenologist, medical radical, and temperance reformer.10 With so many schools tochoose from, it is possible that Snow gravitated to a school that had at least one fac-ulty member who shared his antispirit views, but the Hunterian also offered studentsexcellent facilities, including an extensive pathological museum and a large dissect-ing room. The perpetual fee at the school was £34, which included access to the read-ing room and library, and it was the lowest priced among schools that offered a fullcomplement of courses for dual qualification. Although not attached to a hospital,it was located near several of them.11

Snow found affordable lodgings near Soho Square, a short walk from the Hunter-ian School of Medicine. He rented a room at 11 Bateman’s Buildings, a terrace ofrow houses along an alley that connected Soho Square to Queen Street (now Bate-man Street). Each house in this eighteenth-century speculative development had


Table 3.2. London medical schools, amenities, and “perpetual” fees as of October 1836

Private schools and colleges with a full complement of lecture courses and dissecting Private schools with limited offerings Hospital-based schools with various offerings

Aldersgate School of Medicine(library & medical society; £36 15s)

Blenheim Street School of Medicine(£36 15s.)

Hunterian School of Medicine(library, reading room, museum; £34)

Mr. Grainger’s School, Webb Street(museum; medical society; practiceprivileges at Surrey Dispensary andthe London Fever Hospital; £48 6s.)

King’s College Medical School(£63)

London University College Medical School(£70 10s.)

St. George’s Hospital School of Anatomy andMedicine(£46 4s; including anatomyand demonstrations, £16 16s.)

Westminster School of Medicine(£45)

Mr. Dermott’s Theatre of Anatomy(anatomy, including demonstrations anddissecting, physiology, surgery; £10 10s.)

Dr. Robert’s Lecture Room(Theory and practice of medicine; £5 5s.)

Mr. Smith’s Theatre of Anatomy(anatomy, including demonstrations anddissecting, physiology, surgery; £10 10s.Midwifery, including hospital practice; £5 5s.)

Dr. Waller’s Lectures on Midwifery(cases from the London MidwiferyInstitution; £5 5s.)

St. George’s Hospital Theatre of Anatomy(anatomy, physiology, demonstrations,dissecting; £16 16s.)

Charing Cross Hospital Medical School(only medicine, midwifery, anatomy, andsurgery; £19 19s.)

Free Hospital Medical School(no chemistry or botany; no fees listed)

Guy’s Hospital Medical School(full complement; £69 6s.)

London Hospital Medical School(full complement; £61 19s.)

Middlesex Hospital Medical School(full complement; £45)

St. Bartholomew’s Hospital Medical School(full complement; £66 4s., plus £1 10s.for use of library)

St. George’s Hospital Medical School(£39 18s., no anatomy)

St. Thomas’s Hospital Medical School(full complement; £55 13s.)

Source: Lancet 1 (1836–37): 7–15.

three storeys above ground, as well as rooms in the cellar. Number 11 was one of thesmaller houses, containing approximately 250 square feet of living space per floor,12

but it would have been sufficient as a place to read and sleep. Most of a first-yearmedical student’s time was spent at school, either in a lecture hall or in the dissect-ing room.

Snow the Medical Student

Whether to enhance his qualifications or to establish close relationships with seniorLondon doctors, Snow decided to repeat several courses he had already taken in New-castle. During the winter session of 1836–1837 at the Hunterian School of Medicine,he attended Mr. P. Bennett-Lucas’s lecture course on anatomy and physiology, theassociated anatomical demonstrations, plus dissecting on his own; chemistry withDr. Hunter Lane; and the principles and practice of medicine, still termed physic bythe Royal College of Surgeons, with Dr. Michael Ryan, an Irish physician with par-ticular interests in obstetrics and a medical radical.13 Snow decided to attend Dr.Jewell’s lectures on midwifery and diseases of women and children at the HunterianTheatre of Anatomy, perhaps because the course fee included attendance on cases atthe Royal Lying-in Hospital on Queen Street, near both the Hunterian School andTheatre. This facility was listed as a Hospital for Clinical Midwifery in the Hunter-ian Theatre’s schedule of courses, indicating that students who walked its wards withDr. Jewell would be taught obstetrics, an emerging specialty within general practicealso pursued by Hardcastle and, a few years hence, by Snow himself14 (Table 3.3).

Apothecaries’ Hall expected students to take botany and electives during their firstthree-month summer session in London. John Epps lectured in botany at the Hunter-ian School of Medicine, and Snow completed that course with him, probably dur-ing the 1837 summer session. When he was not in the lecture hall or the physic gar-den, he was probably dissecting in the “dead room.” In all, Snow would take fourcourses from Epps—two in materia medica, one in forensic medicine, as well asbotany.15

During his first year in London, Snow developed a close friendship with a class-mate, Joshua Parsons. “It happened,” recalled Parsons, “that we usually overstayedour fellows [in the dissecting room], and often worked far on into the evening. Theacquaintance thus grew into intimacy, which ended by our lodging and reading to-gether.”16 Each day was built around the lecture courses. The instructors arrived atthe appointed hour, expounded information and opinion (sometimes reading ver-batim material previously published in a medical journal), and then rushed off toresume private practice or do their hospital rounds, but outside the prescribed lec-tures medical education was largely self-directed. It was left to the students to sup-plement lecture notes with textbooks, to observe symptoms on the wards, to notethe appearance of diseases in the glass jars on display in the anatomical museum, to


correlate structures they could dissect with the demonstrator’s cadaver (or, if avail-able, a wax model), to conduct experiments in the chemistry laboratory, and to studymedicinal plants in the physic garden.17 The goal was to amass sufficient informa-tion to pass one comprehensive certifying examination at the very end of formaltraining.

Snow left no diary of his experiences as a medical student, but those who did maybe instructive. For example, James Paget entered the medical school attached to St.Bartholomew’s Hospital two years before Snow began at the Hunterian. “For thegreat majority of students, and for myself at first,” wrote Paget in his memoirs, “workat that time had to be self-determined and nearly all self-guided: it was very littlehelped by either the teachers or the means of study.” For most students “there wasvery little, or no, personal guidance; the demonstrators had some private pupils,whom they ‘ground’ for the College [of Surgeons] examinations, but these were onlya small portion of the school.” The situation was somewhat better, he thought, at thenearby “Aldersgate Street school, where were . . . some active demonstrators, andwhere more ‘grinding’ was done.”18 It appears that Snow and Parsons had neitherthe need nor the resources to hire a grinder. Both were older and more experiencedthan the typical medical student: Snow was twenty-three with almost nine years of


Table 3.3. Snow’s likely schedule of lecture courses during the winter session of 1836–1837

Monday Tuesday Wednesday Thursday Friday Saturday

9:00 |← Chemistry →|

10:00

11:00 |← Practical anatomy and demonstrations →|

Noon

1:00

2:00

3:00 |← Anatomy and physiology →|

4:00 |← Principles and practice of →|medicine (physic)

5:00

6:00

7:00 Surgery a Midwifery b Surgery Midwifery Surgery Midwifery

a We assume he attended these lectures; surgery was not a required course for apothecary candidates andtherefore not listed by Snow’s examiner.b Taken at the Hunterian Theatre of Anatomy, not the Hunterian School of Medicine.

Source: Lancet 1 (1836–37): 12; Society of Apothecaries,“Court of examiners entrance books,” MS 8241/10,61 (“John Snow”).

medical experience, while Parsons, although a year younger, had served a five-yearapprenticeship and had already completed twelve months at the North London Hos-pital. The two friends probably drilled each other until Parsons became dually qual-ified in October and left London to set up a general practice in Somerset.19

Snow, on the other hand, had to take another series of lectures and fulfill the re-quirements for hospital attendance. During the winter session of 1837–1838 he tooksecond courses in materia medica, chemistry, and midwifery with the same instruc-tors as the year before, but in the new academic year Dr. Robert Venables offeredphysic, Mr. G. Jones delivered the lectures in anatomy and physiology, and Mr. Sav-age gave the anatomical demonstrations (Table 3.4).20 In addition, Snow attendedmedical and surgical practices at the Westminster Hospital. It lay relatively far fromhis lodgings, nearly a mile to the south, beyond St. James Park on Broad Sanctuaryby Westminster Abbey and the Houses of Parliament. Although a mile meant littleto an enthusiastic walker like Snow, it seems odd that he avoided University CollegeHospital on Gower Street, St. Pancras, only a third of a mile from his lodgings. Uni-versity College Hospital offered case-study clinical instruction by, among others, therespected surgeons Astley Cooper and Robert Liston. Parsons had attended this in-stitution when it was called the North London Hospital; perhaps he was dissatisfiedwith his training there and had urged his roommate to go elsewhere, or Snow mayhave been dissuaded by a change in the University College fee schedule that penal-ized students who attended practices at the hospital but were not enrolled for lectures.21

For the next twelve months Snow was expected to be at the Westminster Hospi-tal shortly after noon six days a week. Most of the time, apparently, he shadowed the


Table 3.4. Snow’s likely schedule of lecture courses during the winter session of1837–1838

Monday Tuesday Wednesday Thursday Friday Saturday

9:00 |← Materia medica and therapeutics →|10:00 |← Practical anatomy and demonstrations →|11:00 |← Chemistry →|Noon1:002:003:00 |← Anatomy and physiology →|4:00 |← Principles and practice of →|

medicine (physic)5:006:007:00 Midwifery Midwifery Midwifery

Source: Lancet 1 (1837–38): 14–15; Society of Apothecaries, “Court of examiners entrance books,” MS8241/10, 61 (“John Snow”).

resident medical officers. One physician staffed the out-patient clinic each day. Forexample, Dr. John Bright came on Tuesdays and Fridays; Drs. George Roe and JohnBurne covered the other weekdays.22 In clinics physicians diagnosed and prescribedfor patients, most of whom were accident victims, members of the laboring classeswho paid subscriptions to friendly societies and provident funds to cover hospitalcare. After seeing the resident physician the patients waited at the dispensary for thehospital apothecary to compound and distribute medicines. If their complaints wereunrelieved, patients could return the following day and repeat the procedure with adifferent physician. Only nonchronic cases were considered for admission to the hos-pital. Many of those cases required the attention of the house surgeons, of whichthere were four when Snow “walked the wards” at the Westminster: Sir AnthonyCarlisle, Anthony White, George Gurthrie, and B. Lyon.23

These physicians and surgeons were proponents of what came to be called hos-pital medicine. This approach sought to develop the same habits of mind charac-teristic of accomplished practitioners at the bedside, but to do so in metropolitanclinical settings where students had two advantages not available to most appren-tices. First, one could observe many more patients and a broader array of diseasesin urban hospitals than in individual practices. Second, hospitals with morgues inwhich demonstrators could teach dissecting (or even a simple “dead room” in whichstudents were left to their own, often notorious, devices) offered the opportunityto compare one’s clinical observations and diagnoses with anatomical structuresand pathological lesions post mortem. Hospital medicine was touted as the pre-ferred venue for the clinical–pathological method. Next to anatomy, the Lancet con-sidered “Clinical Medicine—the study of disease, by the bedside of the patient, inthe wards of an hospital, and of manual surgery, in the operation theatres of thoseinstitutions—” the most important subject for the aspiring surgeon.24 Snow mayalready have been introduced to this relatively recent medical perspective while at-tending practices at the Newcastle Infirmary, but he most assuredly experienced itat the Westminster Hospital.

The Lancet was typical of advanced British medical thinking in its advocacy ofhospital medicine, although not everyone agreed that experiential empiricism wasits proper foundation. According to this journal, “medicine is, above all other sci-ences, a science of observation,—to be successfully studied only by careful and long-continued watching of the symptoms of disorder, the phenomena of health, and theresults of employing remedial agents for the cure of disease.”25 Methodical observa-tion was often difficult to carry out in the out-patient clinic because there was sucha high turnover of patients. Students could follow the medical staff on the wards for“fever patients” who could not be treated in their own homes, but such admissionsdepended on seasonal fluctuations in infectious diseases. The surgical wards, how-ever, offered numerous learning opportunities during the academic sessions whenhouse surgeons could be assured that the operating theaters were filled with gawk-ing medical students and a few senior students were available (often paying a hefty


fee for the privilege) to assist as dressers and clinical clerks. However, for the ma-jority of students, attending a hospital practice was their best chance to observe agreater variety of diseases than they could possibly have confronted as an appren-tice to a solo practitioner. The Lancet recommended a system for making the mostof this opportunity: “The moment . . . a student enters an hospital he should com-mence making an accurate record of a certain number of cases in the wards. . . .He should . . . make a selection of the most common diseases, or accidents, andthis limitation of his labour will enable him to follow a certain number of cases totheir termination. . . ,” whether to cure or death of the patient. One advantage ofattending hospital practices was that in the event a “case terminate[d] unfavourably,the post-mortem appearances of the subject” should be examined in the dead room.26

The object was to develop a personal collection of case notes that could be consultedfor years thereafter. Snow’s extant casebooks and his remarkable facility at recallingspecific cases during medical society meetings indicate that he mastered this objec-tive, probably a result of a combination of his own initiative, Hardcastle’s tutelage,and training in London.27

Whether a particular student’s experience corresponded to the ideal posed by theLancet depended largely on the views of the hospital staff where one received prac-tical training unless, like Snow, the student had learned to keep case notes at the bed-side during an apprenticeship. Again, James Paget’s recollections of his student yearsat Bart’s are instructive, whether or not they are representative. “In the second win-ter” session of 1835–1836, he wrote in his memoirs, “I gave myself to Hospital prac-tice more than in the first. . . . In the first year, I had not neglected Hospital prac-tice; but I had done little more than go round the surgical wards, . . . seeing whatwas rare, talking about cases, sometimes hearing a very few words of teaching. Be-sides, I had often sat . . . in the outpatients’ room.” Like Snow at the WestminsterHospital, Paget was not a surgeon’s assistant responsible for dressing wounds, “partlybecause the dresserships were expensive (10 guineas at least), partly because theyseemed to offer scarcely more opportunities of studying surgery than I had had inmy apprenticeship.”28 He found the instruction in the medical wards more congen-ial and spent most of his time there, serving several months as a clinical clerk forone of the house physicians. He thought the “teaching was admirable . . . and theirexpectation of what might be learned by continued research” set a standard for theremainder of his career.29 One physician stood out because “he would make thosewho went round with him examine for themselves, and would tell and show themhow to learn, and have his case-books well kept. . . . This precision, and the earlyhours, were too much for the great majority of students,” but the baker’s dozen whoattended the morning rounds “imitate[d] him in his mode of study. . . .”30 Ac-cording to Paget, “I worked steadily all through the winter, still dissecting as muchas I could, and helping in the post-mortem examinations whenever I had a chance.”31

That is, he took full advantage of the learning opportunities the new hospital med-icine had to offer, even at an institution he considered in decline compared to the


teaching available at University College Hospital—and, perhaps, at another relativenewcomer in medical education, the Westminster Hospital.

Several events punctuated the weekly routines during Snow’s twelve-month rota-tion at the Westminster Hospital. At the end of April 1838, he completed the sixmonths on the wards of a London hospital required by the Royal College of Sur-geons. He took the qualifying examination on 2 May. It is likely that his experiencewas similar to Paget’s two years earlier:

The examination was very simple. The ten examiners sat at the outer side ofa long curved table. Each in turn, I think, took a candidate; and, when he hadfinished, others could ask questions. My examiner-in-chief was Mr. AnthonyWhite, of the Westminster Hospital [one of Snow’s teachers]: his questionswere not difficult, and I believed that I brought them to a close by giving anaccount of the otic ganglion and its nerve-communications, in reply to someenquiry about branches of the fifth nerve. That ganglion was then known tofew; and he who knew about it seemed to be thought sure to know all com-mon things. After Mr. White, Sir Astley Cooper asked me some questions, andseemed satisfied. . . ; and then I was courteously dismissed.32

Groups of candidates—those who had completed all required lecture courses andmonths of hospital attendance—entered a room at the Royal College of Surgeons inLincoln’s Inn Fields and were examined orally, one after the other. The examinerswere particularly interested in the candidates’ knowledge of anatomy. Snow musthave satisfactorily answered whatever questions they put to him. Subsequently, theLondon Medical Gazette published a notification: “College of Surgeons. List of Gen-tlemen who have received diplomas. May 1838.” Of 114 successful candidates,“J. Snow, York” ranked seventh. He had become a Member of the Royal College ofSurgeons in London.33

Shortly before Snow earned his first medical title, the apothecary at the West-minster Hospital had resigned his post, and Snow began the process of submittinga full application, including eight references, as his replacement. The work of a hos-pital apothecary was wide-ranging, and, according to the Lancet, the Westminster’shad been extraordinarily effective: “(owing to the exertions of the apothecary andthe matron) the diets are as wholesome and plentiful, the clothing is of as good aquality, and is as clean, and, in short, the whole working machinery is as efficient,as in any hospital in London.”34 Snow was aware that the hospital charter would en-gage only a Licentiate of the Society of Apothecaries, but he assumed that the ex-aminers would permit him, as they occasionally had allowed others, to take the qual-ifying examination several months early, but they refused his request to be examinedat the end of the summer session in July. When he appealed, they reminded him thathis practice obligation would not be met until the end of September and again re-fused to grant him an exception. He was forced to withdraw his application.35 At the


time it was a setback. Instead of building a practice from a base at a major teachinghospital with an annual salary to tide him over, Snow would have to scratch out aliving in an open market glutted with general practitioners. One might wonderwhether he did not later come to consider the legalistic intransigence of Apothe-caries’ Hall a bit of good fortune, for in the same editorial in which the Lancet ap-plauded the Westminster Hospital for the conditions it had established for ward pa-tients, it castigated the house committee for its “mal-treatment of the apothecary bythe imposition on him of unprofessional duties, in addition to those of his own de-partment . . .” such as filling out forms, which was the proper job of a secretary.“What wonder, then, is it that no man of competent ability can be found long to fillthis degraded medical office?”36 Over the years taking the apothecary post at theWestminster Hospital would have resulted in a considerable loss of time and energyfor activities that Snow valued more than financial security—research and medicalsociety meetings.

Snow the Public Health Investigator

In November 1836, during Snow’s second month at the Hunterian School, Dr. Lanelectured on arsenic and its chemical properties. Snow took a special interest in thesubject, so he lingered a bit after the lecture. Dr. Lane called his attention to an ar-ticle in a foreign medical journal that described a new method of preparing cadav-ers for dissecting: injecting a saturated solution of arsenite of potash (potassium car-bonate) into the blood vessels to eliminate most of the dried blood, followed by redink into the arteries to highlight them. At Lane’s suggestion Snow replicated this pro-cedure in the cadaver he was dissecting and later in several others at the request ofsome classmates.

However, Snow had inadvertently introduced a public health problem at the med-ical school. While dissecting one of the prepared cadavers, a student became ill withsevere abdominal cramps, vomiting, and diarrhea. Snow does not appear to haveconsidered arsenic poisoning the cause until “the summer of 1837, [when] I injectedanother body, and dissected it, with five of my fellow students, during the very hotweather of, I think, August. Decomposition was retarded considerably [by the ar-senic solution], but there was only one of us who did not suffer more or less indis-position, principally bowel complaints: and the subject gave out a peculiar odour,which I suspected arose from the arsenic rising in combination with the volatileproducts of decomposition.”37 He did not have time to test his suspicion until theChristmas recess, when he cut out a few portions of the cadaver for examination.He found no evidence of arsenic in the tissue, which supported his notion that thesolution had turned gaseous and disappeared from the tissue. Again his studies tookprecedence, and it was not until “some time afterwards” that he devised “an experi-mentum crucis” to determine if the indispositions he and his fellows had experienced


was due to inhaling arsenic vapors or individual constitutional factors (since noteveryone was identically affected). The phrase that Snow employed in his first knownpublication, a letter to the editor of the Lancet, was defined in a popular contem-porary text, A Preliminary Discourse on the Study of Natural Philosophy: “If more thanone cause should appear, we must then endeavour to find, or, if we cannot find, toproduce, new facts. . . . Here we find the use of what Bacon terms ‘crucial instances,’which are phenomena brought forward to decide between two causes, each havingthe same analogies in its favour. And here, too, we perceive the utility of experimentas distinguished from mere passive observation.”38 Snow’s notion of a crucial ex-periment in this instance involved placing “some animal substances, in a state of de-composition, on a dish, along with solution of arsenite of potash, and also powderedarsenious acid. . . .” He covered the dish with “a bell-glass receiver to collect thegases given off, and, at the end of two or three weeks, . . . added the air containedin the glass to a sufficient quantity of pure hydrogen to make an inflammable mix-ture, and burnt this as it proceeded from a small jet. . . .” The result was “a smallquantity of metallic arsenic”—in short, the arsenic was in the vapor. He informedthe school authorities, who accepted his recommendation to discontinue the “modeof injection” he had introduced at the Hunterian.39

Snow’s investigations of poisonous cadavers coincided with his participation in astudy of poisonous candles undertaken by the Westminster Medical Society. The so-ciety was founded in 1809 by Mansfield Clarke and Benjamin Brodie, the latter alecturer in surgery at the Hunterian School of Medicine in Great Windmill Street,which is why meetings were initially held in the school’s museum. “For some yearsthe Society seemed almost to be an appendage of the school, every student who at-tended the lectures becoming also a member. . . .”40 However, the rules werechanged the year before Snow reached London to include a formal proposal and ap-proval process. Weekly meetings were held every Saturday evening from Octoberthrough April, with a pause for the summer months. Snow did not attend a meet-ing until 8 April 1837, when he was a guest of Dr. John Epps, who was scheduled tocomment on the therapeutic administration of strychnine, bismuth, and arsenic.41

When the 1837–1838 session of meetings resumed in October, Snow was proposedas an ordinary member and approved.42

The society had taken a distinctly radical turn a few years earlier, when five monthsof debate about medical reform “culminat[ed] in motions calling for the merger ofthe three estates into one democratic faculty. These motions were passed by massivemajorities, despite stonewalling tactics by the diehards.”43 Eventually, members whosought a compromise prevailed, although at the expense of defections by extremistsat both ends of the political spectrum.

The Westminster Medical Society had a reputation for debating matters relatingto public health such as the cholera epidemic of 1832, and the members decided toinvestigate “arsenical candles” during Snow’s first year as a member.44 On 28 Octo-ber 1837 Dr. James Scott reminded the membership of potential risks from inhaling


the fumes of stearin candles infused with white arsenic, which were considerablycheaper and burned brighter than candles manufactured from pure wax or sper-maceti. Earlier in the year a Mr. Everitt had demonstrated at a meeting of the Medico-Botanical Society in London that such candles produced vapors containing arsenic;he had boiled candles in water and reduced the precipitate with sulfurized hydrogengas to several grains of arsenic per candle. Whereas some medical men did not be-lieve a moderate amount of arsenic was harmful, Dr. Scott had recently received re-liable information that at least two manufacturers had dramatically increased theproportion of arsenic to stearin in response to public demand. “Now, as these can-dles were not only much in use in private families, but had lately been introducedinto some of the churches, and were likely to find their way into the theatres,” Dr.Scott “thought it would come within the province of the objects of the Society, tostate its opinion respecting the safety of such a quantity of a poisonous mineralburnt, and its vapour inhaled.”45 In the ensuing week Mr. Richard Phillips and “Mr.Snow had succeeded in detecting arsenious acid in these lights,” thereby confirmingEveritt’s findings. Everitt, in attendance as a guest at the meeting on 4 November, of-fered to give a public demonstration for the society later in the month. A commit-tee was formed “to communicate with Mr. Everitt and Mr. Phillips,” who had agreed“to carry on the investigation.”46

Poisonous candles reappeared episodically on the society’s agenda in the ensuingweeks, but a select committee carried out investigations behind the scenes through-out. As promised, Mr. Everitt repeated several chemical analyses on arsenic–stearincandles before the membership in mid-November. Mr. Golding Bird, a recent grad-uate of Guy’s Hospital Medical School, extended the chemical investigation by burn-ing candles in conditions with varying amounts of oxygen present; he detected var-ious arsenic compounds under all conditions.47 The second set of experiments werephysiological in nature. “A lofty and spacious apartment of Dr. Scott’s house in theStrand” was converted into a laboratory in which members of the select committeeconstructed four boxes with ventilation holes and glass fronts for viewing the responses of linnets, green finches, guinea pigs, and rabbits. They burnedarsenic–stearin candles in two boxes and spermaceti candles in the other two over aseventy-two-hour period (in six twelve-hour blocks). Hourly observations wererecorded in a register. Although the guinea pigs and rabbits were unaffected, mostof the birds in boxes exposed to the vapors of arsenic candles died, whereas those“in the boxes with pure lights were as gay at the end of the experiments as beforethey commenced.” The select committee detailed these investigations at a meetingon 9 December and concluded “that the vapour given off . . . during combustionis likely to be prejudicial. In closing their Report, the Committee express their wishto be of service to the public in a matter of so much importance, in the absence ofall medical police in this kingdom, the only country in Europe where the publichealth is so little regarded by the governing powers.” Before the society could voteon whether to accept the committee’s report, however, the bylaws required it to


be printed, distributed to the full membership, and, if approved, made available tothe public. After considerable discussion the society deferred a decision on whe-ther to pay the printing costs and refund the expenses incurred in conducting theinvestigations.48

During the week of 10–16 December 1837, three members of the society under-took additional but ex-officio investigations. Mr. Golding Bird made post-mortemexaminations of five birds exposed to arsenic vapors by the select committee. He de-tected minute amounts of arsenic in the body of one bird but nothing on any feath-ers. The drinking water was heavily contaminated, and “he thought it probable theyhad been poisoned in this manner,” perhaps because the deleterious effects of in-gested arsenic was common knowledge. After he reported his findings at the 16 De-cember meeting, Joshua Toynbee and Snow reported that they had “conducted a se-ries of experiments on these candles, to ascertain the effects of their combustion onanimal life.” First, they had experimented on guinea pigs, but Snow and Toynbee’sanimals, like their counterparts in Dr. Scott’s experiments, presented no symptomsof illness, regardless of the length of exposure or the level of arsenic in the candles.Similar experiments on some birds, however, were inconclusive because the appara-tus ignited during the investigation. The report of the meeting does not mention anydiscussion of the select committee’s report.49

Then the medical media became involved. The Lancet’s leading editorial on 23 De-cember reminded its readers of the coverage it had already given to the WestminsterMedical Society’s investigation of “Arsenical Candles.” The editorial gave additionalinformation on the subject, including a history of their discovery by a French chemistin the 1820s, but thanks to “the vigilance of the French Government,” the candleswere tested, found to be deleterious to health, and their manufacture banned in thatcountry. “‘Cheap wax lights,’“ as they came to be called, made a commercial jumpover the channel, and their investors made a hefty profit “at the expense of the well-being of the English community,” claimed the Lancet.50 The editorial then summa-rized the “variety of experiments” conducted by the select committee from the West-minster society and used the results to condemn the secretary of state for the HomeDepartment of England for permitting the sale of candles that expose “the animaleconomy . . . to the action of five times a greater quantity of arsenic than any pru-dent physician would venture to administer internally. . . .”51 Whereas the Lancetreferred to summations of society meetings by one of its reporters, the London Med-ical Gazette printed actual extracts from the committee’s report, accompanied by aneditorial early in January 1838. At a special meeting early in February, a majority ofthe Westminster Medical Society soundly condemned this caper by a disgruntledmember and decided to spend no more time or money on the topic. The society hadnot repudiated its own committee’s findings, it had acted on procedural grounds be-cause premature publication of significant passages from the report interrupted thedeliberative process called for in its bylaws. 52


A New Scientific–Medical Perspective

While the poison candle caper prevented the Westminster Medical Society from tak-ing an unambiguous position on a public health matter, Snow’s involvement in theinvestigative process is suggestive of the training he was receiving in London. In hisfirst year as a member of the Westminster Medical Society, he aligned himself withthose who considered medicine a science rather than just an art practiced at the bed-side. Like his concurrent investigation of arsenic vapors in the cadavers prepared atthe Hunterian School of Medicine, his chemical analyses and physiological experi-ments conducted for the society were pragmatic investigations designed to addresspotential health hazards, not pure science. The only remarkable aspect of Snow’s in-vestigative method in both instances was its typicality for his cohort. He consideredchemistry one of the collateral sciences of medicine, a common view in the 1830s.For example, the subtitle of the London Medical Gazette at the time was “A WeeklyJournal of Medicine and the Collateral Sciences.” He was part of a cadre of youngmedical practitioners whose training included an emerging laboratory complementto clinicopathological dimensions of hospital medicine.53

The arsenic candles investigations show Snow as a collateral scientist in keepingwith the new scientific approaches to medicine that were part and parcel of his train-ing. His approach to these investigations also reveals a model that would recur in hisanesthesia and cholera research. At an early stage in his career he demonstrated anability to set up a series of experiments that traced an agent as it circulated in a med-ical school dissection room, in rooms where arsenic candles were burned, and in thebodies of everyone who entered them. That is, he was already concerned with chem-ical analysis, employing animal experimentation, and asking questions about whathe would later term modes of communication—the pathways by which a specificpoison was introduced into a community and where and how it lodged in the body.Must arsenic be ingested to be poisonous (the common assumption at the time), orcould it also be poisonous if inhaled (an unusual assumption)? A decade later hewould articulate the principles of how ether and chloroform circulate in the bodyand cause their specific effects; shortly thereafter he would hypothesize how choleracould circulate through the water supplies of a neighborhood, a town, and a me-tropolis. This facility in imagining systems circulation and transmission in terms ofpatterns and pathways was the unifying conceptual orientation in Snow’s work.

The hospital medicine to which Snow was exposed was an English variant ofdevelopments in western Europe associated with the Enlightenment. In mid-eighteenth-century London several surgeons believed that students should base theirknowledge of medicine on anatomy rather than observations accumulated at thebedside as apprentices learning a craft. William Hunter established a private anat-omy school in Covent Garden in 1746. His brother, John Hunter, joined him twoyears later, and the school prospered for more than a decade. In 1766 William Hunter


on his own purchased and renovated a house at 16 Great Windmill Street as a com-bined residence and school, the forerunner of the Hunterian School of Medicine. Al-though its successful run was nearly over when Snow arrived, anatomy schools suchas the Hunterian that emphasized morbid anatomy had set the stage for the incor-poration by English hospital-based medical schools of the more expansive curricu-lum pioneered in France.54

In Paris between 1790 and 1830, a group of medical reformers, the Idéologues,augmented the provision of care and surgery in Parisian hospitals by the introduc-tion of teaching and research. They believed that conventional Hippocratic–Galenicnotions of humoral imbalance needed to be replaced by a scientific form of medi-cine within an Enlightenment worldview: modeled on the natural sciences, foundedon the principles of Lockean empiricism, and pragmatic in the sense of under-standing the “human economy”—how individual and social systems functioned.55

Their covering law, the medical equivalent to Newton’s theory of gravity, was thatspecific diseases were connected to particular organs or tissues in the body. They be-lieved enlightened medical thinking should correlate empirical observation of indi-vidual patients at the bedside, statistical manipulation of multiple observations inclinical settings, and pathological findings from postmortem dissecting. Supportersof the Idéologue orientation gained control of several hospitals in Paris, where theyreconfigured medical education to include training in sciences collateral to their vi-sion of enlightened medicine, especially anatomy, physiology, mathematics, andchemistry.56 A leading figure was Pierre Louis (1787–1872), who devised the “nu-merical method,” involving statistical analysis of many cases in the Paris clinics toshow that venesection was only minimally effective in the treatment of pneumonia.57

Statisticians like Louis were among the adherents of the new scientific–medicalperspective in England during the middle third of the nineteenth century, but thegeneral tendency was to think of hospital medicine as a branch of natural philos-ophy. Natural philosophy was the inquiry into the principles and laws underlyingphenomena in nature, and in 1830 John Herschel had published a primer for ac-tualizing it that was still popular reading during Snow’s training period.58 Accord-ing to Herschel, natural philosophers should limit their searches to verifiable prox-imal causes; they should seek to trace, in whatever discipline they investigated, “theoperation of general causes, and the exemplification of general laws. . . . Everyobject which falls in his way elucidates some principle, affords some instruction,and . . . [gives] a sense of harmony and order.”59 Experience acquired by obser-vation and experiment (what Bacon termed active observation) was the founda-tion of natural philosophy. Herschel’s “perfect observer” was acquainted “not onlywith the particular science to which his observations relate, but with every branchof knowledge which may enable him to appreciate and neutralize the effect of ex-traneous disturbing causes.” We should observe until we are in a position to de-duce general conclusions that encompass more than our experience, then test thevalidity our deductions by experimentation and further observation. That is, “the


successful process of scientific enquiry demands continually the alternate use ofboth the inductive and deductive method”—or, in our term, hypothetico-deductivereasoning.60

The view that corollary sciences and analogical reasoning were central to the studyof medicine lay at the core of natural philosophy. According to Herschel, “there isscarcely any natural phenomenon which can be fully and completely explained inall its circumstances, without a union of several, perhaps of all, the sciences. . . .Hence, it is hardly possible to arrive at the knowledge of a law of any degree of gen-erality in any branch of science, but it immediately furnishes us with a means of ex-tending our knowledge of innumerable others. . . .”61 For example, Herschel’s jus-tification for analogical reasoning and horizontal moves among collateral sciencesparallels Snow’s decision to use chemistry when investigating two medical problemsassociated with potential arsenic poisoning. Only in his mid-twenties, Snow was al-ready the “perfect observer” and keen experimenter that Herschel considered centralto scientific progress.

* * *

Snow qualified as an apothecary in October 1838.62 He had already decided to re-main in London, having moved the month before to lodgings in Frith Street, only afew blocks from Bateman’s Buildings. Here, in the heart of Soho, he set up a surgeryin his apartment and hoped to establish himself as a general practitioner and ac-coucheur. Starting his own practice in central London “seems crazy.”63 There was asurfeit of surgeon–apothecaries in the metropolis as a whole, a half-dozen within afew blocks of where Snow hung his shingle. None of the conventional routes musthave been available or seemed sufficiently attractive. Most medical students from theprovinces returned to their home districts after qualifying, often relying on medicalrelatives to help them become established or joining an existing practice as a juniorpartner.64 Snow had burned his bridges to Yorkshire and Northumberland severalyears before. He does not appear to have had substantial medical connections inYork, a city also suffused with medical men. If he had chosen not to continue asHardcastle’s assistant (or never been asked) in 1833, there seems little reason to thinkhe would return five years later to the city where his former master still maintainedan active practice. In addition, Warburton’s oldest son was already a partner and dueto inherit his father’s practice, which ruled out any temptation Snow may have hadto renew his temperance activities from a base in Pateley Bridge.

Opening a practice in London had certain advantages that must have outweighedthe risks. The Westminster Medical Society offered a scientific community and thekind of comradeship that might equal the friendships he had made in the Yorkshiretemperance movement. He lacked the connections, the affluence, and the patronageusually required to secure a hospital appointment in the metropolis, but he couldhope to become a lecturer in one of the medical schools. What is more, London now


had a university that would grant a doctor of medicine to someone who had not at-tended Oxford or Cambridge, which meant that Snow could aspire to become aphysician and, perhaps, shatter the glass ceiling of social advancement that kept med-ical men of his background from attending patients in the upper classes.

Notes

1. Richardson, L, v. Galbraith suggested the motive for the stopover in Liverpool; personalcommunication, 4 October 2000. For the probable daily pace of a long-distance walker in the1830s, see Galbraith, JS-EY, 49.

2. He may have spent as much as £170 on his London training, of which it seems unlikelythat he could have saved more than half as an assistant apothecary from 1833 to 1836; S. Snow,JS-EMP, 147–48. By 1836 William Snow was an established farmer, perhaps with an annualincome around £120; Ibid., 46.

3. “Regulations of Apothecaries’ Hall and College of Surgeons,” Lancet 1 (1836–37): 6–7.Apothecaries’ Hall required a five-year apprenticeship in addition to lectures and hospitalrounds and set the minimum age for qualification at twenty-one. The Royal College of Sur-geons expected at least five years devoted to acquiring professional knowledge, which couldinclude a short apprenticeship; candidates for qualification had to be at least twenty-two yearsof age.

4. In chemistry, medicine, materia medica, therapeutics, surgery, anatomy, and physiology;G. G. Turner and Arnison, Newcastle upon Tyne School, 17–20. See also Richardson, L, vii–viii.

5. Society of Apothecaries, “Court of examiners entrance books,” MS 8241/10, 61 (“JohnSnow”).

6. Bailey, “The medical institutions of London,” British Medical Journal 1 (1895): 1289;Clark-Kennedy, “London Hospitals,” 111–12; Peterson, Medical Profession, 15, 71.

7. It was not until the 1850s that “private education in the anatomy schools was co-optedor destroyed by the hospital medical schools”; Peterson, Medical Profession, 64–65, 72. See alsoDesmond, Politics of Evolution, 12–13.

8. “Advertisement,” Lancet 1 (1836–37): 5. See also Peterson, Medical Profession, 66. For theeditorial policy of the Lancet and the medical radicalism of its founding editor, Thomas Wak-ley, see Desmond, Politics of Evolution, 14–15, and passim.

9. Peterson termed it a “supermarket approach to medical education” (66).10. John Epps, MD, was from Edinburgh and in 1826 a member of the Phrenological So-

ciety there. He was editor for the London Medical and Surgical Journal, author of a book onhomeopathy and dropsy, and contributor to the Lancet and M-CR; Medical Directory, 1845.See also Desmond, Politics of Evolution, 166, 421.

11. Richardson, L, v–vi. See also Snow, “Arsenic as a preservative of dead bodies” (1838),264, where he mentioned taking chemistry and performing dissections “at the school in GreatWindmill-street.” Mr. Smith, who examined Snow for the LSA, noted the number of lecturecourses completed between October 1836 and October 1838 and the names of the instruc-tors; Society of Apothecaries, “Court of Examiners entrance books,” MS 8241/10, 61 (“JohnSnow”). All but one of the instructors were on the faculty of the Hunterian School of Medi-cine; “Hunterian School of Medicine,” Lancet 1 (1836–37): 12. In the previously cited letter tothe Lancet, Snow described dissecting in August 1837—between sessions, when only perpet-ual students had access to the school’s facilities. See also Cope,“Private medical schools,” 91–92,and Peterson, Medical Profession, 72.


12. Monmouth House and various ancillary buildings occupied an entire city block southof Soho Square until demolished in 1773. Two large houses facing the square were subse-quently erected and leased by Lord Bateman, along with a collection of houses created for theartisans involved in the construction. Part of their pay included grants of subleases to thehouses in which they lived, which came to be called Bateman’s Buildings; see Sheppard, Parishof St. Anne Soho, 113–14. Stephanie Snow estimates rent for a room was 13–18 shillings perweek; JS-EMP, 147–48. In 1841 (three years after Snow moved out) a census enumerator listed17 persons at 11 Bateman’s Buildings, among the most crowded of the sixteen houses in theterrace; UK, Home Office, 1841 Census, H.O. 107/730/2A, 1–8.

13. P. Bennet Lucas became a member of the Royal College of Surgeons of Edinburgh in1833. In London, besides his appointment at the Hunterian School of Medicine, he was a sur-geon at the Metropolitan Free Hospital. Among his writings is a text entitled Anatomy andSurgery of the Arteries and an article on asphyxia in the Cyclopaedia of Practical Surgery. Hewas a contributor to the Lancet and the Provincial Medical and Surgical Journal. John HunterLane was from Surrey but qualified as a surgeon (1829) and received the MD (1830) fromEdinburgh. He lectured on chemistry and forensic medicine in the Liverpool School of Med-icine before coming to the Hunterian. He was a regular contributor to the London medicaljournals; Medical Directory, 1845. Michael Ryan read medicine in Ireland, received the MDfrom Edinburgh, and focused his practice on obstetrics. He was for a time editor of the Lon-don Medical and Surgical Journal; see Desmond, Politics of Evolution, 171, 427. According tothe Apothecaries’ Act of 1815, Scottish graduates could not practice in England unless theyreceived an English qualification, whether the LSA, the MRCS of London, or an MD fromOxford, Cambridge, or (eventually) University College London. Apparently, few bothered toadd English credentials and practiced without them.

14. We have not found biographical information on Jewell. The weekly schedule we con-structed from the course descriptions in Lancet 1 (1836–37): 12 is the most likely scenario forfulfilling the courses noted in Society of Apothecaries, “Court of Examiners entrance books,”MS 8241/10, 61 (“John Snow”). It is possible that he attended lectures in surgery offered byJames Wardrop (1782–1869), MRCS of Edinburgh, and highly recommended in Lancet 1(1836–37): 20. The Society of Apothecaries did not require comparative anatomy, which wastaught at the Hunterian during the 1836–1837 session by Robert Grant, a surgeon and physi-cian educated in Edinburgh, Lamarckian evolutionist, lecturer in comparative anatomy at Uni-versity College London, and fiery agitator for radical medical reforms; Medical Directory, 1845;see also Desmond, Politics of Evolution, 422. We do not know if Snow attended Grant’s lec-tures in 1836–1837.

15. Society of Apothecaries, “Court of examiners entrance books,” MS 8241/10, 61 (“JohnSnow”).

16. Quoted in Richardson, L, v.17. Although the Anatomy Act of 1832 made it easier for medical schools to obtain ca-

davers legally, wax models were still used for demonstration purposes; see LMG 19 (1836–37):32. A collection of wax models from the early nineteenth century is on display at the GordonPathological Museum of Guy’s Hospital, London.

18. S. Paget, Memoirs of Sir James Paget, 40–41.19. Galbraith, “Joshua Parsons,” 108.20. Lancet 1 (1837–38): 14–15; Society of Apothecaries, “Court of examiners entrance

books,” MS 8241/10, 61 (“John Snow”). Robert Venables, MA and MB (1823) from Oxford,published his “Lectures on clinical history, pathology, and treatment of urinary disease” inLMG (1837–38); Medical Directory, 1845.

21. “Advice to students,” Lancet 1 (1837–38): 20; see also 11, 15. The North London Hos-pital in Gower Street was opened in 1834, replacing the University Dispensary in Euston Square


that had provided practical training for medical students of the newly founded University ofLondon between 1828 and 1833. In 1838 the name was changed to University College Hos-pital; Newman, Medical Education, 113–14.

22. Snow was not trained by Richard Bright, a physician at Guy’s Hospital, a respected clin-ical researcher on kidney diseases, and the developer of a chemical test for the kidney diseaselater named for him.

23. Lancet 1 (1837–38): 15. Westminster Hospital had been a dispensary in James Streetuntil 1834, when it moved to a new location and added a medical school; Newman, MedicalEducation, 113. For the reputation of the medical officers and the method of teaching at West-minster Hospital, see S. Snow, JS-EMP, 135–37.

24. “Advice to students,” Lancet 1 (1837–38): 20. For the significance of the shift from the“history taking” in conventional bedside medicine to the study of physical signs in hospitalsettings, see Peterson, Medical Profession, 14–15, and her citations of studies by Figlio andWaddington.

25. “Advice to students,” Lancet 1 (1837–38): 20.26. Ibid., 21.27. There are parallels between the Lancet’s ideal case report and Snow’s format set forth

in the extant casebooks (CB) from the last decade of his life, although the latter contains idio-syncrasies evolved over many years by a skilled experienced practitioner. Moreover, a numberof his publications include statements such as the following: “The following case from mynote-book”; in “Case of malignant hæmorrhagic small-pox” (1845), 585–86.

28. S. Paget, Memoirs and Letters, 59–60.29. Ibid., 60.30. Ibid., 61.31. Ibid., 63.32. Ibid., 64–65; Newman, Medical Education, 20, appears to be based on Paget’s account.33. According to the Charter of 1822, examiners had to be selected from the twenty-one

members of the council, and examinations were held in the college building; see Bailey, “Med-ical institutions of London,” British Medical Journal 2 (1895): 1291. “College of Surgeons,”LMG 22 (21 July 1838): 688.

34. “Editorial—1 April 1837,” Lancet 2 (1836–37): 60. The hospital apothecary, Mr. Thur-man, also retired as secretary of the Westminster Medical Society in October 1837; Lancet 1(1836–37): 177.

35. Richardson, L, vi–viii; S. Snow, JS-EMP, 140–43.36. Lancet 2 (1836–37): 59–60.37. Snow, “Arsenic as a preservative of dead bodies” (1838), 264.38. Ibid.; Herschel, Preliminary Discourse, 150–51. John Herschel (1792–1871), a mathe-

matician, chemist, researcher in optics, astronomer, and translator of various literary works,was the son of William Herschel (1738–1822), also an astronomer.

39. Snow, “Arsenic as a preservative.”40. Bailey,“Medical Institutions of London,” British Medical Journal 2 (1895): 26, and British

Medical Journal 1 (1895): 1389. See also Hunt, Medical Society of London, 16–17; S. Snow,JS-EMP, 170.

41. S. Snow, JS-EMP, 172; see also “Westminster Medical Society,” Lancet 2 (1836–37): 123,where Epps is recorded as warning that even “small doses of liquor arsenicals . . . in deli-cate females, soon brought on uterine hæmorrhage, though he had never witnessed a case inwhich it had gone to an alarming extent.” Official minutes or reporters’ abstracts of meetingswere regularly published in the London medical journals.

42. Galbraith, JS-EY, 54. “Westminster Medical Society. To the Editor. . . ,” Lancet 1(1836–37): 232. According to the new bylaws, three members had to propose a candidate for


membership, and a majority of the society had to approve. Successful candidates had to payan introductory fee of one guinea, which also covered annual dues for three years.

43. Desmond, Politics of Evolution, 105.44. “Westminster Medical Society,” Lancet 2 (1831–32): 21–24, 51–54, 85–88, 146–50; dis-

cussions of cholera occurred on 31 March , 7 April, 14 April, and 28 April 1832.45. “Westminster Medical Society,” Lancet 1 (1837–38): 212. It is possible that Everitt was

a misspelling of David Everett, LSA (1839).46. Ibid., 243. There were several medical men named Phillips, of which the most likely in

this instance was Richard Phillips, LSA (1836), MRCS (1837).47. Ibid., 425. While still apprenticed, Golding Bird became a student at Guy’s, where he

soon developed a reputation as an accomplished chemist. He received the LSA in 1836 andearned an MD from St. Andrews in 1838; see Coley, “The collateral sciences in the work ofGolding Bird.”

48. “Westminster Medical Society,” Lancet 1 (1837–38): 425–27.49. Ibid., 463.50. Editorial, Lancet 1 (1837–38): 457.51. Ibid., 458.52. “Poisonous Candles,” LMG 21 (1837–38): 577–80; “Westminster Medical Society,” LMG

21 (1837–38): 585–88; “Westminster Medical Society,” Lancet 1 (1837–38): 722.53. However, the institutional approach to laboratory medicine did not develop as early in

England as it did in France and the German states. See also Seale and Pattison, Medical Knowl-edge, 33–35.

54. See Cope, “Private medical schools,” 90–93; the Hunterian School of Medicine wassometimes called The Great Windmill Street School. See also Hays, “The London lecturingempire”; S. Lawrence, “Entrepreneurs and private enterprise”; Long, History of Pathology, 95;and Newman, Medical Education, 82–111.

55. Holloway, “Medical education,” 303–04. The Idéologues sought to emulate GiovanniMorgagni (1682–1771), whose essay De sedibus (1761; The Seat and Causes of Disease, 1769)argued for the correlation of clinical symptoms with pathological manifestations discoveredduring autopsies—which made morbid anatomy central in a medical student’s education.Leading figures among the Idéologues included Pierre Cabanis (1757–1808),physician–philosophe, and Marie F. X. Bichat (1771–1802), who substituted tissues for hu-mors as basic units of health and disease; see Porter, Greatest Benefit, 306–07.

56. Teaching was integrated with research as hospital clinicians devised nosological systemsfor classifying diseases as distinct entities, either by “distinguishing separate diseases that hadpreviously been believed to be the same, or . . . unifying as a single disease category a dis-parate collection of manifestations previously thought to be separate diseases” as in the re-search showing that different types of consumption were one disease, tuberculosis; Seale andPattison, Medical Knowledge, 33.

57. See Porter, Greatest Benefit, 316–18, on the influence of the Paris “school” of hospitalmedicine in London. The Paris school of medicine included, besides Louis, René T. H. Laen-nec (1781–1826), a physician at two large Paris infirmaries, the Salpêtrière and Hôpital Necker,and developer of the stethoscope; Jean N. Corvisart (1755–1821), physician to EmperorNapoleon, proponent of morbid anatomy and the clinicopathological approach to under-standing internal diseases; and Gaspard L. Bayle (1774–1816), physician at the Charité hos-pital and researcher on phthisis (tuberculosis) and cancer pathology. See Porter, Greatest Ben-efit, 312–13.

Contemporary validation that the ideas from the Paris school were debated during Snow’smedical training is found in Edwin Lankester’s “Essay on the uncertainty of medical science,and the numerical method of M. Louis,” London Medical and Surgical Journal 10 (1836–37):


468–76, read at a meeting of the Medical Society of London in November 1836. Lankester(with whom Snow would later work very closely) argues that Louis’s method is not just a me-chanical collection of facts. Instead, a judicious use of the method would assist those whowished to move medicine from an art to a science. Some critics “will feel disposed to say, that,from the very nature of medicine, it is impossible to reduce it to the rank of a true science.To this I would answer,” wrote Lankester, “that it is as possible for the mind of man to havethe relation of cause and effect in one series of actions as in another. . . . If the astronomerhas thus succeeded, surely it is not too much to suppose that the medical philosopher mayequally give laws to the relations of bodies infinitely more accessible to the apprehension ofthe sense” (476). However, the manner in which Lankester presented the numerical methodindicates that its use in England was not the norm.

58. In an 1831 letter to W. D. Fox, Charles Darwin wrote, “If you have not read Herschelin Lardners Cyclo—read it directly”; Darwin, Correspondence, 1: 118. Herschel’s PreliminaryDiscourse (1830) was republished in Dionysius Lardner’s Cabinet cyclopædia in 1831.

59. Herschel, Preliminary Discourse, 87; quotation from 15.60. Ibid., 132; 174–75.61. Ibid., 174.62. “Apothecaries’ Hall. List of gentlemen who have received certificates. Thursday, Octo-

ber 4,” LMG 23 (1838–39): 144; “John Snow, York,” was eighth on a list of ten.63. Christopher Hamlin’s phrase, taken from his review of an early draft of the manuscript.64. In the sample used by Digby, seventy-eight per cent of GPs in the north of England

had their “main place of practice in [the] area of birth”; British General Practice, 74.


IN OCTOBER 1838 John Snow “nailed up his colours” as a surgeonat 54 Frith Street, part of the parish of St. Anne-Soho, one of Victo-

rian London’s most densely populated areas.1 A jumble of trades, shops, markets, of-fices, and residences, Snow’s new neighborhood was a mixture of the genteel and thehumble, of family and industry. Once home to foreign aristocrats and Huguenot im-migrants, this part of Soho was by the 1830s an area in flux. At its northern end wasSoho Square, built around a central garden, with houses occupied by lawyers, den-tists, architects, the publisher Routledge, and Crosse and Blackwell’s manufactory ofcondiments. At the northwestern edge of the square was the Soho Bazaar, a closedmarket originally established at the end of the Napoleonic Wars as a venue wherethe widows and daughters of army officers could rent stalls cheaply by the day tosell their handicraft, mainly jewelry, millinery, gloves, lace, and potted plants. 2 Snowlived at the opposite end, near where Frith dead-ends into King Street.3

According to the 1841 census, 540 people resided in the 600 feet that constitutedFrith Street.4 It was a densely packed thoroughfare; on average, each house had nineresidents, and many exceeded the average by a considerable margin. Twenty-ninepeople were listed in the five flats at number 19. William Searle, a fifty-five-year-oldbookbinder and his wife, Lucretia, aged forty-five, headed one household contain-ing two adult sons and three more children ranging in ages from nine to thirteen.Nine people shared another flat, and in yet another lived a forty-year-old woman of

81

Chapter 4

Forging a London Career,1838–1846

independent means, a boy of twelve, a painter’s apprentice, and a female servant. Inthe fourth flat lived a painter with his wife and their four children. The fifth con-tained a sixty-five-year-old gold-laceman, his wife, and an unmarried daughter oftwenty-five.5 Londoners lived cheek by jowl with recent immigrants and migrantsfrom the country. Apprentices lived next to picture dealers and solicitors. Tailors,embroiderers, music sellers, bookbinders, engravers, bakers, iron- and cheese-mongers, tea merchants, and stay makers all made their home and living here. Therewas also a violin and guitar maker, a language teacher, a glass enameler, a coffeehouse, and a public house, the “Coach and Horses.” Young and old, day laborers andartists, dentists and doctors all crowded into the street, but 54 Frith Street was some-thing of a refuge from the hubbub. The 1841 census indicated that just four peoplelived there: Sarah Williams[on], fifty-five and independent; her thirty-year-olddaughter, Harriet; Jane Weatherburn, a female servant, aged thirty, born outside thecounty; and John Snow, surgeon, twenty-five years of age.6

Four other surgeons were located within a few doors of him—August Sannier at56 Frith Street, George and Joseph Toynbee at 58 Frith Street, and Alexander Angusat number 66. Peter Marshall, with whom Snow would work regularly, had premisesin Greek Street, which ran parallel to Frith. Like Snow, these were all men hustlingto make a career for themselves in the great emerging medical middle class of Lon-don. The nearest physicians lived in Golden Square, a quarter-mile to the southwest.7

Snow’s practice for the first eight or nine years largely depended on patients fromthe area in which he lived. It would not be surprising if he often questioned his de-cision to start from scratch in a metropolis oversupplied with GPs, many of whomwere having great difficulty attracting patients.8 Consequently, there was consider-able turnover in general, and Snow’s part of Soho was no exception. For example,by 1841 J. L. Curtis and Co., surgeons, had set up shop at 7 Frith Street, the Toyn-bees and Sannier were no longer listed in the city directory, and Hugh W. Diamond,another surgeon who would go on to pioneer psychiatric photography, had movedinto number 59.9 Curtis headed a group practice, Diamond brought an apprenticewith him, Alexander Angus had an assistant, and Snow remained at 54 Frith Streetuntil 1852. For those who could make a go of it, there was obviously demand in thisdistrict for general practitioners.10 Initially, at least, Snow followed custom in secur-ing appointments as surgeon to four friendly societies, or sick clubs; 64 percent ofGPs in a sample covering the years 1820–1879 had at least one nonhospital ap-pointment such as a friendly society.11 These voluntary associations, forerunners ofthe capitation schemes of the next century, collected a few pence per week from everylaborer and paid practitioners an annual lump sum—often quite small—for treat-ment of the workers and, sometimes, their families.12 Snow had an intense bent to-ward research, but there were no paid positions as a medical scientist in London un-til after midcentury. Not until the Public Health Act was passed in 1859 was thereany provision for the paid employment of “investigatory” medical staff, and eventhen there were very few such positions and only on a temporary basis.13


Before the advent of anesthesia, John Snow was largely able to make a living as aGP in London and still have time for research and medical society meetings becauseof his thrift and his energy. His modest means never exceeded his expectations.Richardson remarks that Snow “managed by his frugality to lay in store for a rainyday for himself, and to help such friends as needed.” A teetotaling vegan during hisfirst five years as a London GP and a temperate vegetarian thereafter, he was a healthenthusiast his entire adult life. He dressed plainly and remained a bachelor.14

Finding His Way, 1838–1839

Snow’s marginal success in general practice was all the more remarkable because heevidently did not possess an easy bedside manner. The word on John Snow was: “Aquiet man, very reserved . . . not easily to be understood and very peculiar.” Hehabitually spoke in a husky voice, which “rendered first hearings from him painful,”and he sometimes had trouble making himself heard in meetings.15 When Snow didmeet with success from using anesthesia, it was widely assumed that he got rich frommilking this practice. While an obvious research talent, he was in some ways lack-ing in humanity. In his memoir Richardson felt compelled to defend Snow fromthese criticisms but readily conceded that “He did not become the idol of the peo-ple in common practice, far from it.”16 Richardson felt that Snow’s lack of popular-ity was a sign of his medical integrity. Richardson relates that in Snow there was toomuch of the skeptic to be popular and none of the quackery or “routine malprac-tice which the people love,” and as a poor boy from York he had no entrée to “thebedsides of dowagers of the pill-mania dynasty.”17 Such skeptics did not become richby writing prescriptions or compounding medicines. Undoubtedly, he was never oneto tell people what they wanted to hear for the sake of popularity. Nonetheless, hisanesthesia casebooks indicate that he was very capable of putting nervous patientsat ease. Additional factors not addressed by Richardson include Snow’s temperance,which likely alienated him from the heavy-drinking working clientele in his neigh-borhood. The casebooks occasionally reveal his impatience, sometimes downrightirritability, with what he perceived as general ineptitude among his neighbors. In anexample from April 1850 that ties together his antipathy toward alcohol and his skep-tical attitude toward the locals, Snow consulted on a case of delirium tremens. Hisfriend and colleague Peter Marshall asked for his assistance with a long-time alco-holic who had been unable to sleep for two days. The man was shrieking, shakingviolently, and hallucinating when Snow was called in. His course of treatment wasbasically to sedate the patient with opium and to induce ordinary sleep by way ofchloroform. The strategy seemed to be working but was undermined because theman was, as Snow complained in his notes, “surrounded by a lot of ignorant peoplewho made him more excited by boisterous attempts to keep him quiet.”18 Eventu-ally the patient was removed to St. George’s Hospital for further treatment in a more

Forging a London Career, 1838–1846 83

stable setting, but Snow’s remark does suggest the distance between him and the gen-eral public on how to behave when a medical man was in attendance. His candorabout the deleterious effects of alcohol also came between him and his patients.

On the other hand, he was immensely respected by his colleagues, and not justthe research oriented. He was an acute diagnostician in regular practice, and his col-leagues in Soho regularly consulted him about difficult cases. Marshall was in aweof Snow’s practical knowledge and encyclopedic knowledge. One area in which Snowexcelled was in the care and delivery of babies. His interest in midwifery, which inhis day included the study of diseases of women and children, probably began dur-ing his apprenticeship experiences at the lying-in hospital in Newcastle and was nur-tured during his London training by Drs. Ryan and Jewell. When Snow began pre-senting case reports in journal articles and at medical society meetings, he often drewon his practical expertise in obstetric, gynecological, and pediatric practice.19 Ob-stetric work helped build up a practice, although it was time consuming, and the regular fee for a delivery in the poorer practices was only ten shillings and six-pence or even less,20 but it was a way in which a doctor might become the familyphysician.

Having assured himself of at least a modest practice and the attendant income,Snow proceeded to solidify and deepen his relationship with the Westminster Med-ical Society, which he had first joined as a student.21 His career as a medical scien-tist and his involvement with the Westminster Medical Society were closely inter-twined. Richardson stated, “I have often heard him say, both privately and publicly,that, upon this early connexion with the ‘Westminster Medical,’ his continuance inLondon depended, and all his succeeding scientific success.”22 The Westminster Med-ical Society had once had 1,000 members, but by the time Snow joined its fortuneswere sinking. Soon after Snow completed his studies, the Hunterian Medical Schoolin Great Windmill Street closed down. This was a double calamity for the West-minster. Most of its membership had been drawn from the student body of theschool, and it had enjoyed rent-free use of the school’s facilities for meetings formany years. It suffered a dramatic decline in membership and depleted its financialreserves as it had to rent temporary quarters. In 1843 it reached low ebb, with onlya dozen members remaining. Snow stuck with the Westminster during its dark daysand was a faithful participant. In the first five years of his membership, he attendedmore than 90 percent of the weekly meetings on Saturday evenings, taking a guestmore than a third of the time.23 Over time he was elected to various offices. For ex-ample, he was on the advisory committee for the 1842–1843 and the 1846–1847 ses-sions and vice-president in 1848–1849.24 Meanwhile, the society added new mem-bers, eventually reaching 275. It continued to be dogged by financial concerns, so in1849 the officers sought amalgamation with the like-minded Medical Society of Lon-don, in part because the two societies had a large number of members in common.

The Medical Society of London had been founded in 1773 by Dr. John Lettsom,a forerunner of the medical radicals who came into prominence in the 1830s. Sixty


years earlier he perceived the need for a society that would admit physicians, sur-geons, and apothecaries on an equal footing and that would allow Quakers and Dis-senters to be members, but after thriving for a long period, the Medical Society ofLondon had, like the Westminster, fallen upon hard times. An amalgamation of thetwo was a natural solution, but the joint society had to take the name of the formerorganization because of a technicality in the Medical Society of London’s lease onits property.25

In the early days of Snow’s career, however, the Westminster retained a distinctidentity, and it provided him with a comfortable environment to meet most of hisprofessional and social needs.26 While Snow’s fondness for the Westminster was deepand abiding, it was not exclusive. In 1843 he was elected a fellow of the Royal Med-ical and Chirurgical Society, but, according to the society’s Transactions, he gave fewpapers at this staid society of medical conservatives, and the medical press recordedfew comments by him.27 The more bellicose side of Snow, who had argued withHardcastle over the brandy treatment for cholera and who set out to clean up Wat-son’s surgery without first consulting his principal, was reserved for the Westmin-ster, where he could participate in the rough-and-ready debates without making en-emies. Generational differences in the membership brought stark disagreements. Theolder generation at the Westminster consisted mostly of men whose formal Londontraining involved far fewer courses than Snow was required to take, occurred at atime when Cullen and Brown were considered “modern” theorists, and preceded thewave of Continental ideas and foreign influences that transformed medical school-ing in the 1830s.28 The newer generation, by contrast, either had the social advan-tages necessary to travel to the Continent for additional training or became awareof the newer work in hospital and laboratory medicine through journals.29 Snowshaped his nascent career by allying himself with the new generation and (as politelyas possible) lecturing to the older generation to insist that the hospital and labora-tory approaches received a fair hearing. Because the norm for research, especiallylaboratory research, at that time was still solo investigation, Snow indicated his al-legiance to the new generation primarily by citing the same authorities and refer-ring to the same published works.

This generational divide and Snow’s position in it was evident in the early papershe delivered at the Westminster. On Saturday, 7 December 1839, he read a lengthyaccount of twelve cases of scarlet fever that had been followed by severe edema, withfour deaths. His conclusion was that “disorganization of the kidney might be occa-sioned by scarlet fever.”30 The context for his discussion of these cases was recentmedical research, not empirical medicine. His review of the literature featured thediscovery by Dr. Richard Bright of the relationship between albumin in the urineand certain diseases of the kidney.31 Then he showed how Bright’s findings could ex-plain the cases he had treated. The first was a girl aged twelve whose severe form ofscarlet fever was followed by a generalized swelling involving the chest and abdomen,eventually leading to death. His postmortem examination—Snow laid the specimens


before the society—showed that her kidneys were grossly enlarged. In two of theother deaths the kidneys were found to be much congested postmortem, the lungswere edematous, and there was pericarditis (inflammation of the membrane sur-rounding the heart). In ten of the twelve cases albumin had been found in the urineand was probably present in the other two, but the tests had been inadequate.32 Headded that generally the urine was dilute and low in urea content; these findings in-dicated that urea was accumulating in the blood. It had often been detected by oth-ers in such cases, and Snow suggested that a rise in circulating urea might be thecause of some of the problems, including disease of the heart itself. In terms of treat-ment he recommended, in view of the congestion, that blood-letting at the com-mencement of the disorder should be beneficial, together with free purgation.

Snow was immediately challenged by William Addison.33 Dr. Addison was un-convinced by Bright’s researches that the kidney was the source of the problem indropsy. Instead he attributed all the symptoms described by Snow, including the dis-ease of the kidney, to a peculiar state of the system that might be induced by in-temperance and a variety of other causes. He thought it more likely that the entirehuman “economy” had been disrupted, and the cause could not properly be local-ized to a single organ. He was ready to dismiss a laboratory discovery—albumin inthe urine—as a mere epiphenomenon providing no basic insight into the diseaseprocess.

However, Dr. Golding Bird, recently appointed an assistant physician at Guy’s Hos-pital, took up the torch for the new generation while still disagreeing with Snow’sinterpretation. He doubted whether increased urea in the blood contributed to thesymptoms. He noted that François Magendie (1783–1855) had injected urea into theblood, and no bad effects had resulted. Bird’s citation of data from the laboratory ofMagendie, a skilled neurophysiologist and experimental pharmacologist, positionedhim with Snow as an advocate of a new approach to clinical medicine in which the-ory and laboratory research structured one’s interpretation of diseases.34

This relatively early case report and discussion provides a glimpse of the youngSnow’s progress. He enjoyed an advanced grasp of basic concepts of pathophysiol-ogy, especially when understanding a disease process required seeing the relation-ships among various organ systems and tracing fluids from one body compartmentto another. He also demonstrated facility in performing postmortem examinations,but his suggestion that blood-letting and purgatives could be the treatment of choiceshows that current options in therapeutics differed little from Watson’s and hisdrawer of used blisters.35

Snow’s Early Publications

The free debate tradition in the Westminster shaped Snow’s earliest attempts at sci-entific publication. From the outset he structured his written arguments as if he were


presenting a lecture: identifying a clinical or public health problem, surveying themost recent medical literature on the topic, and dealing in advance with anticipatedobjections—in short, using the medical journal as a forum to deliver the same mes-sages he articulated in person at society meetings. He also floated trial balloons be-fore his colleagues. Reading a paper allowed him to weigh criticism from his peersand to decide whether the material was worth sending to a journal, having it pub-lished as a pamphlet at his own expense (or both), or leaving it as a presentation.The latter approach had some payoff, too, because reporters for the Lancet and LMGgenerated detailed summations of papers. Because the reports of what transpired atthe medical societies usually included the reactions of each commentator, Snow couldalso make his mark by responding to papers presented by his colleagues and the oc-casional guest lecturer. Snow was no exception to the generalization that, for Lon-don medical men in the nineteenth century, participation in medical society affairsbrought professional recognition, and regular publication was a critical aspect of ca-reer advancement.36

His first four publications were letters to the editor written in response to articlespublished in the Lancet and LMG. These letters were not, however, purely ad hoc re-joinders. His reply to a Professor Goodeve on the use of arsenic to preserve cadav-ers included a description and analysis of the experimental inquiry he had under-taken during his student days. Thomas Wakley, editor of the Lancet, added a sentenceto the effect that Goodeve had reported no ill effects from his arsenic-treated ca-davers. Wakley’s comment was as revealing as it was gratuitous. He was an old-schoolsurgeon who considered medicine solely an inductive science and appeals to exper-imental medicine either faddish or harmful,37 but Snow was undeterred. In January1839 he sent another letter to the Lancet because a recent article by John Goodmanon the “Physiology of the mechanical action of the heart” was “open to some ob-jections.”38 Mr. Goodman had proposed that the auricles (atria) of the heart, beingless muscular than the ventricles, had no need for muscle fibers in their walls. Heargued that when the ventricles contracted, the diminution in their volume produceda vacuum in the pericardium; atmospheric pressure acting on this vacuum squeezedthe auricles, emptying them into the ventricles without the need for them to con-tract. He reasoned that the rib cage and the diaphragm were of such constructionas to be able to withstand “the pressure of the atmosphere, generally understood tobe 15lbs. on every square inch of surface. . . . The bony arch, by its unyieldingstructure, presents itself to the oppressing forces with the firmness of the oak, in anarched and resisting form, while the more yielding diaphragm, like the willow be-fore the wind, bending beneath the atmospheric pressure, presents a concave, butstill resisting and equally protecting surface.”39

Snow began his rejoinder with the above quote, minus the sylvan flourish. Heagreed with Goodman that “the most delicate structures on the earth bear the pres-sure of the atmosphere without detriment, so long as it is equal in all directions; adistended bladder, and bubbles blown in soap and water, bear it because it is equal


inside and out; but this is not what Mr. G. means. . . .”40 The anatomy and physi-ology of the thorax, according to Snow, did not support Goodman’s conclusions: “Athorax 10 inches deep and 30 inches in circumference (not a very large one), has 300square inches of surface, and would, in this case, have to resist a force of 4500 pounds,or more than two tons; and, in addition, the diaphragm and the parts closing thetop of the thorax, would have to resist half as much; this would require thick wallsof cast iron, instead of mere flesh and bone. The truth is, that with very slight vari-ations the pressure on every part of the thoracic viscera is exactly the same as on theexterior of the chest.”41 The walls of the thorax are movable and elastic, and atmo-spheric pressure on them and inside the lungs keeps the surfaces of the lungs in closecontact with the inside walls of the chest. The only variations in pressure betweeninside and outside occur during inspiration and expiration. These are slight, Snowexplained, having quantified them by measuring his own intranasal pressure whilebreathing with both a mercury and a water manometer.

The rest of the letter proceeded in like manner, with quotes from Goodman fol-lowed by correctives drawn from current medical authorities and his own clinicalexperience. He cited a recent paper by Magendie on blood pressure in dogs and sug-gested that Goodman’s confusion stemmed from a misreading of Johannes Müller’sPhysiology, a textbook that served as the most advanced European treatise on thesubject during the 1830s and 1840s (Snow quoted from the English translation).42

Müller (1801–1858) belonged to a generation of natural historians who believed sci-entific truth lay somewhere between the warring perspectives of their elders. ForMüller, Enlightenment physiology was too mechanistic and reductionist to accountfor life forces, whereas the archetypal forms and Platonic ideas in Romantic Natur-philosophie struck him as “fables.” His alternative, a “rational creative force,” was akinto vitalism and served as the organizing principle in his discussion of embryology,43

but Snow used Müller’s principles of physiology to expose fallacies in Goodman’sreasoning. As such, Snow was not out to score debating points at an opponent’s ex-pense.44 His agenda was to advance the cause of a new scientific generation. Althoughhe lacked the resources to travel to France or Germany to study under such teach-ers, he could read their works and position himself within the larger movement ofexperimental physiology and chemistry that was transforming laboratory medicine.Goodman could have done likewise and would not have gone astray had he fully un-derstood the contributions of Müller and Magendie.45

A few months later another opportunity arose for Snow to enter the lists as an ad-vocate of the new medical science. Someone who identified himself as “M.H.” sub-mitted a brief note to the Lancet on “Respiration and asphyxia.” After commentingon the various nerves responsible for stimulating respiration, “M.H.” argued thatwhat incites the first breath in the newborn cannot be the same mechanism that in-cites breathing in the mature animal, because the latter depends on “evolved car-bonic acid” produced by the animal after it has begun to breathe oxygen.46 The au-thor went on to claim that asphyxia was closely allied to epilepsy because of the


convulsive nature of the attempts of the asphyxiated animal to breathe. Snow, in re-ply, would very likely have alluded to the fact that the fetus in utero produces car-bon dioxide that is chemically indistinguishable from that produced by the organ-ism after birth. As he would write later, there was no reason in his mind to arguethat whatever causes the newborn to take its first breath is different from what causesit to take its second or third breath.47 We will never know what Snow’s letter to theeditor contained because Wakley chose not to print it. Instead, the 25 May 1839 is-sue of the Lancet included the following notice: “The remarks of Mr. John Snow ona recent communication from M.H., on the physiology of respiration, have been re-ceived. We cannot help thinking that Mr. Snow might better employ himself in pro-ducing something, than to criticising the productions of others.”48 Wakley’s state-ment can be read as a snub: Snow was an upstart trying to make a name for himselfby finding fault with his elders. It can also be read as the reaction of a prickly edi-tor who thought Snow was criticizing him for including flawed articles in his jour-nal, and it can be read as a gentle, if ham-fisted, warning by a senior colleague thatSnow should temper himself at so early a stage of his career. Whatever Wakley’s in-tent, his comment was patently unfair to Snow. His first letter to the editor had de-tailed arsenic experiments, and the Lancet had reported on Westminster Society meet-ings at which Snow had read several papers on his research activities. He appears tohave taken offense, for he found a friendlier reception in LMG.49

Setting His Own Agenda, 1839–1843

Snow took Wakley’s comment to heart in that he refrained from sending further let-ters to editors for the next few years and used this period to stake his own claim toexperimental territory and to establish areas of special interest. The territory he laidclaim to included the physiology of respiration and the chemistry and physics of in-haled gases, with special attention to their implications for midwifery. Although atfirst glance Snow’s early research and scholarship might seem eclectic in subject mat-ter, his persistent interest was the physiology and pathology of respiration. He in-vestigated the mechanics of breathing and ways to restore vitality when respirationwas interrupted. He studied the properties of inhaled toxins and gas exchange at thetissue level. His understanding of factors that stimulated or depressed respiration,or that supported or interfered with gas exchange, would prove enormously usefulwhen his major professional challenge became finding the middle ground betweenpreventing pain and suppressing breathing when administering anesthetic gases. Inaddition, his deep understanding of the inhalational route of toxins led in a directpath to his skepticism of the miasmatic origin of cholera. One should not read Snow’sarticles and presentations during the next half-dozen years as anticipations ofWilliam T. G. Morton’s discovery of ether or of the return of cholera to England,but it is highly unlikely that without the insights Snow derived from these forays into


medical science, he could have so successfully addressed the twin problems of anes-thesia and cholera.

Snow’s emerging focus was in evidence at the Westminster Medical Society in March1839, when Dr. Golding Bird read a paper on how carbonic acid gas produced deathin animals. Snow thought the paper so interesting that he requested a continuationof the discussion. At the next meeting he began by noting that Bird’s paper had “in-duced him to modify his opinion as to the modus operandi of charcoal fumes. Hehad formerly entertained the idea that carbonic acid [carbon dioxide], like hydrogenand nitrogen, produced death simply by the exclusion of oxygen; but the experimentsof Dr. Bird and Collard de Martine had convinced him of the contrary . . .”—thatcarbon dioxide was deleterious, although he was not ready to accept Bird’s view thatit was an active poison.50 During the week after this presentation Snow had under-taken several experiments on small birds and white mice using various mixtures ofatmospheric air, carbon dioxide, and oxygen. He described his results in detail andconcluded that oxygen could act, to some degree, as an antidote to carbon dioxide,and that while the physiological action of carbon dioxide was unclear, its destruc-tive powers might arise from constant stimulation of “the mucous membrane of theair-cells.”51

This extended comment indicates Snow’s facility in planning and conducting a setof experiments designed to answer a specific question. The chemical procedures hedescribed required a considerable amount of apparatus and of skill, and his com-ments reveal an understanding of the physical and physiological principles involved.He was particularly interested in the public health implications of these investiga-tions. He cited a recent study that “death might be produced in an atmosphere whichsupported the flame of a candle.” Because such a flame went out in an experimen-tal atmosphere containing four percent carbon dioxide, “a fortiori, such an atmo-sphere could not support life.”52 This conclusion was at odds with the reassurancesof chemists that charcoal-burning stoves lacking a chimney were safe for domestic use.

When Snow published his next paper in 1841, he provided further evidence thathe was carefully focusing his investigations (Table 4.1).53 From a general interest inthe chemistry and physics of inhaled gases, he began to turn his attention increas-ingly to aspects of asphyxia, notably the increased resistance to blood flow throughthe lungs and the site of the metabolic processes.54 He also showed a predilectionfor inquiring into instances and mechanisms of poisoning, particularly if the poi-sonous substance were inhaled. He demonstrated both an interest and a facility inthe invention and design of apparatus.

Snow resumed his publications with an article on deformities of the chest andspine in children.55 While he focused on how abdominal enlargement might proveto be the basic cause of chest deformities in the growing child, he was especially con-cerned about the impact the deformities had on respiratory function and lung de-velopment. About six months later Snow published a paper initially read at the West-minster Medical Society on 16 October 1841.56 His explanation of the resuscitation


Table 4.1. Snow’s published research, 1836–1846

Experiment Apparatus Involved Involved Collateral sciencesTopic Datea conducted constructed respiration, gases poisons used

Arsenic as preservative of 1836–1837 X X X Chemistrydead bodiesb

Action of recti musclesb 1838 Anatomy, physiology, physics

Mechanism of respirationb 1839 X Physiology, Physics

Action of recti musclesb 1839 Anatomy, Physiology

Distortions of chest in 1841 X Anatomy, pathology,children with abdominal physiology, clinical caseenlargement report

Resuscitation of stillborn infants 1841 X X X Physiology, physics

Paracentesis of thorax 1841 X X Physiology, physics

Uterine hemorrhage with 1842 Physiology, clinical caseretention of placenta report

Circulation in capillaries 1843 X X Physiology, physics,

microscopy

New kind of pessary 1843 X Clinical case report

Lead carbonate poisoning 1844 X Pathology, chemistry,clinical case report

Hemorrhagic smallpox 1844 Pathology, clinical casereport

Pericarditis after scarlet 1845c Pathology, clinical casefeverb report

(continued)

Table 4.1. Snow’s published research, 1836–1846 (Continued)

Experiment Apparatus Involved Involved Collateral sciencesTopic Datea conducted constructed respiration, gases poisons used

Atmospheres with 1846d X X X Chemistry, physics,reduced oxygen and physiologynormal carbon dioxide

Strangulation of ileum in 1846 Pathology, clinical casemesentery report

Alkaline urine 1846e X Chemistry, physiology,clinical case report

aDate given is that of publication unless the article states specifically that the observation or experiment was carried out at an earlier time.bReply to previous publication by another author.cReports case that occurred in 1844.dRefers to research conducted in 1839.eReports case that occurred in 1842.

of the stillborn infant draws on several of his research interests, including respira-tion and asphyxia, as well as a practical interest in designing apparatus. In a moregeneral way, it illustrates important features of Snow’s thought and writing and theextent to which he had achieved a level of scientific competence at this relativelyearly stage of his career. The paper is dense in ideas and material, while the style isclear and brisk.

Snow began this paper by reviewing a number of physiological and philosophicalquestions relating to asphyxia and marshaled experimental evidence to show thatanimals tolerate lack of oxygen much better at low temperatures than at high tem-peratures. He cited many physiological experiments performed by authorities he citedby name, the best known being Lorenzo Spallanzani (1729–1799) and Marie FrançoisXavier Bichat (1771–1802). After explaining why many commonly used resuscita-tion methods were unsatisfactory because they were at odds with this large body ofexperimental data, Snow turned to the new device produced after his own plans byMr. John Read of Regent Circus and described its use and advantages.57 The appa-ratus consisted of two syringes placed side by side, one to withdraw air from thelungs via the mouth and the other to push fresh air into the lungs via the nostrils.

Atmospheric air, provided by an efficient device such as Read’s, ought to be suf-ficient by itself to restore respiration if the asphyxia were reversible at all. Snow addedthat should the physician desire to add oxygen, “oxygen gas can be generated in greatpurity, in a few minutes, from chlorate of potash, by means of a spirit-lamp and asmall retort.”58 After a few comments on possible uses of mild electric shocks in stim-ulating respiration, Snow mentioned the experiment he had performed on a guineapig to show that he could restore some heart action an hour after death by artificialrespiration. He concluded his paper with some observations on the mechanism thatcauses the newborn to take its first breath—perhaps held in reserve from his never-published reply to M.H. in the Lancet—and how long after cessation of placentalcirculation fetuses of various ages would survive.

This paper seemed to stimulate the Westminster Medical Society almost as muchas Read’s apparatus was said to stimulate newborn respiration. The society took theunusual step of extending discussion of the paper into the next two meeting ses-sions, 23 and 30 October. For the most part, the many comments and criticisms fromthe other members reflected the tradition of bedside medicine, although Mr. WilliamD. Chowne added a statistical dimension: He reviewed his records and found onlysixteen stillborns among his last 500 obstetrical cases, leading him to dispute Snow’sone-in-twenty figure as grossly inflated. Mr. Forbes Winslow attacked Snow for notdistinguishing between two causes of asphyxia, plethora and collapse, and arguedthat only blood-letting would help in cases of plethora. Many shifted the course ofdiscussion to the question of resuscitating nearly drowned adults and debated howmany minutes without breathing might pass before it became impossible to restorerespiration. Each speaker had a case report to prove the point he was making, oftenflatly contradicting the lesson of someone else’s case report. Only Sir Benjamin Brodie


offered a comment that seemed on the same plane as Snow’s discussion of experi-mental physiology, claiming that artificial respiration could not be effective if theheart had stopped.59

When Snow was granted time to reply to these objections on 30 October, he hadobviously used the intervening period to prepare his remarks carefully. He turnedaside the plethora/collapse distinction by carefully defining his terms, arguing thatthe correct current usage restricted the term asphyxia to “the pathological state oc-casioned by the stoppage of the respiration.”60 He considered asphyxia a unitary phe-nomenon, physiologically, and therefore the experimental data he had originally citedwere applicable. He also took up the question of the resuscitation of nearly drownedadults. Many of the cases cited by the members at the previous meeting had occurredin the Serpentine pond at Hyde Park, and the Royal Humane Society had erected areceiving-house specifically for the purposes of treating such victims. Snow expresseddismay that the society recommended immersion in a warm bath (always at theready) before attempting to restore respiration. Instead, the authorities should havean apparatus like Read’s (adult-sized) in the boat that was sent out to pull the vic-tim from the water and work to restore respiration before reaching the receiving-house.

These remarks of Snow’s were only the lead-up to what he considered his con-clusive rejoinder. Since delivering his own paper, he had located one in the Philo-sophical Transactions of the Royal Society written by John Hunter, the eighteenth-century surgeon and founder of the school of anatomy in Windmill Street. Hunterhad recommended a bellows for artificial respiration, designed on a principle almostidentical to Read’s two-syringe device. He had performed some experiments with hisbellows on a dog whose heart had been exposed and showed that the heart actionwould flag soon after artificial respiration ceased and pick up again after artificialrespiration was resumed. He was able to restart the dog’s heart ten times using hisbellows, even after the heart had ceased to beat for as long as ten minutes. If Sir Ben-jamin Brodie doubted the evidence of Snow’s own guinea pig experiment, he couldhardly maintain his objection in the face of this experiment by Hunter, whom Snowconsidered “one of the greatest physiologists that ever lived.”61

Snow’s Evolving Scientific Thought

The paper on newborn resuscitation illustrates a complex method of attacking aproblem in medical science. Snow had found a comfortable balance among newerperspectives in hospital and laboratory medicine and an updated version of bedsidemedicine. For him the ideal form of clinical observation, whether conducted per-sonally at the bedside or in hospital wards and supplemented by reports from med-ical journals, consisted of a long series of cases that had been carefully recorded andcould be statistically analyzed, but conclusions were tentative unless confirmed by


laboratory findings. In this instance he had to resolve an apparent dichotomy be-tween laboratory experiments showing that cold was desirable and accumulated bed-side experience suggesting that heat was desirable. He rejected neither out of hand,however. Instead, he offered a distinction to try to reconcile the laboratory and thebedside findings—warmth might be preferable if the infant were to begin sponta-neous breathing soon; cold might be preferable if attempts at resuscitation were go-ing to last indefinitely.

Snow also demonstrated ease in moving among different scientific disciplines. Hisresuscitation paper was based largely on applied physiology, but he also made de-tours into chemistry, anatomy, and physics just as readily as he moved between lab-oratory and bedside. It was a pattern he followed his entire career, specifying the pre-cise relationship between medicine and its collateral sciences.62 Snow was asystems–network type of reasoner. He seldom dealt with linear chains of cause andeffect but rather with interacting networks of causes and effects. He viewed the hu-man organism, and the world it inhabits, as a complex system of interacting vari-ables, any one of which, isolated temporarily for careful study, might provide a use-ful clue to the clinical–scientific problem—but only when seen in its proper context,and only when the variable, having once been isolated for study, was then put backinto its place in the system and restudied in its natural environment. The heat–colddiscussion in the stillborn-resuscitation paper provides a limited example of thismode of thought. At the chemical level, the temperature controls the rate at whichreactions occur. If a chemical reaction consumes oxygen, it will consume it faster ifthe temperature is increased. At the physiological level, changes in temperature willaffect the animal’s nervous system and occasionally stimulate a nervous reaction, in-cluding a reflex inspiratory effort. Snow was equally comfortable isolating these vari-ables for study at one level of biological organization or seeing their interactions atthe multiple levels that make up the intact organism within its environment. In someclinical circumstances the positive effects of heat in stimulating the nervous systemcompensate for any negative effects heat might have in causing increased consump-tion of the limited oxygen that is available. In other circumstances the opposite wouldhold true.

Snow showed further evidence of his understanding of the physics and physiol-ogy of respiration, as well as his ability to put that knowledge to clinical use, whenhe discussed a new apparatus for paracentesis of the thorax at the Westminster twomonths after delivering the paper on stillborn resuscitation.63 Paracentesis is thewithdrawal of fluid from the pleural space (the space surrounding the lungs) to al-low the lungs to expand fully and relieve labored respiration. Conventional meth-ods of draining fluid from the pleural cavity allowed air to flow in as the fluid waswithdrawn. Snow’s explanation of why this was undesirable began with a brief re-view of the mechanics of respiration. “In the normal condition there is no vacantspace within the thorax. The pleura on each side of the chest is a vacant bag, merelylubricated on the inner surface with serum; and the pulmonary and costal portions


glide gently over each other during respiration. Whenever any fluid, whether aliquid or a gas, accumulates within the pleura, it is desirable that we should getrid of it.” When the diaphragm is depressed during normal inspiration, the pres-sure in the lungs becomes slightly less than the pressure of the atmosphere, andair comes in through the trachea, expanding the lungs to fill the space made avail-able. “But so soon as an artificial opening is made into the pleura, the atmosphericpressure is at once equal on the inner and outer surfaces of the lung on that side;it collapses in accordance with its own elasticity, and remains unaffected by themotions of the ribs and diaphragm.” When the diaphragm is depressed underthese circumstances, it sucks in air through the opening in the pleura, which com-presses the lung and does not allow it to expand. “It follows from this that at thecompletion of paracentesis, performed in the usual way, the lung must be col-lapsed, and the space between it and the ribs occupied by air, provided all the liq-uid has been removed. And, in fact, with the stethoscope applied to the chest dur-ing the operation, the air can be heard passing in by bubbles as the liquid flowsout.” By replacing one fluid in the pleural space (pus or serum, depending on theunderlying disease process) with another fluid (air), one has done nothing to re-lieve the basic problem.64

Snow then outlined an ingenious procedure that would work. He believed that,“provided the serum can be removed without making a communication betweenthe external air and the pleura, I do not see why tapping may not be performedon the thorax with . . . safety and success. . . .” A Glasgow physician, Dr. David-son, had tried but failed to prevent the ingress of air by applying a cupping glassover the canula. Snow showed his colleagues an instrument manufactured for himwith great accuracy, again by Mr. Read of Regent Circus. It consisted mainly ofan outer hollow tube (canula) and an inner solid tube (trocar). Both trocar andcanula had beveled ends so that when one was placed within the other, the entireapparatus formed a thick, solid needle suitable for puncturing the pleural cavity.The trocar could then be withdrawn, leaving the canula as a hollow tube con-necting the pleural cavity with the outside, suitable for sucking out fluid. Thenovel feature was a stopcock near the outer end of the canula. This had been ex-tended so that the accurately machined trocar, which bore a mark, could be with-drawn beyond the stopcock while maintaining an airtight fit. The stopcock wouldthen be closed, the trocar removed, and an elastic tube connected at one end toa double-action valved syringe like a stomach pump. Fluid could thus be removedwithout allowing air to enter, and “the integrity of the chest as a pneumatic ap-paratus is not impaired during the operation.”65 With characteristic generosity,driven by the belief that the practice of medicine should be a public service, helaid before the society a drawing of the instrument that any member could havedevised by his own instrument maker. Snow had provided both a clear physio-logic rationale and a practical way to bring that wisdom to the bedside for the re-lief of the patient.66


Deeper Into Asphyxia

Snow’s interest in the mechanisms of asphyxia was again evident two years laterin a published paper on circulation in the capillary vessels.67 Again, he reasonedback and forth between the realms of physiologic theory and practical therapeu-tics. The medical question at issue was whether the pumping force generated bythe heart fully accounted for the circulation of blood in the capillaries. A numberof experimental findings suggested that it did not, and he reviewed the relevantliterature. He then proposed a unifying explanation: Capillary flow was assisted bythe “attractions and repulsions” caused by the “mutual changes which take placeat the capillaries, between and blood and the tissues.”68 As some substances moveout of the bloodstream to nourish the surrounding tissues, and as other substancesmove into the bloodstream to be carried away from the tissues, all these processesof exchange create and impart a motive force to the flow of blood in the capillar-ies.69 One piece of evidence he offered in support of his hypothesis was the arrestof the pulmonary circulation in a state of asphyxia. Once the exchange of gaseshas ceased to occur within the pulmonary capillaries, the motive action of the heartis insufficient to propel the blood through the pulmonary circulation. He arguedsimilarly that camphor and other volatile medicines were capable of assisting dif-ficult and impeded respiration. By virtue of the fact that they were exhaled withthe breath in chemically unchanged form, these medications exerted an increasedattractive force upon the pulmonary circulation that could help to remedy the ef-fects of certain lung diseases.

Snow suggested that this group of medicines might be called “diapnetics,” basedon their analogy of function with diuretics—the former enhanced excretion throughthe lung, the latter through the kidney.70 His reason for claiming the privilege ofnaming this group of medicines was a peculiar one. He did not claim to have dis-covered any of the medications. He claimed, instead, to have discovered the fact thattheir common medicinal and chemical properties allowed them to be classified as afamily of agents. The family resemblance lay both in the chemical fact that they un-derwent no alteration in the body before they were exhaled and in the (purported)therapeutic fact that they could assist impeded respiration. While the individualdrugs had been known previously, Snow now suggested that the profession had failedto appreciate the family resemblance and its underlying chemical mechanism. Hewas tentatively exploring the notion that a hypothesized family resemblance amonga class of drugs could henceforth guide his research into the properties and mecha-nisms of these and related drugs, both in the laboratory and at the bedside, and hisattempts to better integrate laboratory findings with bedside observations. Chem-istry was the laboratory science Snow was most likely to employ. If microscopic examination was of value, however, he referred to what others described. He mayhave considered this collateral science insufficiently developed to be helpful in manyinstances.71


Although his research focus was on respiration, Snow remained engaged in thefull range of topics discussed at the Westminster Medical Society.72 When com-menting he occasionally referred to experimental work of his own, such as the useof dogs and cats as subjects, differences between ordinary respiration and cough,chemical studies of the absorptive actions of the gut, experiments relating to dia-betes, and the effects of woorara poison on guinea pigs.73 In February 1839 he com-mented about malformations in birds and reptiles, and in April he discussed ap-propriate treatment of mental diseases. Some years later he discussed mind–bodyinterdependence, the relationship between plague and outside temperature, and howhe had counted an adult lion’s heart rate at sixty by observing the pulsations of theradial artery.74

Snow’s may have been a shy man who either kept to himself or kept his colleaguesat a polite social distance, but he did have some close friendships. One was surelyPeter Marshall, the surgeon in Greek Street who lived near him. In three publica-tions, Snow referred to Marshall as “my friend.”75 Marshall was also Snow’s generalpractitioner. In the summer of 1845, when he developed a protracted illness sug-gesting a kidney disease, Marshall undertook his medical care, eventually consultingDrs. Richard Bright and William Prout, both notable authorities on kidney disor-ders.76 They persuaded him to take a vacation, an unusual practice for him. He vis-ited his friend and one-time roommate, Joshua Parsons, in Somerset. Parsons wassurprised to find that Snow was now taking a little wine and eating some meat. Thephysicians must have convinced him that teetotalism and a strict vegetarian regimenwere unsuited to his delicate state of health. He ended his summer vacation with ashort visit to the Isle of Wight and then returned to London and resumed his nor-mal schedule.77

Seeking an Academic Position

The dual qualification MRCS and LSA that Snow obtained in 1838 was the basic le-gal requirement for general practice, but Snow wanted more than what the life of atypical GP had to offer. In addition to involvement in medical societies and experi-mental research in his home laboratory, he wanted an academic post and certifica-tion as a physician.

Two pathways to an academic post in medicine existed at the time. Each hospitalappointed two or three surgical and medical “visitors.” These were unsalaried posts,but they brought their occupants many referrals and prestige. Well-heeled patientsexpected their surgeon or physician to be experienced, and where better to gain itthan on the bodies of those who had no choice but to go to a hospital? In Londonthe most sought-after visitor posts were at the hospital-based medical schools, whichgave one an academic appointment and often first chance at the second pathway, alectureship in surgery, medicine, or obstetrics. There were, of course, other subjects


to teach and therefore other posts available. Qualification as a surgeon made “Mr.Snow,” as he was referred to in the medical journals, eligible for an appointment assurgical visitor, and Richardson states that he found a vacancy in the outpatient de-partment at the Charing Cross Hospital. However, he is not listed as such on anyrecords housed in the hospital archives, so at best he had an informal arrangementthat never eventuated in a formal position.78

Only physicians were eligible to be medical visitors, and many medical school lec-tureships also fell to doctors of medicine; whatever his ultimate goal, Snow decided hewanted to attain the triple crown in his field. The bachelor of medicine (MB) was aprerequisite, and only Oxford and Cambridge had offered these degrees in England forseveral centuries, but since 1828 the University of London in Gower Street, within walk-ing distance of Snow’s flat, had offered both degrees. Table 4.2 lists the requirementsfor the MB, along with remarks on Snow’s ability to meet each of them. The Hunter-ian School of Medicine was a “recognized” institution, which permitted Snow to by-pass the required lecture courses and proceed directly to the examination when he felt


Table 4.2. Prerequisites for a bachelor of medicine (MB) degree examination at the University of London in 1844

Prerequisites Snow’s Status

At least 19 years old Age 30 in 1843

Degree in arts from recognized university, No degree in arts; exempted from or passed University of London matriculation examination after matriculation examination translating a portion of Celsus’s

De Re Medica

At least 2 years’ attendance at recognized Completed full curriculum, Hunterian medical school School of Medicine; one year of

courses in Newcastle

Attended course of lectures in four of the Attended ten of these courses, either following subjects: descriptive and surgical at the Hunterian or in Newcastleanatomy, general anatomy and physiology,comparative anatomy, pathologicalanatomy, chemistry, botany, materiamedica and pharmacy, general pathology,general therapeutics, forensic medicine,hygiene, midwifery, surgery, medicine

Nine months of dissection Completed at the Hunterian

Course in practical chemistry and ability Satisfied at the Hunterian; publicationsto carry out common laboratory procedures demonstrated this facility as well

Practical knowledge of preparation of Qualified as LSAmedicines

Source: University of London Calendar, 1844, 44–45; Alun Ford to David Zuck, 27 February 2001; JuliaWalworth, University of London Library, to David Zuck, 4 August 1989.

he was prepared.79 He took the examinations given on 23 November 1843. To pass hehad to demonstrate both theoretical and practical knowledge, answering, among oth-ers, questions on how to tell blood spots from rust spots, the poisonous dose of lau-danum in an infant and the symptoms it would produce, the determination of preg-nancy in a variety of cases, the anatomy of the portal system, the nature of ciliary motion,and the auditory apparatus of the cuttlefish, a fish, and a reptile. He passed, placing inthe second division.80 Upon gaining this degree, custom permitted him to replace hissurgeon’s designation with the physician’s title, Dr. Snow, although it was increasinglyexpected that “Dr.” should be reserved for recipients of the MD.81

A year later he was among the candidates at the University of London who hopedto pass the arduous oral and written examinations for the MD degree. All had toshow proficiency in philosophy and logic in the form of written commentary on ex-cerpts from Locke, Berkeley, and Leibnitz. All had to translate passages from Frenchand Latin. They had to discuss a case of rheumatism accompanied by chest pain anda heart murmur, a surgical case involving management of bladder stones, and a mid-wifery case with secondary arrest of labor followed by spontaneous delivery. Finally,they were asked questions on displacement of the heart, scarlet fever, pneumonia,pleurisy, diarrhea, and delirium tremens.82 This time Snow was placed in the firstdivision. Passing this academic milestone also provided a suitable occasion for hav-ing his portrait painted for the first and only time (Fig. 4.1).83 Snow now possessedthe credentials required for a medical school post.

The medical schools of London were in considerable flux at this time; those of thelarge teaching hospitals, with their attached clinical facilities, were growing in statureand influence and displacing the private ones, a number of which, like the Hunterian,had closed. In the eastern part of London, however, the private medical school in Alders-gate Street had for some time provided stiff competition for the nearby St.Bartholomew’s Hospital Medical School. For many years the Aldersgate school hadboasted a string of popular lecturers that the hospital school could not match and forsome time brought St. Bartholomew’s (“Bart’s”) to the brink of closure.84 Alfred Bar-ing Garrod, a friend of Snow’s through the Westminster Medical Society, had joinedthe Aldersgate Street School in 1844 as a lecturer in materia medica. Two years laterthe lectureship in forensic medicine became vacant, and Snow was appointed. His workon poisons and his knowledge of obstetrics would have been applicable to the sub-ject.85 His first lectures on forensic medicine were duly advertised in the fall issue ofthe Lancet: one course to be offered in the summer session of 1847. Enrollment re-quired a ticket costing two pounds, two shillings.86 Snow thought highly enough ofhis academic appointment to add his description as “lecturer in Forensic Medicine atthe Medical School, Aldersgate Street” to several papers published in 1846 and 1847.87

However, the school’s fortunes soon fell as its rivalry with Bart’s took a dramati-cally different turn. Some five years earlier, Bart’s had scored a double victory overits rival by attracting Mr. James Skey, a well-respected lecturer in anatomy, away fromthe Aldersgate and by appointing the extremely popular James Paget as its new lec-turer in physiology. As the years went by it became clear that the Aldersgate School


could not offer a staff of lecturers in the most basic subjects to rival the reputationof the new Bart’s faculty.88 It was in disarray by the fall of 1848; it was late in pub-lishing a prospectus for the coming session, and when it did the lecturer in forensicmedicine was not mentioned. In all likelihood, however, Snow offered the course.The school closed completely at the end of the 1848–1849 session, and the final re-ward from his short association with it was the privilege of helping pay off its debts.89

Alfred Baring Garrod transferred to University College Hospital, but Snow appar-ently made no move to seek another academic post.

Snow in 1846: The Mind Prepared—For What?

In his first ten years out of medical school, Snow was able to make a living as an urban general practitioner. He attained considerable scientific skill, some degree ofprofessional recognition, and a level of education and certification that took himnear the top of his profession. In some other ways he seemed hardly to have left therural north. He cared daily for the same class of working poor among whom he had


Figure 4.1. John Snow, age about 33 (portrait by Thomas Jones Barker, courtesy of Geoffrey

Snow; black-and-white reproduction supplied by David Zuck).

grown up in York, reinforcing his generally egalitarian outlook. His austere lifestylefit well with his habitual moral rectitude. He had personally investigated a wide rangeof medical problems, many of them suggested by his experiences as a practitioner.He had identified with and learned from a group of authorities who represented themost advanced thinking in physiology and chemistry. He had developed rare skillsthat allowed his mind to flow easily among the three realms of bedside, hospital, andlaboratory medicine. Given any medical issue, Snow could readily imagine whatwould be seen when one examined a patient at the bedside, what sorts of statisticalregularities one might uncover by considering a series of cases, how one might elu-cidate basic mechanisms through laboratory experiments—and, finally, how onecould take back to the bedside the fruits of one’s research to improve the care of thepatient and the general public health.

Snow’s research skills were widely applicable, but he tended to focus rather thanscatter his research efforts. From the beginning he had identified respiration and as-phyxia as his special province. He devoted special attention to the effect of respira-tion on the circulation and the chemistry and physics of inhaled gases. He was prov-ing adept at designing apparatuses based on a clear understanding of underlyingscientific mechanisms and well adapted to practical needs. He had illustrated hisskills and interests in his entire series of scientific publications, perhaps none morestriking than the 1841 paper on the resuscitation of the stillborn infant. It was in-formed by major philosophical questions: What exactly was the dividing line be-tween life and death, living and nonliving? What was the basic difference betweenan infant born apparently dead but destined to live, and one who would remaindead? What made states of near-death reversible or irreversible? What was the rela-tionship between the oxygenation of the organism and its state of sensibility or in-sensibility to stimuli such as pain? How could asphyxia be distinguished from otherstates that resembled it but that had fundamentally different properties? What roledid temperature play in all of these processes? All of these questions provided aframework for the scientific investigation of related puzzles that might present them-selves to Snow in the future. As 1847 approached Snow had much to be thankful for.

Nonetheless, he remained a relatively obscure general practitioner, little knownoutside two London medical societies and a small private medical school whose bestyears were behind it. He still had a flat in Frith Street, and he still worked long hoursserving working-class patients for the most part. The time and energy available formedical research were limited. No change for the better was on his horizon. Thencame news about ether anesthesia.

Notes

1. Richardson, L, ix.2. Mozart had lodged in Frith Street, Constable had lived there, and Hazlitt had died there.

Hare, Walks in London, 126–132; Weinreb and Hibbert, London Encyclopaedia, 295, 779; Cun-ningham, Hand-Book of London, 193, 445–46.


3. Robson, Royal Court Guide, 29. We are grateful to Agnes H. Widder of the MichiganState University Library for providing research assistance with the city directories and 1841census reports.

4. UK Home Office, 1841 Census, H.O. 107/730/3, 10–32 (County of Middlesex, Liberty ofWestminster, parish of St. Anne-Soho; Registrars’ districts, Strand/St. Anne Westminster/3).The population may be somewhat inflated because enumerators included overnight visitors.

5. Ibid., 15–16; Pigot and Co., Royal Street Directory of London for 1840, 122.6. Pigot and Co., Royal Street Directory of London for 1840, 122; Robson, London Directory

for 1840, 132. The first city directory listing for Snow that we have found was in 1840. In 1841the enumerator wrote Williams; UK Home Office, 1841 Census, H.O. 107/730/3, 27. Ten yearslater, the spelling changed to Williamson, the same used by Richardson; 1851 Census, H.O.107/1510/82; and Richardson, L, ix.

7. Robson, London Directory for 1838, 163; for 1839, 129; for 1840, 132; for 1841, 136–37;for 1843, 121. “Physicians,” Pigot & Co., Directory of London, 1839, 180–81.

8. S. Snow, JS-EMP, 331–32. For a discussion of the travails of the fledgling Victorian physi-cian trying to set up practice in a town where he has no social relations and connections, seePeterson, Medical Profession, 90–135. Peterson relies heavily on the fictional Dr. Stark Munro,a character created by Arthur Conan Doyle in his semiautobiographical novel The Stark MunroLetters (1895). Peterson argues that the problems faced by Stark Munro were typical of theentire Victorian period. Doyle provided a condensed portrayal of Dr. Stark Munro, with “morein his brains than in his pocket,” in the better-known character of Dr. Percy Trevelyan in theSherlock Holmes story “The Resident Patient”; Doyle, Memoirs of Sherlock Holmes, 177–78.We are grateful to Christopher Hamlin for pointing out that contemporary medical autobi-ographies, such as that of Thomas Watson, confirm these points; private communication.

9. On Diamond see Gilman, The Face of Madness.10. Robson, London Directory for 1841, 136–37; UK Home Office, 1841 Census, H.O.

107/730/3, 11.11. Richardson, L, xii; Digby, British General Practice, 79.12. In the 1830s some medical men were paid as little as 2 shillings per person per year;

Peterson, Medical Profession, 114–15.13. John Simon, as head of the medical department of the Privy Council, created a Labo-

ratory Investigation Division in 1865 that employed several physicians on a part-time basisand whose employees eventually became leading medical scientists; Lambert, Sir John Simon,279–84. Full-time positions attached to medical schools employing physician–scientists re-mained the vision of reformers rather than an accomplished reality; Worboys, SpreadingGerms, 27.

14. Richardson, L, ix–x, xl. He also stated that Snow in later life regretted not having mar-ried and had children, noting vaguely, “the fates had been against him permanently on thatscore”; Ibid., xxxviii.

15. Ibid., x, xxxiii. A reporter at a December 1838 meeting of the Westminster Medical So-ciety noted that “Mr. Snow now made some observations in a very low tone, and consequentlyhis meaning could not be very well caught”; LMG 23 (1838–39): 426. The reporter for theLancet at the same meeting apparently was sitting closer to Snow and was able to report hisstatement, which had to do with chemical affinity between gases and the role that played inthe amount of oxygen the lungs could extract from the air; “Westminster Medical Society,”Lancet 1 (1838–39): 419. Similar remarks about Snow’s lowness of voice may be found in“Westminster Medical Society,” LMG 23 (1838–39): 954.

16. Richardson, L, xxxix.17. Ibid., xii.18. Ellis, CB, 121.


19. Snow listed himself as a general practitioner in the 1845 London Medical Directory butby 1847 had changed his designation to “physician and accoucheur,” indicating the signifi-cance he attached to obstetric work in his evolving career; S. Snow, JS-EMP, 209. Between Oc-tober 1849 and September 1850, fully half the new patients Snow added to his practice wereobstetrical cases; Ibid., 286. By then he was also increasingly restricting himself to adminis-tering anesthesia.

20. Peterson, Medical Profession, 99–100.21. We might wonder how Snow was regarded as a practitioner by his peers. At least some

colleagues viewed Snow as a shrewd clinician who could be a valuable ally when faced with apuzzling case. Richardson described Snow’s talents: “He had great tact in diagnosis; an ob-servant eye, a ready ear, a sound judgment; a memory admirably stored with the recollectionof cases bearing on the one in point, and a faculty of grouping together symptoms and fore-shadowing results, which very few men possess.” Richardson, L, xxxix. Richardson stated thatanother close associate of Snow’s who had in fact consulted with him on a number of diffi-cult cases, Mr. Peter Marshall, would concur item by item with this description. Richardson’spraise was part of a eulogistic memoriam, and Richardson did not meet Snow until fifteenyears after these events. Nevertheless, Snow’s published case reports and commentaries seemto lend some support to Richardson’s opinion.

22. Richardson, L, viii–ix. The importance of medical societies for the development ofnineteenth-century medicine, of which Snow’s experience might be seen as a microcosm, isstressed by S. Snow; JS-EMP, 173.

23. S. Snow, JS-EMP, 172. The annual sessions of the medical societies generally ran fromearly October to early May.

24. Lancet 1 (1842–43): 327; Lancet 1 (1843–44): 163. Snow’s election as vice-president wasnoticed in AMJ 1 (1853): 218; he added “Vice-President of the Westminster Medical Society”to his by-line in the fourth paper of an eight-part series, “On narcotism by the inhalation ofvapours,” LMG 41 (1848): 330–35.

25. “The Westminster Medical Society,” BMJ 2 (1896): 26; Hunt, Medical Society of Lon-don, 3–5, 15–18, 73–74. We are grateful to Roy Porter and Caroline Overy for aiding us inidentifying these sources. Richardson apparently was still grieving the old Westminster namewhen he reported in 1858 that the venerable organization had “sunken into” the Medical So-ciety of London; L, viii. However, it was very important that the Medical Society of London’stitle to its property not be jeopardized, because it was precisely as a result of owning its ownmeeting house that the new amalgamated society could be financially secure.

26. Snow’s election as fellow of the Royal Medical and Chirurgical Society was announcedin M-CT 26 (1843): xxii.

27. On the social and political orientations of the society, see Desmond, Politics of Evolu-tion, 223–25.

28. See Hardcastle’s requirements for certification as an apothecary; Society of Apothe-caries, “Court of Examiners entrance books,” MS 8241/1, 213.

29. A reflection of the new interest in medical affairs outside Britain was the inaugurationof the British and Foreign Medical Review in 1836.

30. “Westminster Medical Society,” Lancet 1 (1839–40): 441–44. Snow’s paper was “Theanasarca which follows scarlatina”; only the reporter’s summation exists. Scarlet fever was adreaded disease right up to the introduction of sulphonamide drugs in the mid-1930s; valvu-lar disease of the heart resulted from the associated rheumatic fever. Bright himself was awareof the causative association between kidney disease and an earlier attack of scarlet fever; Peitz-man, “From Bright’s disease to end-stage renal disease.” We are grateful to Dr. Peitzman forthe further information that William Charles Wells and John Blackall, between 1810 and 1820,had described the relationship between scarlet fever and dropsy, although they did not view


the dropsy as representing renal disease. While Snow’s observations were thus not original,the recognition of the relationship between scarlet fever, dropsy or anasarca, kidney disease,and albumin in the urine was still fresh in 1839, thereby justifying the reporting of a series ofcases; e-mail message; Peitzman to Brody, 27 February 2002. See also Maher,“Origins of Amer-ican nephrology.”

31. R. Bright, Reports of Medical Cases and “Cases and observations.” See also P. Bright, Dr.Richard Bright, 131–42.

32. The test most commonly used for albumin in the urine at that date was gross andqualitative—heating a teaspoon of urine over a candle flame to see whether coagulationoccurred; Peitzman, “Bright’s disease.”

33. No first name is given, but the content of the remarks make it unlikely to have beenThomas Addison of Guy’s Hospital.

34. Golding Bird, it appears, by this time accepted the basic fact that urea accumulated inthe blood in Bright’s disease of the kidney. In 1833, as a young student at Guy’s, he had madehimself somewhat notorious by engaging in a running debate (in the pages of the LMG) withanother student of Bright’s, George Owen Rees, in which Bird had taken the losing side onthe question of whether urea was increased in the blood; Peitzman, “Bright’s disease,” 316. Seealso Coley, “The collateral sciences in the work of Golding Bird.”

35. Snow’s prescribing habits and general mode of practice were not noticeably differentthan those of the usual general practitioner of his time; see Earles, “Prescription records,” CB,xliv–l. The new discoveries resulting from hospital and laboratory medicine were only slowlyapplied to therapeutics and did not affect daily practice until very late in the nineteenth cen-tury; see Warner, The Therapeutic Perspective, and Durey, The Return of the Plague, 133.

36. S. Snow notes the importance of journal publication in advancing the careers of physi-cians; JS-EMP, 184. She also notes that when Snow listed his name in the 1845 London Med-ical Directory, he mentioned five papers he had published and also noted that he was inven-tor of a new instrument for paracentesis of the thorax and of a sponge pessary; Ibid., 209.

37. Snow, “Arsenic as a preservative” (1838). Wakley’s comment seems gratuitous becauseSnow had himself admitted that not all dissectors fell ill and that illness might depend onvariables such as room temperature. Wakley was an advocate of the clinical–pathologicalmethod introduced to London medical schools by Scottish trained surgeons; see editorialsabout the need for ready access to autopsies and complete case notes for students walking thewards in Lancet 1 (1836–37): 16–17. For his view of scientific medicine, see the book reviewthat “wisely advises” that “the progress of medicine, as an inductive science, is retarded by theconstruction of hypothetical theories . . . and by the deduction of general principles or con-clusions, from a limited number of facts”; Lancet 2 (1831–32): 153.

38. Snow, “Mechanism of respiration,” (1839). Goodman’s paper, read to the ManchesterMedical Society, had appeared in Lancet 1 (1838–39): 515–19.

39. Goodman, Lancet 1 (1838–39): 515.40. Snow, “Mechanism of respiration,” 653.41. Ibid.42. In Goodman’s defense, Magendie and investigators following the line of Lavoisier’s in-

vestigations of the chemistry of respiration were proposing new concepts in physiology sorapidly that one medical man complained, “How often does it fall to the lot of the student ofphysiology to unlearn what he has been at pains to acquire!” See Williams, Observations, 7.

43. Desmond, Politics of Evolution, 342, 346–47.44. For a contrary interpretation, see P. E. Brown, “Autumn loiterer” and “Another look.”

Snow’s harshest critic, Brown considered him an upstart who sought instant visibility by at-tacking an older, established medical man.

45. For brief synopses of the work and influence of these two figures in nineteenth-


century medical science, see Porter, Greatest Benefit, 327–29, 333–34, 337–38. Müller and Ma-gendie were perhaps less influential than the students they trained—Hermann von Helmholz(1821–1894) and Karl Ludwig (1816–1895) in Müller’s case, Claude Bernard (1813–1878) inMagendie’s. Snow lacked the expanded laboratory facilities those investigators enjoyed someyears later on the Continent. Snow remained in the generation of experimental physiologistswho mostly studied intact animals and who had limited abilities to derive quantitative data.The capability of isolating specific organs and tissues for physiological experiments and de-riving precise measurements of their functions was beyond Snow’s facility at that time.

46. “M.H.,” “Note on respiration and asphyxia,” Lancet 2 (1838–39): 240.47. Snow, “On asphyxia, and the resuscitation of still-born children” (1841–42), 227.48. Lancet 2 (1838–39): 352.49. Snow did not publish in the Lancet again until 1846, when he sent a brief epistle at-

tacking homeopathy, with which he believed Wakley would sympathize; Lancet 1 (1846): 229.Indeed, Wakley appended a favorable comment.

50. “Westminster Medical Society,” LMG 24 (1838–39): 60, 62.51. Ibid., 61. Snow published these results several years later; see “On the pathological ef-

fects of atmospheres vitiated by carbonic acid gas, and by a diminution of the due propor-tion of oxygen” (1846). Because it is difficult in this article to separate the experiments he un-dertook in 1838 from those that came later, we have relied on the synopses reported in themedical journals.

52. Ibid.53. We have omitted from Table 4.1 Snow’s letter “On the use of the term ‘allopathy’“(1846),

in which he dismissed homeopathy as an unscientific fad. The letter is not properly a scien-tific report but rather an expression of political opinion.

54. S. Snow agrees that the contents of these early papers show Snow concentrating on res-piration, but she also claims that he indicated an equal interest in “epidemic disease”; JS-EMP,203. We have found no evidence of the latter.

55. “On distortions of the chest and spine in children” (1841).56. Snow, “On asphyxia, and on the resuscitation of still-born children” (1842); “West-

minster Medical Society,” Lancet 1 (1841–42): 132–34. Shephard considers this paper partic-ularly significant for Snow’s later anesthesia research; JS, 45.

57. Owen, “A man called Read.” Read (1760–1847) was born in Sussex and trained as a hor-ticulturalist. He invented a brass syringe for spraying plants and, having read reports of deathsfrom poisoning, modified it for use as a stomach pump. He was taken up by Sir Astley Cooperand opened a workshop in Southwark, near Guy’s Hospital, moving later to Oxford Circus.Versions of his pump, which was used also as an enema syringe, are illustrated in Brockbank,Ancient Therapeutic Arts, 53–56.

58. Snow, “On asphyxia,” 226.59. “Westminster Medical Society,” Lancet 1 (1841–42): 149–51.60. “Westminster Medical Society,” Lancet 1 (1841–42): 212.61. Ibid., 213; Hunter, “Proposals for the recovery of persons apparently drowned,” dis-

cussed by Zuck, “Diagnosis of death.”62. The remarks in which Snow most fully developed his vision of medicine and the col-

lateral sciences came later, when he assumed the presidency of the Medical Society of Lon-don; “Medical Society of London,” Lancet 1 (1855): 292.

63. Snow, “On the paracentesis of the thorax” (1841).64. Ibid., 705–06.65. Ibid., 707. In a footnote the editor of LMG added that although Snow had provided a draw-

ing of the instrument, the description in his text was so clear that it was not thought necessary


to have an engraving made. According to Zuck the innovative nature of Snow’s apparatus hadnot been fully appreciated; “John Snow on paracentesis of the thorax.” His invention was the pre-cursor of all trocars and canulas and all exploring and spinal needles fitted with a stopcock, ofwhich there are many to be found in instrument catalogues. Until 1920 the routine treatment forempyema was still rib resection and open drainage, and many died as a result. Matters came toa head during the 1918–1919 influenza epidemic, when a large number of victims suffered fromthe complication of streptococcal empyema. The death rate among American servicemen as a re-sult of open drainage was so appalling, seventy percent in some centers, that an Empyema Com-mission was set up to find the cause. Its report pointed out the fatal error of the neglect of thephysiology of the open chest wound; Coope, Diseases of the Chest, 376–77.

66. After Snow presented his new instrument for paracentesis, he had to defend the propo-sition that it was bad for air to be admitted into the pleural space as the pathologic fluid waswithdrawn. Dr. William Addison, Dr. Frederick Bird, and Dr. Golding Bird all defended theview that air in the pleural space was harmless—or at any rate, that as air was much moreeasily compressible than a liquid, replacing the pathologic fluid with air would be a thera-peutic advantage. Snow had to go back and restate the basics of the physics and physiologyof respiration, adding that while air was an elastic and compressible fluid, in the pleural cav-ity it would expand during inspiration and be compressed during expiration, thereby im-peding lung movement. In this instance, at least, resistance to Snow’s ideas crossed the “gen-eration gap” within the society; “Westminster Medical Society,” Lancet 1 (1841–42): 484–86.

67. Snow, “Circulation in the capillary blood-vessels” (1843). Snow had mentioned his pre-ferred theory of capillary circulation in “On asphyxia” (1841), 224.

68. Snow, “Circulation in the capillary blood-vessels” (1843), 810.69. Snow was at his most preliminary and least speculative mood in this paper: “I have

nothing to advance respecting the intimate nature of the attractions and repulsions which ac-company the changes of composition at the capillaries, and which tend to move the blood ina definite direction. I have carefully avoided such terms as chemical, electrical, and vital, bothin order that I might not be misunderstood, and because I look upon chemical affinity, elec-tricity, and vitality, rather as expressions which are useful to us in the infancy of science thanas forces which have a separate and defined existence”; Snow, “Circulation in the capillaryblood-vessels” (1843), 813. By contrast, in CMC ten years later Snow would speculate morefully on the (chemical) nature of these forces and processes.

70. “Circulation in the capillary blood-vessels” (1843), 813. Snow’s proposal to classify aseries of medications as belonging to a single family might at first glance appear to be a stan-dard move of his time, following in the Linnaean tradition made popular in English medi-cine by Sydenham and Cullen. What seems to us distinctive is Snow’s use of underlying chem-ical properties and mechanisms, and not merely similarities in clinical effects, as part of therationale for creating the “family.”

71. Porter, Greatest Benefit, 320–21. In the 1840s and 1850s microscopes had relatively poorresolution, and no chemical stains were available. Snow’s avoidance of microscopy ran counterto the recommendations of one of his virtual teachers, the physiologist Müller, who particu-larly emphasized that branch of science; Ibid., 327.

72. Richardson provides a picturesque account of the timid young Snow being largely ig-nored when he ventured his first comments at the meetings of the Westminster and only veryslowly winning the respect of his elders; L, ix. The records of the meetings as published in theLancet and LMG suggest otherwise. Snow seems to have been an active discussant almost fromthe beginning of his involvement with the Westminster, at least following his role in the in-vestigation of the arsenical candles. If anything, he spoke with greater frequency during hisearly years in the society than later.


73. For these meeting reports see the notices for “Westminster Medical Society”respectivelyin LMG 24 (1838–39): 255–56; Lancet 1 (1842–43): 184; MTG 4 (1852): 22–24; MTG 10 (1855):167–68; and Lancet 1 (1855): 242–43.

74. “Westminster Medical Society,” Lancet 1 (1838–39): 771–73; “Westminster Medical So-ciety,” Lancet 2 (1838–39): 200; “Psychotherapeia,” MTG 6 (1853): 331–33; “The Indian plagueand the Black Death,” MTG 7 (1853): 614–15; “Physiological meeting,” MTG 7 (1853): 541–42.

75. Richardson, L, xiii. One would guess that any friend of Snow’s from those days wouldprobably be active in the Westminster Medical Society. Peter Marshall served as president ofthe Medical Society of London in 1869, the year following Richardson’s term in office. On atleast one occasion Snow returned the favor and assisted Marshall in some research. On 14September 1846 Marshall read a paper on sudden death before the Westminster and ac-knowledged that Snow assisted him in the autopsy; Lancet 2 (1846): 586.

76. Snow’s health appears to have been indifferent from his student days. Parsons recalledthat Snow periodically suffered from fever and rapid pulse after minor injuries and often ex-perienced fatigue, even though Snow was able to complete all but the last mile of a fifty-mile,one-day walk on Easter Monday, 1837; Richardson L, vi. Sometime before 1845 he also de-veloped symptoms suggestive of incipient pulmonary tuberculosis but “took plenty of freshair, and recovered”; L, xiii.

77. The modern view is that Snow suffered from longstanding hypertension that causedhis premature death by stroke; Shephard, JS, 70. Hypertension could result from kidney dis-ease or could itself be a cause of kidney disease.

78. Richardson, L, x. An exhibit about Snow at the London School of Hygiene and Tropi-cal Medicine in May 1855 included a poster that stated, “In 1838 he became a visitor to theOut-patient Department at Charing Cross Hospital”; Clover/Snow Collection, VIII.2. He isnot listed as such in the hospital minute books between 1834 and 1845, although an infor-mal appointment is a possibility because Charing Cross Hospital was affiliated at that timewith Westminster Hospital, where Snow trained in 1837–1838; search undertaken by HowardHague (assistant librarian, Charing Cross Hospital), electronic communications to Brody, 27March 2002 and 21 June 2002. Although Snow never included an affiliation with CharingCross as a by-line in his early articles, he began a late paper as follows: “On commencing, inthe year 1839, to see a considerable amount of practice amongst the poor of London, chieflythe out-patients of a public hospital, I was very much struck with the great number of casesof rickets”; “Adulteration of bread as a cause of rickets” (1857), 4.

79. For a contrary but undocumented view that Snow had to complete additional lecturecourses, see Shephard, JS, 38.

80. These questions, mostly from the forensic medicine portion of the exam, were reprintedin Lancet 1 (1843): 195–96. Julia Walworthy (University of London Library, PaleographyRoom) in a letter of 4 August 1989 to Zuck confirmed Snow’s position among the successfulcandidates.

81. Richardson, L, xii. The reported minutes of the meetings of the Westminster MedicalSociety reflect this change in Snow’s title.

82. Shephard, JS, 39–40. Copy of the original MD examination from the University of Lon-don Library provided by Zuck, who believes that some of Snow’s research papers in 1843 and1844 may have been by-products of preparations for the MB and MD examinations.

83. For specific questions, Walworthy to Zuck, 4 August 1989. The name of the portraitistand the year it was painted remained unknown until Zuck, “Snow, Empson and the Barkersof Bath.”

84. In 1829 the Lancet advised St. Bartholomew’s prospective students to divide their at-tention: “Follow the teaching of Lawrence, Stanley and Earle at Bart’s, and go to the Alders-


gate Street School to learn from Clutterbuck in medicine, Cooper in chemistry and pharmacy,Waller in midwifery, King and Evans for demonstrations in anatomy”; Lancet 1 (1829–30):47, quoted in Cope, “The private medical schools of London,” 101. Dr. Henry Clutterbuck(1767–1856), besides being a distinguished lecturer on medicine, was an early president of theWestminster Medical Society; Story, “Henry Clutterbuck.”

85. “Gossip of the week,” MT 14 (1846): 68. A number of legal issues in medicine relatedto paternity and determining whether a woman was pregnant and the date at which she be-came pregnant. Other legal issues related to determining cause of death, including cases ofpoisoning. One of the few publications in which Snow assumed the role of a forensic spe-cialist was ON, Part 14 (1850), in which he addressed the question of detecting chloroformadministered antemortem in dead bodies. He mentioned several times having consulted withDr. Alfred Swaine Taylor, author of a popular textbook of medical jurisprudence and perhapsthe foremost forensic expert of the day, and he described his own investigation of tissues takenfrom “a woman who was found dead, under mysterious circumstances, in the WandsworthRoad” (327), which turned out to be negative for chloroform.

86. Lancet 2 (1846): 345. A similar notice appeared the next year: Lancet 2 (1847): after362.

87. The first such paper was “Some remarks on alkalescent urine and phosphatic calculi”(1846). This paper, incidentally, earned Snow praise from another quarter. Golding Bird wrotea treatise on urinary deposits that went through four editions. In the last he praised Snow’sexperiment on urine alkalinity for its elegance and conclusiveness. Snow’s experiment involvedkeeping newly voided urine in an upper vessel at a temperature of 100�F and dripping it intoa lower one at about the rate at which it enters the bladder. The upper vessel was emptiedcompletely and washed every six to eight hours, while the lower one always had a few dropsof the stale urine left in it. The result was that the urine in the lower vessel was always alka-line, while that in the upper was constantly acid; summation by Zuck. Bird concluded that“These researches afford a strong argument in favour of the practice of frequently washingout the bladder, in cases of alkaline urine”; Urinary Deposits, 280. The problem of alkalineurine, as both Bird and Snow explained, was that it predisposed to the precipitation of phos-phates and the formation of encrustation and stones.

88. Cope, “Private medical schools of London,” 103–04.89. Lancet 2 (1848): 376, 412. For Snow’s sense of irony about paying the debts, see Richard-

son, L, xiii.


110

ON SATURDAY, 19 December 1846, a London dentist, JamesRobinson, demonstrated the use of ether for the first time on his

side of the Atlantic. The demonstration occurred in the study of Dr. Francis Boott,an American living in London, who had learned of the new drug from friends inBoston.1 Sponges saturated with ether were placed in a glass vessel attached to anelastic tube and a mouthpiece. Robinson held this apparatus while Miss Lonsdaleinhaled the gas and was rendered unconscious. Robinson quickly extracted a firmlyfixed molar from her mouth and just as quickly she regained consciousness. The pro-cedure had taken a scant three minutes. The patient had felt no pain and had noteven moved a muscle.2

On receiving his letters from America, Boott had also notified Robert Liston, pro-fessor of surgery at University College Hospital.3 Liston and his medical student as-sistant, William Squire, arrived after the dental surgery performed on Miss Lonsdale,and they observed Robinson administer ether with considerably less success to threeor four other patients.4 Liston then consulted Peter Squire, William’s uncle, thequeen’s pharmacist, at his shop in Oxford Street. After another unsuccessful trial ofether (from a cloth), Liston had Squire construct an inhaler from part of a Nooth’sapparatus, a device for carbonating water. This apparatus worked better.5 On Mon-day afternoon, 21 December, with many influential people in attendance, Liston prepared to perform two operations, an amputation at the thigh and removal of a

Chapter 5

Ether

toenail, at University College Hospital. He was uncertain if ether would make pa-tients insensible during major surgical operations. Some practitioners of animal mag-netism claimed that they could induce insensibility in test subjects, but mesmericdemonstrations to date were more entertaining than medical. Would William Mor-tonís claims prove more conclusive? The benches in the operating theater werepacked, apparently with medical men and lay folk who were curious about the newagent and its first use in a London hospital.6 Liston is reported to have announced,“We are going to try a Yankee dodge today, gentlemen, for making men insensible,”but when the operation concluded successfully, he exclaimed, “This Yankee dodge,gentlemen, beats mesmerism hollow.”7

Robinson was still worried about the unpredictability of ether when given withthe modified Nooth apparatus. He developed alternative specifications for a new in-haler and mouthpiece.8 After several successful dental operations a week later, Robin-son was emboldened to give Boott another demonstration, which was successful.Then on Monday, 28 December, Robinson performed a dental operation with etheranesthesia “with the most perfect success in the presence of my friends—Mr. Stocks,Mr. Snow, and Mr. Fenney.”9 In this way John Snow saw with his own eyes what ethercould do.

Medical and Public Reaction

News of ether as an anesthetic agent had begun to swirl about London even beforeRobinson’s first demonstration. A day earlier LMG trumpeted, “animal magnetismsuperceded—discovery of a new hypnopoietic.” The editor noted that the writerclaimed “the process simply consists in causing the patient to inhale the vapour ofether for a short period, and the effect is to produce complete insensibility, —or

. . . intoxication.”10 But LMG’s endorsement was conditional: “Ether is a strongnarcotic, and its vapour speedily produces complete lethargy and coma. . . . It mustbe regarded as producing a state of temporary poisoning in which the nervous sys-tem is most powerfully affected.”11 By equating the drug’s power to induce sleep withits ability to kill pain, the editor had begun to ponder the mystery of this new condition.

Within a week of the announcement in LMG, Liston hailed anesthesia as successfulbased on his two cases of 21 December,12 but he was soon disappointed when otherpatients could not be put under at all, or insufficiently so to prevent pain.13 Mostmedical professionals, however, immediately endorsed ether as one of the importantdiscoveries of the age. In a time when medicine could deliver to the patient preciouslittle in the way of effective treatment and surgery was usually a last resort—a riskyand excruciating ordeal—ether seemed to promise a new era in the alleviation ofpain and suffering. Despite difficulties in administration and even some deaths at-tributed to the agent, a general consensus soon emerged that William Morton had

Ether 111

introduced “a radically new remedy to a profession undergoing massive changes”that orthodox practitioners could use to restore public trust after decades of in-creasing disillusionment with their heroic therapeutics.14 For example, Robinson de-scribed Morton’s discovery fancifully, calling the vapor of ether a form of “steam.”15

Just as steam engines were revolutionizing industrial production and transportation,Robinson believed ether would revolutionize the practice of medicine.

The lay press was not far behind the medical journals in addressing the new phe-nomenon. On 9 January 1847 the Illustrated London News, a popular magazine, car-ried an illustration of an ether inhaler. The Times blew hot and cold, and the humormagazine Punch greeted ether as a cure for scolding wives.16 If the public thoughtthat the world of medical practice had been turned upside down by this new dis-covery, they were not far off the mark. Ether brought the lower echelons of medicalpractice into contact with the elite. It brought dentists into the surgical theaters ofteaching hospitals and, in a short while, into the accoucheurs’ chambers as well.17 Itpermitted medically untrained entrepreneurs to engage in broad and sometimes riskymedical practice. Many of the important early discoveries and innovations with etherreflected this confluence of the different social strata of medicine. In the United Statesdentists like Morton and Horace Wells argued from the outset over patents and pri-ority, while Harvard medical men authorized the validity of their claims. Indeed,ether precipitated great activity along the entire spectrum of medical practice, fromstorefronts to hospital operating theaters. In 1847 most practitioners were contentto enjoy whatever financial benefits ether might bring or, like James Young Simpsonin Edinburgh, to flamboyantly champion a powerful drug that magically took awaypeople’s pain. An English physician publicly commenting on ether during the firstfew weeks of 1847—as Snow did—would initially have been seen as merely one ofa number of practitioners jostling for attention.

Snow’s Initial Approach to Ether

A variety of English medical opportunists were quickly off the mark and “gettingquite into an ether practice” within a fortnight of hearing about its new use as a painblocker.18 Richardson wrote that Snow encountered “a druggist . . . [who] withoutthe remotest chemical or physiological idea on the subject,” was bustling about townwith an apparatus under his arm and evidently doing a brisk business. “If he can getan ether practice,” Snow told Richardson, “perchance some scraps of the same thingmight fall to a scientific unfortunate.”19

In 1847 Snow was, in his own words, a “scientific unfortunate”—a telling phraseabout the nature of London medical society at midcentury. Nearly ten years of ded-ication to medical science, including active participation in the Westminster Med-ical Society and frequent contributions to major medical journals, had brought Snowlittle recognition as a medical man. The ether phenomenon, however, permitted him


to bring his laboratory experience and work at the bedside and in hospitals to bearon a number of problems with a chemical agent that was as potent as it was myste-rious. He realized straight away that the mixed reviews of the drug’s efficacy weredue not merely to technical problems with the apparatus. The problems revealed abasic ignorance about the quantity of the drug to administer and its precise actionswithin the body. Bedside medical experience was effective in deciding how muchpowder or solution to measure out for particular patients with certain symptoms,but only laboratory medicine could offer clues to the precise doses of a vapor to ad-minister and for how long.20 In this setting his approach took the form of combin-ing more than a decade of experience with the chemistry and physics of gases, aswell as clinical knowledge and experimental interest in respiration and asphyxia, intoa scientific understanding of anesthesia with lucrative practical applications. How-ever, for Snow personal gain from the practice of anesthesia was a by-product of hiscommitment to science and public health. While in America Morton struggled topatent his discovery, Snow never patented any apparatus he designed. On the con-trary, he published clear descriptions, including engraved figures, so that others couldcopy them if they chose.

There were problems in the administration of ether, as Liston had quickly real-ized. Some patients went under peacefully, while others resisted mightily, sometimesspewing vulgarisms that upset the ladies on the observation benches at the operat-ing theater. Robinson tinkered with the inhalation apparatus, especially the mouth-piece, and endorsed his own model. Within a month of the announcement in LMG,there seemed to be as many different inhalers on the market as there were peoplewho called themselves anesthetists.21 Robinson and others were interested in creat-ing a device that was easy to use, but the principles of design were not based to anygreat extent on the chemistry of ether or the physiology of inhalation.

When Snow first witnessed the administration of ether as an anesthetic, he wasalready familiar with many of its properties. He had experimented several years ear-lier with “æther and . . . other volatile medicines” while studying the capillary cir-culation. He had found that ether “separated from the blood in the lungs and es-cape[d] with the breath . . . in the gaseous form with the carbonic acid gas andwatery vapour, . . . in this way lessening congestion and relieving its attendant dis-tressing symptoms.”22 While experimenting in 1843 with ether as a “diapnetic” forpromoting respiration, Snow concluded (hastily) that it could be used to promotenormal mechanisms of respiration.23 In other words, he had already considered etheras an inhaled medicine that had a discrete impact on the circulatory system.

Soon after he saw ether administered, a research agenda took shape in his mindthat would occupy him for the next few months. Animal experiments led him to be-lieve that all sentient creatures were susceptible to the effects of ether. Consequently,the inconsistencies Robinson and other pioneers in ether inhalation were encoun-tering could not be due to constitutional variations among the patients; the causemust be that the patients were not receiving as much ether as the administrators

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thought. It was common knowledge among chemists and chemically inclined med-ical men like Snow that the amount of ether in saturated air depended on temper-ature, so he decided to determine the concentration of ether vapor in a standardamount of air at different temperatures. The second part of his research agenda wasto design an inhaler that would allow control of the amount of ether administered.When Snow began this enterprise he did so working largely at home on his own.24

The medical community began to describe the process of etherization as anesthe-sia, an eighteenth-century coinage meaning insensibility or the suspension of sen-sation (its most useful and astonishing effect), but a new science was required tomake sense of it.25 In the United States ether was promoted as Letheon—in classicalGreek mythology the river in Hades that rendered drinkers oblivious to their past.26

While others may have let this new powerful gas go to their heads, Snow managedto bring an analytic perspective to the mystery of ether. He sought not only to iden-tify its problems but to solve them on all levels, clinical and theoretical, physiologi-cal and chemical, individual and collective. His success would transform him froman obscure, struggling Soho GP into a doctor who “was in constant requisition byall the principal London surgeons at their operations, and . . . devoted himself toit as his chief branch of practice.”27

By September 1847 Snow had published On the Inhalation of Ether, a practical andcomprehensive guide to the clinical use of ether anesthesia. This book shows that heaccomplished four major goals in nine months. First, he had addressed the matterof temperature and determined the precise dose of ether to be given under variousconditions. Second, he had designed an inhaler that took advantage of the chemicaland physical properties of ether to control the dose in a reliable fashion. Third, hehad conducted animal experiments, for which he was sometimes one of the ex-perimental animals, to begin to demonstrate the basic mechanisms by which in-halation anesthesia worked. Fourth, he developed an active ether practice, bringinghim a wealth of clinical experience and observations as well as needed financial re-sources. All four accomplishments occurred simultaneously in the first half of 1847(Table 5.1).

Controlling the Dosage

Two and a half weeks after he had seen his first ether demonstration, Snow attended ameeting of the Westminster Medical Society, where members commented on the in-halation of ether. Most offered case descriptions relating the outcome of attempts to ren-der patients insensible prior to operations—sometimes successful, sometimes not, but,

Dr. Snow said that the great effect of temperature over the relations of atmo-spheric air with the vapour of ether, had apparently been overlooked in theconstruction and application of the instruments hitherto used. This circum-


stance would explain, in some measure, the variety of the results, and accountfor some of the failures. The operators did not at present know the quantityof vapour they were exhibiting with the air; it would vary immensely accord-ing to the temperature of the apartment, as would be seen by some calcula-tions he had made, and suspended in the room.28

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Table 5.1. Snow’s anesthesia research and practice from December 1846 to September 1847

16 October 1846 Morton administers ether for an operation in Boston

19 December 1846 First use of ether for anesthesia in London by James Robinson

28 December 1846 Snow witnesses ether administered by Robinson for dentalextraction

16 January 1847 Preliminary table for calculating the strength of ether vapor bytemperature

23 January 1847 Displays ether apparatus he designed to control temperature

28 January 1847 First administers ether with new apparatus at St. George’s Hospital

29 January 1847 Revised table for calculating the strength of ether vapor bytemperature

4 February 1847 Administers ether with modified apparatus at St. George’s Hospital

13 February 1847 Reads paper at WMS, “Observations on the vapour of ether, andits application to prevent pain in surgical operations”

20 February 1847 Discusses new experiments showing that ether is exhaledunchanged and that production of carbon dioxide is reducedduring anesthesia

18 March 1847 Administers ether using apparatus with wider (3/4 inch) tubing

19, 26 March 1847 “On the Inhalation of the vapour of ether”

3 April 1847 Demonstrates a portable apparatus for ether inhalation

6 May 1847 Uses Sibson’s facepiece on his own apparatus at St. George’sHospital

12 May 1847 “Lecture on the inhalation of vapour of ether in surgicaloperations”

10 June 1847 Modifies Sibson’s facepiece, adding two swing valves to admit air

September 1847 On the Inhalation of the Vapour of Ether in Surgical Operations

12 November 1847 “Dr. Snow on the effects of ether vapour”—letter to editor of LMG

28 January–2 September Administers ether in fifty-two cases at St. George’s Hospital

3 May–8 September Administers ether in twenty-three cases at University CollegeHospital

Source: Lancet 1 (1847); LMG 39 (1847); Lancet 2 (1847); LMG 40 (1847).

Snow’s previous work with ether and his extensive experience with the chemistryand physics of gases and the physiology of respiration had obviously allowed him tohit the ground running. He was beginning work on the science of inhalation anes-thesia while most of his fellows reported only anecdotal cases in the London med-ical journals.

Snow realized that the volatile nature of ether was the source of the speed withwhich it acted and subsided and the source of its many difficulties. The colorless,highly flammable anesthetic liquid we know as diethyl ether was commonly preparedby the reaction of sulphuric acid and ethyl alcohol. Chemists had readily synthesizedit for many years before its anesthetic properties were discovered. Snow was fortu-nate that the first anesthetic had been so widely studied from a chemical point ofview. In 1802 both Joseph-Louis Gay-Lussac and John Dalton had used it in studiesof the rates of expansion of gases.29

Dalton had also investigated ether’s elastic force, its ability to change states eas-ily at room temperature from liquid to gas, as had the chemist Andrew Ure, a mem-ber of the Royal Medical and Chirurgical Society. Snow was familiar with Ure’s ex-tensive 1818 paper on “The leading doctrines of caloric,” in which he reviewedDalton’s findings and produced a table showing the variations in the elastic forceof ether, among other vapors, by temperature.30 Snow was also familiar with Dal-ton’s work showing that “all vapours in contact with the liquid which gives themoff ” saturate the air in a proportional manner, depending on the “elastic force,” orwhat would be known today as its saturated vapor-pressure.31 “It occurred to mymind,” Snow wrote after the fact, “that by regulating the temperature of the airwhilst it is exposed to the ether, we should have the means of ascertaining and ad-justing the quantity of vapour that will be contained in it.” Several experiments on“the quantity of ether vapour taken up at various temperatures corresponded withcalculations” of elastic force in Ure’s table.32 Hence, Snow felt comfortable usingUre’s formula and table in developing the “Table for calculating the strength ofether vapour” (Fig. 5.1) he presented at the 16 January meeting of the Westmin-ster Medical Society.33 He soon realized, however, that while his numbers matchedUre’s, they had both tested ether that was not altogether free from alcohol. He fash-ioned “a graduated tube, bent in the form of Dr. Ure’s eudiometer” with one legblocked with mercury and introduced a few drops of ether through the mercuryand up the tube. Then he plunged the device into a temperature-controlled waterbath, took a reading, repeated at another temperature, and in this way collectedhis data. He found that saturation ratios were the same, but there were four-de-gree differences in temperature; at constant barometric pressure, what occurred at40°F with unwashed ether occurred at 36°F for washed ether (ether from whichthe alcohol has been replaced by water). By March Snow had constructed a revisedtable using washed ether, which he considered the most suitable form for inhala-tion, and presented the results in a way that reflected more closely what takes placephysiologically during inhalation.34


Designing an Inhaler

When Snow published (in two parts, on 12 and 19 March) his first survey “On theinhalation of the vapour of ether,” he immediately hammered out the clinical im-plications of his laboratory researches: “It will be at once admitted that the medicalpractitioner ought to be acquainted with the strength of the various compoundswhich he applies as remedial agents, and that he ought, if possible, to be able to reg-ulate their potency. The compound of ether vapour and air is no exception to thisrule. . . .”35 Regulation meant being aware of the concentration–temperature prob-lem with ether and then designing an apparatus that could administer precise

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Figure 5.1. Table “suspended in the room” at the 16 January 1847 meeting of WMS and pub-

lished on 29 January (Lancet 1 [1847]: 99; LMG 39 [1847]: 219).

amounts of the agent. At the time of his first communication to the WestminsterMedical Society (16 January 1847), after describing his findings on “air, saturatedwith the vapour of ether” at various temperatures, he announced that he would soonbe able to demonstrate a “cheap and portable” instrument, currently being contrived“on the plan of the inhaler of Mr. Jeffreys. . . .”36

Even the first, imperfect table for determining the amount of ether in air at var-ious temperatures was sufficient for Snow to design an ether inhaler quite differentfrom others on the market. The inhaler used in Liston’s operations, “contrived byMr. Squires [sic], of Oxford-street,” was mentioned often in January 1847.37 TheLancet published illustrations and descriptions of various apparatuses for adminis-tering ether. On 13 January the Pharmaceutical Society exhibited a variety of inhal-ing devices.38 Many of the early inhalers were made of glass and contained a spongeonto which liquid ether was poured. A chemist, Jacob Bell, had devised a new sim-plified glass flask inhaler that was used in a normally excruciatingly painful litho-tomy; the patient felt no pain “after blowing the horn,” and remained in a “dreamyand ‘very comfortable state’” during the evening following the operation,”39 but, ingeneral, the results of administering ether with these inhalers were inconsistent. Snowreasoned that as the ether changed state from liquid to gas, it absorbed heat fromthe surrounding atmosphere. Because glass is a singularly poor conductor of heat,the air temperature inside the inhaler dropped, reducing the quantity of ether va-por at full saturation. Patients as a result inhaled insufficient amounts to render theminsensible. Snow, therefore, designed an inhaler in which the administrator couldcontrol the air temperature by “placing it in a bason [basin] of water, warmed orcooled to a given temperature. . . .”40

On Saturday, 23 January at the meeting of the Westminster Society following hisfirst communication on ether, he demonstrated the apparatus constructed on thebasis of his design by Mr. Daniel Ferguson, surgeon’s instrument maker and cutlerin Giltspur Street. It consisted of a round tin box four or five inches in diameter andtwo inches deep (Fig. 5.2). There was an opening at the edge through which the airentered a metal tube coiled around the outside of the box, which led to the inside.The idea was to warm the inhaled air before it entered the vaporizer. Internally thevaporizer had been designed to maximize ether uptake. It contained a metal spiral,or volute, which directed the inhaled air over a much longer ether surface than itsarea would otherwise have allowed. The spiral plate had been soldered internally tothe top surface and almost reached the bottom, and the air had to circle over thesurface of the ether three or four times. Snow chose a diameter (6˝) and depth (1.25˝)of the chamber and size of the coils (5/8˝ between coils) that maximized the surfacearea contact between air and ether and that could contain enough ether, withoutsloshing, as the patient breathed. From the center of the top of the box a removableflexible tube led the saturated vapour mixture to a mouthpiece, which containedvalves to prevent the return of expired air into the apparatus. There was no spongeto create an obstruction, and the box was made of metal, which was a good


conductor of heat. The apparatus was portable and cheap. In use it was placed in abasin of water at a temperature that corresponded to the proportion of vapour thatthe operator wished to give.41 The metallic chamber easily conducted heat from thewater bath to the air–ether mixture passing through it, preventing the ether fromcooling for the relatively brief duration of most operations.

Snow based the shape of the coils in the spiral chamber of his inhaler on the de-sign of Julius Jeffreys’s volute humidifier published in LMG in 1842.42 This is an-other instance of the way Snow retained a ready acquaintance with nearly everythingpublished in the London medical journals in his lifetime. Jeffreys’ device was an ap-paratus designed for the amelioration of chronic bronchitis by the humidificationof air. Snow had consulted Jeffreys’s 1842 article describing the humidifier when writ-ing his capillary circulation paper. He had used the humidifier in his clinical prac-tice, and in 1846 he immediately saw its potential for modification into an ether in-haler. Because ether was more volatile than water, Snow’s spiral did not require thedegree of involution that Jeffreys had given his.

Snow’s inhaler was subsequently modified several times. For example, a tap wasintroduced to allow air to be drawn in to dilute the ether mixture (Fig. 5.3) Snowalso removed the external tube for warming the air. Possibly he came to realize thatthe very low specific heat of air would hardly influence the uptake of ether, so thisadded complication of construction was not worthwhile, but his methodology for

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Figure 5.2. Snow’s first inhaler, demonstrated at the WMS on 23 January 1847. “It consisted

of a round tin box, two inches deep, and four or five inches in diameter, with a tube of flex-

ible white metal, half an inch in diameter, and about a foot and a half long, coiled round and

soldered to it. There was an opening in the top of the vessel, at its centre, for putting in the

ether, and afterwards attaching the flexible tube belonging to the mouth-piece. In the interior

was a spiral plate of tin, soldered to the top, and reaching almost to touch the bottom” (Lancet

1 [1847]: 120–21).

knowing and controlling the strength of vapor was very simple and immediatelyclear. The operator should read from the table the temperature corresponding to thevapor concentration required and adjust the temperature of the water bath accord-ingly. The specific heat of water being so much greater than that of ether, the tem-perature of the water bath would remain relatively constant for the short durationof the majority of operations then being performed. Snow mentioned that in onecase, with the water at a temperature of 70°F, anesthesia had been induced in half aminute. Soldering the spiral volute to the top plate rather than the bottom made itmuch easier to pour the ether in and out, and it was also easier to construct.

Early in April in response to a request for a portable inhaler, he “laid before the[Westminster Medical] Society a small and very neat apparatus for the inhalation of


Figure 5.3. Snow’s first modification of his inhaler. Snow first administered ether to surgical pa-

tients on 28 January 1847. Because “the sudden access of air highly charged with ether produces

irritation and cough in some persons, I was desirous of having the means of diluting the vapour

to any extent, and Mr. Ferguson, of Giltspur Street, who has taken great pains to carry my wishes

into effect, got a tap cast of wide calibre, opening two ways, by means of which the patient can

begin by breathing unmedicated air, and have this gradually turned off as the etherized air is

admitted in its place. This tap offers the further advantage of enableing the medical attendant

to keep up the state of insensibility during an operation by a more diluted vapour than that

which was necessary to produce that state” (LMG 39 [19 March 1847]: 500–01).

ether.”43 Also made by Mr. Daniel Ferguson, this inhaler was small enough to be car-ried in the pocket of a coat, yet affixed with wider tubes for the admission of moreair than the earlier model. Snow had provided a pocket-sized inhaler, although “hedid not intend it to supersede the [larger model], which was better adapted for ex-act observations.”44 He had also increased the width of the tubing on the large in-haler, and both models employed “a ferule to admit external air into the tube, nearthe mouth-piece, when required” instead of a “two-way stop-cock” in the tube as itemerged from the inhaler.45 The two versions of the inhaler Snow described in Aprilwere little changed in the final model (Fig. 5.4) he described and illustrated in theclinical manual published early in the fall. In this definitive version of the inhaler, aportable “box of japanned tin or plated copper, of the size and form of a thick oc-tavo volume,” functioned as the housing for the spiral chamber and water bath whenthe apparatus was in use.46 Between operations the box could be emptied of waterand used as a storage space for the tubes and face masks.

In 1846 the idea of compelling patients to get their air through tubes and valveswas, as Snow remarked, “perfectly new” (E, 21). All early inhalers, even Snow’s, ob-structed the patients’ breathing to some degree.47 Valves were frequently too small.In some cases the inhaler was placed above the patient’s head so that the heavier

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Figure 5.4. Snow’s ether inhaler, used exclusively from June 1847. His description: “A. Box of

japanned tin or plated copper, of the size and form of a thick octavo volume, serving as a wa-

ter-bath when the apparatus is in use, and at other times containing the elastic tube and face-

pieces. Attached to this by clasps, and moveable at pleasure, is B. The spiral ether chamber, of

thin tinned brass, or copper plated with silver. C. Opening in ditto for putting in and pour-

ing out ether, and for screwing on, D. Brass tube, by which the air enters which the patient

inhales. E. Another opening in ether chamber for screwing on F. Elastic tube about three feet

in length. G. Face-piece. H. Inspiratory valve of ditto. I. The same face-piece compressed, to

fit it to a smaller face. S. Section of spiral ether chamber, B” (Snow, E, 16–17).

ether flowed into the patient’s lungs while the lighter air sat on top, unmixed anduninhaled. Often in these cases anesthesia failed, or worse, insensibility was inducedby way of partial asphyxiation. After administering ether for several weeks, Snow de-cided that the primary cause of most failures was the use of “tubes of too narrowcalibre” (E, 21).48 The apparatus he demonstrated in April was fitted with a tubethree feet long with an internal diameter of 3/4˝ (after a 5/8˝ tube had proved in-adequate). He reasoned that the tube “must be wider than the trachea, to compen-sate for the resistance arising from friction of the air against the interior” (E, 21).

Finding a satisfactory mouthpiece was considerably more troublesome than themodifications required to perfect the basic apparatus. Snow’s first mouthpieces didnot cover the nostrils (see Fig. 5.3), so the patient had to breathe through the mouthwhile the nostrils were pinched shut. Although this method often functioned quitewell, it caused trouble for those patients who tried to breathe through their blockednoses—they drew air through their tear ducts, turned blue, or both. In such instancesSnow had to free the nose and let them breathe air, delaying the whole process. Hetried and discarded several mouthpieces before settling in early May on a face mask“invented by Mr. [Francis] Sibson, of the Nottingham General Hospital. It was madeof metal and covered with silk, in the form of a partial mask, and admitted of res-piration both by the mouth and nostrils, the border of it contained pliable sheet lead,which could be moulded to the peculiarities of the features, and retained the formgiven to it.”49 After a month, however, he “introduced two swing valves into it, to su-persede the spherical valves he had previously used. The expiratory valve is made tobe moved gradually at will from the opening it covers, so as to admit external airand supersede the two-way tap.”50

So, by late spring of 1847 Snow had a complete apparatus with which he couldcontrol the dosage of ether. With its constancy of temperature and the anesthetist’sability to control the concentration of vapor, it became popular, was manufacturedby four instrument makers, and was often recommended in the medical journals.Unlike Morton, Snow made no attempt to secure a monopoly on the use of his ideas.He wrote and lectured on his experience and gave freely of his knowledge. His re-ward was the recognition of his ability by the leading surgeons of his time, whichassured an increasing number of consultations and a growing and lucrative anes-thesia practice.

Basic Research into Anesthesia

While Snow was determining the dosage and concentration of ether at various tem-peratures and designing his initial apparatus, he was also beginning basic researchinto the mechanisms of anesthesia. He set out to answer several questions. How uni-form was the effect of ether on different species and on individuals within the samespecies? How did ether render the animal unconscious and free from pain? What


observable signs and symptoms correlated with different levels or degrees of anes-thesia? Snow was so successful at this research program that in a few months he elu-cidated and formulated most of the basic principles that anesthesiologists use todayto design anesthetic vaporizers.

At the Westminster Medical Society on 13 February, Snow delivered his first for-mal paper on ether. He outlined what was known about the compound’s properties,including the fact that in the gaseous state it occupies space when mixed with air.However, he had found by experiments on mice that ether did not produce insen-sibility by excluding oxygen from the air—that is, cause asphyxia—because “sup-plying the displaced oxygen did not counteract the effects of the vapour.”51 The dis-tinction between etherization and asphyxia was critically important and poorlyappreciated by many at the time because the forms of primitive apparatus then inuse commonly interrupted breathing and caused a degree of asphyxia of which theoperator was unaware. Asphyxia, while it produced insensibility to pain, was a greatdanger to life and ended in death. Ether, Snow determined, worked by a very differ-ent route. Although its precise physiological mechanism was uncertain, animal ex-periments suggested to him that ether “allowed the blood to be changed from ve-nous to arterial in the lungs, but probably interfered with the changes which takeplace in the capillaries of the system. He had ascertained that a little vapour of ethermixed with air would prevent the oxidation of phosphorus placed in it, and consid-ered that it had a similar effect over the oxygen in the blood, and reduced to a min-imum the oxidation of nervous and other tissues.”52 This paper shows the range ofSnow’s thinking and his creative linking of inorganic chemistry with biology.53

At the society meeting on the following Saturday, on 20 February, Snow broughthis earlier experiments to their logical conclusion. Reduction of the metabolic pro-cess implied reduced carbon dioxide production, and this he had now demonstrated.Since the last meeting “he had completed some experiments, by which he had as-certained that the vapour of ether was given out again from the lungs unchanged,and that the amount of carbonic acid gas produced during the inhalation of etherwas less than at other times: these circumstances he considered confirmed the ex-planation of the modus operandi of ether which he had previously given.”54 If, as pre-viously, he had been working with mice, the accuracy of his measurements was im-pressive.

There were many reports in 1847 of outright failures to induce insensibility by theinhalation of ether as well as of patients crying out and struggling to varying de-grees. When employed in some operations, Snow wrote in his clinical manual, “theether has often been left off, and given up as a failure, on account of the excitementproduced by it, under an impression that it was producing an opposite effect to itsusual one, and acting as a stimulant instead of sedative” (E, 33). Such responses wereusually attributed to individual susceptibility.

Snow disagreed. He thought that every sentient being was susceptible to ether. Hehad commented early in 1846 on results from experiments conducted on various

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animals seven years earlier: “We find that the birds were uniformly sooner distressedand killed than the mice by corresponding atmospheres [containing differentamounts of oxygen, carbon dioxide, etc.]. The human being, as regards his respira-tory function, is placed between the bird and the rodent, and we may therefore con-clude that the fatal effects of vitiated atmospheres on him will likewise be interme-diate.”55 It appears that in his apartment Snow kept a large supply of laboratoryequipment (graduated cylinders, pneumatic troughs, etc.), chemicals, and amenagerie of thrushes, linnets, rodents, frogs, and fish upon which to experiment.When he began investigating the physiological responses to the inhalation of ether,his home laboratory was as prepared as was his mind.

In January 1847 he made “a few experiments on small animals” (E, 33). In one heplaced a bird inside a jar filled with known proportions of ether and air for very spe-cific periods of time, generally one to fifteen minutes. He carefully monitored theeffect of the gas on the subject, noting how quickly the bird went under and howquickly it recovered, pricking it to check for a reaction to pain. He repeated theseexperiments with small rodents and soon reached the conclusion that “ether acts ina very uniform manner on the various classes of animals. The difference in the timethey take to become affected and to recover, depends on the difference in the activ-ity of the respiratory and circulatory functions.”56 He found that birds reacted mostquickly, rodents less so, frogs slower than rodents, and fish, breathing air via water,slower still. The respiratory law was the same as in his earlier experiments on viti-ated atmospheres. “There may be persons,” Snow asserted, “on whom [ether] doesnot act favorably, but I believe that no sentient being is proof against its influence.”57

He undoubtedly confirmed the “principle that there is no person who cannot be ren-dered insensible by ether” (E, 33) on his own thirty-three-year-old body, using atimepiece to determine rates of induction, unconsciousness, and recovery. Variationsin human reactions depended mostly on size and respiratory and circulatory factors,not a vague and unprovable constitutional disposition. Children and youths werelike linnets, with rapid breathing and small bodies and therefore easier to anesthe-tize than adults. If some adults became excited when administered ether or some al-coholics seemed impervious to its influence, the explanation was simple: the quan-tity of ether had been insufficient to suspend their “cerebral functions . . .altogether” (E, 33). In very short order Snow had established two basic principlesthat would inform much of his research: (1) There is a universal susceptibility toether, and (2) the rate at which a regular dose of ether affected a body was depen-dent upon the rate and efficiency of breathing and blood circulation.

Five Degrees of Etherization

In early May 1847 Snow’s portrait was on display in the National Gallery in Trafal-gar Square in the rooms occupied by the Royal Academy of Arts. In addition, he had


been invited to present a lecture–demonstration at the United Service Institution forits medical members, including physicians in the army and the Royal Navy.58

Snow used this lecture to cover many aspects of ether anesthesia. Early in the lec-ture, he suffered a mishap. He placed a thrush in a jar containing one-third ethervapor and two-thirds air. He turned to his audience and summarized the two prin-ciples of etherization he had formulated—that while all animals are susceptible, dif-ferences in the time it takes to render a particular animal insensible and to recoverdepend on “differences in the activity of the respiratory and circulating functions.”59

When he next looked at the jar the bird was dead. Snow was embarrassed and im-mediately admitted, “It is a result I did not intend, and it has arisen from my goingon with the lecture, and looking at my notes, instead of directing my whole atten-tion to the animal.” Snow recovered quickly even if the thrush did not. He immedi-ately emphasized the object lesson: “This accident shows the power of the agent.”60

Ether required the administrator’s undivided attention. Such an accident shouldnever happen to human patients as long as they were carefully monitored by trainedand observant medical men. Snow thus had an opportunity to emphasize anotherof his basic themes—anesthesia is a medical procedure and should not be left to den-tists, druggists, or the unskilled people who were then often employed to adminis-ter ether. Ether is dangerous and requires conservative dosages. He had determinedthat an upper limit of fifty percent ether to air was required to induce insensibility,but only ten to fifteen percent to maintain it.

Snow went on to describe his anesthesia technique in great detail and to suggestits various military applications. On the battlefield ether would reduce mortality bysaving wound victims from a second shock, the shock of an operation without anes-thesia, which often compounded the damage done by the initial shock of the wounditself.61 Off the battlefield, where malingering was a common problem in militarymedicine, he suggested ways in which anesthesia might be used to help distinguishbetween feigned and real disability or deformity. On this occasion he emphasizedthe way he had combined his experiences in the laboratory and at the bedsides ofpatients to determine the precise symptoms and signs that allowed him to gauge thedepth of anesthesia:

I let the patient begin by inhaling only air, and then turn the two-way tap alittle at each inspiration, till the etherized air is admitted, to the exclusion ofthe other. This prevents the coughing which the sudden access of the vapouroccasions in some persons. . . . I usually get the tap quite turned on in aquarter of a minute. I find that consciousness and the power of voluntary mo-tion are soon lost, generally in the first minute, and for some time before asurgical operation could be commenced without causing pain, and awakeningthe patient. . . . As the patient gets under the influence of ether, the limbsbecome relaxed, and drop down, if not supported, but the eyelids still retaintheir sensibility, and close again on being opened by the finger, but in a little

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time they cease to do so, or close feebly; the breathing becomes deep, regular,and, as it were, mechanical; and the eyes generally turn upwards, as in sleep.When these phenomena take place, an operation may be commenced, with-out fear of its causing cries or struggles, or being felt by the patient.62

Snow added that “an observant medical man will have no difficulty” determiningwhen patients are sufficiently insensible for a painless operation. “I have not once been mistaken,” he said, “with respect to the time when the operation mightbe commenced.”63

By the time that Snow condensed his clinical observations into his eighty-seven-page monograph, On the Inhalation of the Vapour of Ether in Surgical Operations, hehad organized the important signs into five degrees of etherization.64 The degreeswere, “in some measure, arbitrary” because they gradually ran into one another andwere not always clearly distinguishable (E, 1). Nonetheless, Snow considered themnear-infallible guides to monitoring patients undergoing anesthesia (Table 5.2).65

Snow was not the only researcher in 1847 to divide etherization, a continuum, intodiscrete degrees. In England Plomley had suggested three broad stages early in 1847;Snow’s five degrees parsed the same effects differently (E, 13). In France Longet un-dertook animal experiments on how the inhalation of ether affected nervous sys-tems and proposed two stages.66 M. Flourens, experimenting on dogs, determined


Table 5.2. Snow’s five degrees of narcotism

Degree Symptoms

First Patients know where they are and what is happening to them, can directvoluntary movement, and experience tingling in limbs, singing in ears,and dizziness. Some absence of sensation when returning to this stageafter insensibility.

Second Mental functions and voluntary actions may be performed, but in adisordered manner. Patients appear asleep, but groaning, talking,dreaming, and struggle may occur.

Third Mental functions and voluntary motions cease, eyes no longer react and tendto incline upward; muscle contractions and respiratory contractions mayoccur, as well as rigidity and spasms. Unintelligible muttering or cryingout may occur as patients are being subdued. Conjunctiva does notrespond to touch.

Fourth Breathing stertorous, pupils dilated, no movements except respiration. Thisdegree is seldom necessary for complete insensibility.

Fifth Respiration becomes difficult, then feeble and irregular. Respiration eventually reaches paralysis or ceases while heart continues beating for a short time.

Source: Snow, E, 3–13.

the sequence in which ether shut down the brain and nerve centers; Snow usedFlourens’s study as a physiological basis for the signs he described.67

Snow’s refined formulation suggests that he was concerned with degrees of nar-cotism as distinct from simple etherization. That is, he was interested in the total ef-fect of the agent on the body, not just the the elimination of pain. His scheme en-abled the anesthetist to read the signs of an etherized body. Snow remainedcommitted to the general principle that all humans, like all animals, were subject tothe influence of ether, but he had seen in the laboratory how some factors, such asbody size and respiratory rate, could predictably alter the response. As he gained in-creased clinical experience and as he organized his anesthesia experiences into a for-mal case series, he realized that individual differences reflecting class, age, body type,and health might also affect response to anesthesia in understandable and predictableways.68 For example, the effects of ether might be different in patients suffering fromdiseases of the lungs or heart. He could also be quite precise in predicting how longeach degree might endure. For example, he wrote: “If etherization is carried to thefourth degree, complete insensibility usually continues for three minutes after theinhalation is discontinued . . . A state of unconsciousness usually lasts five min-utes longer, a period during which any pain there might be would not be remem-bered afterwards” (E, 42). Snow’s specific concerns with degree and duration of anes-thesia reveal a broad and abiding commitment as a clinician. In the previous examplehe was informing surgeons how much time they should expect to have for a partic-ular operation on a patient in a given state (in this case a harelip, which would ne-cessitate removal of the face piece).69 He was also suggesting that conservative ap-proaches to anesthesia were highly desirable for patient welfare: Use as little aspossible to keep the patient as deep as necessary, but no more.

In his elaboration of five degrees of narcotism, Snow continued an intellectualprocess from his student days. His fundamental premise, that susceptibility to nar-cotism is a universal phenomenon affecting all classes of animals, challenged a cen-tral tenet of traditional bedside medicine—that the unique constitution of each pa-tient always trumps what physicians know about human physiology in general,whether conceptualized as humoral fluids, inflammation, nervous irritation, etc., butinstead of rejecting the bedside medical perspective outright, Snow reconfigured itas a practical extension of hospital and laboratory contributions to a new medicalspecialty. He made careful observations of patient reactions during etherization,and these observations constituted case studies of the sort urged by practitioners ofhospital–clinical medicine. Because the variables Snow observed were qualitative anddid not vary in kind among the patients in the case series, there was no need for astatistical analysis, and there was always the laboratory in which to deepen his un-derstanding. As he wrote a year after his first presentation on ether inhalation at theWMS, “There can be no doubt that these degrees of narcotism correspond with different proportions of vapour which are dissolved in the blood at the time—proportions which I hope to be able to determine.”70

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Snow’s Anesthesia Practice

Snow’s anesthesia practice—in the operating theaters of hospitals for the lower classesof patient and in the private quarters of surgeons and dentists for the upper classes—came to serve two major purposes. It brought him increasing financial security andvaluable contacts within the social world of London medicine, and it served as a vi-tal extension of his home laboratory. His success as a skilled administrator with areliable inhaler gave him entrée to the surgical theaters in a number of London hos-pitals, especially St. George’s and University College Hospital.71 By the time he ad-dressed the military surgeons and physicians at the United Service Institution on 12May 1847, he could state that he had “given the ether for a great number of opera-tions in private practice, in addition to twenty-eight operations, most of them seri-ous ones, in St. George’s Hospital.”72 When he published On the Inhalation of theVapour of Ether in September, he could include detailed reports of seventy-five op-erations (E, 56–76).

Snow first administered ether publicly during three operations at St. George’s Hos-pital on 28 January. He did so “by means of the inhaler described and depicted in[the] last number” of the Lancet. He was then still trying to refine his apparatus andhis technique and experimented with water-bath temperatures of 65°, 70°, and 75°F.73

On 4 February three operations at St. George’s were carried out “in which the vapourof ether was exhibited again by Dr. Snow, in the presence of Sir B. C. Brodie, Mr.Keate, and a numerous assembly of spectators.”74 Two of the patients, a man beingoperated on for fistula and a woman having a mastectomy,“began by inhaling merelyatmospheric air, and when a little initiated to the process, etherized air from the ap-paratus was gradually let on, by means of a tap, opening two ways, which had beenadded since the previous week, and which Dr. Snow said Mr. Ferguson, the instru-ment maker, had contrived” (Fig. 5.3). One of the two surgeons, Mr. Caesar Hawkins,addressed the audience on the benches of the operating theater afterwards: “hewished publicly to express the thanks of himself and colleagues to Dr. Snow” for in-venting an apparatus “he considered . . . very much superior to those they had pre-viously used; and it had the great advantage of enabling us to regulate the propor-tion of vapour administered.” 75 In May, when Snow was the anesthetist for Liston,the surgeon was so impressed that he changed from skeptic to cautious advocate ofether inhalation when administered according to Snow’s guidelines: “Dr. Snow man-aged the ether better than he had previously seen it given.”76

At this early stage in his practice, Snow made a few mistakes, even if he did notreadily admit to them. During his eighth operation as anesthetist at St. George’s Hos-pital, a woman about to undergo a mastectomy

inhaled for four minutes, when it was ascertained by Dr. Snow that the capwhich admits air to the ether was not removed, and, consequently, she got noether, and but little air. This was remedied, and she had the disadvantage of


beginning the inhalation of ether rather out of breath. It excited some cough-ing, and in three or four minutes the face was becoming purple, and the pulsefeeble and quick, and the features rather distorted. The inhalation was ac-cordingly discontinued, and the operation commenced. She struggled andmoaned during the operation; but at the termination of it, having recoveredher faculties, she said that she had felt no pain whatever, and seemed in veryhigh spirits.77

His own case report published several months later tells a rather different story: “Thispatient was suffering from bronchitis at the time of the operation, and the ethercaused a good deal of coughing, and was left off somewhat prematurely on this ac-count, and the operation performed” (E, 58). Although the surgeon had mentionedthe bronchitis at the time to explain the coughing, Snow omitted his own error notedby the Lancet reporter.78 On another occasion Liston stood ready to excise a diseasedelbow joint as

Dr. Snow, who administered the ether, placed his apparatus in the cold waterof the operating theater, which was 65°[F], and put into it two ounces of etherwhich was there [sic], a quantity which generally suffices for an operation.The patient inhaled quietly, and the operation was commenced at the end offive minutes. . . . It was found soon after, that the ether was finished, andsome one went to another part of the hospital for more; in the meantime,the incisions and directions preparatory to sawing the bones having been completed, the man began to complain, and Mr. Liston waited till he was ren-dered again insensible, which was in about a minute after the inhalation wasresumed . . . .

A couple of days later, Snow again administered ether for one of Lister’s patients,“This patient found the ether disagreeable, and wished to leave it off when partlyunder its influence, but with a little trouble she was partly persuaded and partly com-pelled to persevere, and soon became quite insensible, and had her finger removedwithout feeling it.”79 In his own case report, Snow just noted that the elbow excision“went on favourably” (E, 72) and that Mary Mills was “discharged, cured,” thirteendays after her finger amputation (E, 73).

Snow’s mistakes were minor and did not affect the outcome of any operation.From his point of view, perhaps, there was no point in reciting them later in a clin-ical manual intended to show that ether was safe if administered as he described.Certainly the surgeons whom he assisted had great respect from the outset for hisfacility as an anesthetist. Besides regular work in the operating theaters of St. George’sand University College Hospitals, Snow very quickly developed a thriving privatepractice in administering ether, particularly in dental operations. He was renownedfor his skill in controlling the dosage emitted from an inhaler that was easy to

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use and designed to adapt ether’s physical properties to the alleviation of human suffering.

Between mid-May and early September Snow was the anesthetist for twenty-fourmore operations at St. George’s Hospital, for a total of fifty-two, all of which he de-scribed in the clinical manual published shortly thereafter (E, 56–71). In four caseswhich could not wait for the weekly operating day (Thursdays), another surgeongave ether using Snow’s inhaler. He also administered ether for twenty-one opera-tions at University College Hospital during this period, for a total of twenty-three atthis institution (E, 72–76). Of these operations, twenty-six were amputations oflimbs, five lithotomies, six radical mastectomies, and there were a number of oper-ations for hemorrhoids, polyps, diseased testicles, and scirrhous and encysted tu-mors. Six patients died, five of them from complications after amputation. Snownoted that such mortality rates were superior to those of other hospitals and sug-gestive that the inhalation of ether augmented the surgeons’ success rate—and cer-tainly did not reduce it. Snow’s purpose in reviewing these cases was to show that“in none of the six cases that ended fatally . . . can the event have been caused, orin any degree promoted, by the inhalation of ether, since there are very sufficientand well-recognized [other] causes to account for the result” (E, 76). He also hopedto demonstrate his own success as an anesthetist: “in no case in which I have givenether did the patient know anything of the operation, except, two or three times,some trivial part of it, such as the tying an additional small artery after the inhala-tion had been discontinued” (E, 55).

The patients Snow anesthetized in hospital settings ranged in age from four yearsold to seventy-six and were, more often than not, working class. They includedWilliam Cowen, a twenty-three-year-old groom thrown from a horse, with a man-gled and infected leg, and Samuel Richards, “aged 9, a boy of colour,” with a diseasedankle. Anne Atkinson, an extremely feeble eleven-year-old girl with a badly infectedand abscessed leg, survived her surgery but never regained strength and died. Whileoperations on more affluent patients were typically conducted in the patient’s homeor the surgeon’s personal premises rather than a publicly accessible operating the-ater, some hospitals had private wards for people like “A.H., a woman aged 27,” op-erated on for hemorrhoids; and an unnamed female, from whose nose “Mr. Listonextracted a polypus” (E, 74).

Working in hospitals and in private homes as a professional anesthetist must havegiven Snow a certain epidemiological perspective. Watching all walks of life comeunder the surgeon’s knife and the controlled doses of his own gas mask gave himample opportunity to judge the aggregate effects of ether. If his first thought hadbeen to convince himself of the universal power of ether, his hospital work gave himthe opportunity to assess its powers on the broadest array of individuals in an ex-traordinary number of medical, dental, and surgical situations. In short, this expe-rience allowed Snow to generalize about the varied states of anesthesia and to es-tablish norms. He had realized from the outset that when administering ether “to


determine when it has been carried far enough” was the “point requiring most skilland care” (E, 1). Consequently, he had refrained from administering ether in surgi-cal settings until he had developed a method to deliver precise dosages in a uniformmanner. Once he had developed accurate saturation tables and a suitable inhaler, hekept meticulous clinical records on his patients’ responses to different concentra-tions and undertook parallel laboratory investigations on animals.

His knowledge of the chemistry of gases and respiration, skill in designing appa-ratuses, and attention to the nuances of symptomatology all contributed to an ap-proach to the difficulties of etherization that differed from the ways most of his col-leagues responded. Snow’s apparatus was critical to his contributions to anesthesiain its early months, but while his apparatus reflected a physiologically precise, con-stantly testable, and increasingly sophisticated concept of narcotism, other appara-tuses only yielded gradually improved techniques for delivering unregulated amountsof ether to patients. The advances in the latter were technical; the advances in Snow’swere both technical and scientific. Even as Snow’s achievements as an anesthetistwere greeted with applause, the medical community of the day often failed to dis-tinguish between Snow’s in-depth, comprehensive approach and the unscientific tin-kering of other operators. Even before Snow’s monograph on ether garnered praisein a three-column review in the Lancet, that periodical had given considerable at-tention to an approach far different from Snow’s.80 In a letter to the Lancet in July,William Morton had announced an improvement he had made in the mode of ad-ministering ether. Despite the various modifications he had made to his original glassglobe and its valves, he had never been satisfied with any apparatus for the purposeof inhalation. Further experiments had resulted in his abandoning his old inhalerand replacing it by a sponge. This was about the size of the open hand or a littlelarger and concave, to fit over the nose and mouth. It was thoroughly saturated withether, applied to the nose and mouth, and the patient directed to inhale as fully andfreely as possible. Morton had found the result more sure and satisfactory and thedifficulty of inhalation very much reduced or entirely removed. “The beauty and im-portance of this means is its perfect simplicity.”81 Thus, for some, conveniencecounted for more than science, but even if Snow might privately have decried thesedevelopments, the popularity of Morton’s sponge and similar throwbacks did noth-ing to reduce the size of his growing practice in London.

The Vicissitudes of Ether

As Snow increasingly focused his practice on administration of anesthesia, it becameevident that the benefits of ether were growing more complex, as well. It not onlyprevented pain and shock, it kept patients still. With ether dislocations could be re-laxed and treated in minutes, whereas in the past gradual applications of warm bathsand emetics were typical and marginally effective treatments. Snow’s comments to

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the military physicians on the use of ether to detect some cases of malingering, re-vealing as it is of Snow’s willingness to apply ether to all sorts of practical situations,is equally suggestive of the heady power with which ether seemed to render the bodyopen for medical inspection and medical operation. For good or for ill, ether couldinspire “a devotion to technological evidence,” could become a means of bypassingthe patient’s words, an agent by which the sick person was silenced and convertedinto an object, a disease entity.82

Ether also seemed to offer new access to the recesses of the mind. In his first for-mal publications on ether in March, Snow offered some observations about the ef-fects of anaesthesia on the mental processes that were involved in the perception ofpain.“Metaphysicians [like Descartes, Locke, and Hume] have distinguished betweensensibility and perception—between mere sensation and the consciousness or knowl-edge of that sensation, though these two functions have, as they supposed, alwaysbeen combined.” However, he had observed something different. “Ether seems to de-compose mental phenomena as galvanism decomposes chemical compounds, al-lowing us to analyse them. . . . During the recovery of the patient, consciousness,which first departed, generally returns first, and the curious phenomenon is wit-nessed of a patient talking, often quite rationally, about the most indifferent mat-ters, whilst his body is being cut or stitched by the surgeon.”83

Snow observed that many patients dreamed of early periods of life or “that theyare travelling” (E, 11). By the end of his life he would elaborate on this phenome-non, attributing this feeling to a particular set of symptoms. When anesthetics takeeffect, he explained, patients would frequently experience singing in the ears, dizzi-ness, tingling limbs, darkening vision, and a loud noise; “it not unfrequently hap-pens that a person feels as if he were entering a railway tunnel, just when he is be-coming unconscious.”84 For Bernard and Flourens the power of ether to close downthe body’s systems in a particular sequence helped to reveal physiological principles.Similarly, for Snow the shutting down of consciousness gave a glimpse into the mech-anisms of consciousness.

He observed that dreaming took place only in the lighter phases of anesthesia, de-spite the testimony of patients who recalled having lengthy dreams. He argued that“impression of the length of dreams can of course be no argument as to how longthe person was dreaming, and that the impression is often of a longer time than thewhole period of insensibility” (E, 11). In one case Snow recorded an example of “thesmallest amount of etherization with which an operation can be satisfactorily per-formed” (E, 49). A knighted gentleman underwent an operation for “two sinuses bythe side of the rectum” (E, 50). Toward the end of the operation, which lasted a to-tal of three or four minutes, as the surgeon was thrusting lint into the wound, “thepatient flinched and uttered an angry expression; and directly afterwards tried toraise himself up from the sofa, but was easily prevented. In less than a minute, hesaid he had been in Lancashire disputing with some people” (E, 50). Only eight anda half drams of ether were used. Upon learning that the operation was over he was


surprised and satisfied. Snow concluded that the “dream about the conversationprobably occurred at the moment when he first spoke” (E, 51). Because he was deeplyinterested in determining whether a given patient experienced pain, he used his de-grees of anesthesia to pinpoint the instant of the dream within the hypnagogic flowof ether. He recognized that dream states were dependent on basic mental functions.“I think that there is every reason to presume, that there can be no dreams or ideasof any kind in [deep anesthesia], and that for a short time there is not only, as in asound sleep, the absence of mental functions, but also the impossibility of their per-formance” (E, 11). Snow was beginning to explore the possibility that a chemicalagent, which temporarily suspended certain molecular processes in human tissues,could affect in a basic way the stuff that dreams and ideas are made on.

On the Inhalation of Ether was Snow’s attempt to present the gist of his researchin a way that was readily useful for the surgeon and anesthetist alike. It promotedhis inhaler and the beneficent and effective use of ether. The reviewer for the Lancetthought Snow had accomplished his purpose and recommended it,85 but the re-viewer for LMG resisted the entire spirit of Snow’s work and challenged most of hiscentral assertions.86 While Snow’s apparatus was ingenious, the sponge appeared tohave superceded “more elaborate contrivances.”87 Snow was insistent that ether couldprovide pain-free surgery in a safe manner to virtually anyone, but the reviewer wasnot so sure. Snow considered children to be favorable candidates for ether, yet thereviewer worried whether children with “latent tubercular disease of the brain,” acutehydrocephalus, or meningeal lesion might prove exceptions.88 Where Snow foundether to increase heart rate, the reviewer feared that it might stop the heart. WhereSnow defined the five stages of etherization and advocated a reliable method of dis-tinguishing among them, the reviewer emphasized their arbitrariness and the fluid-ity with which patients slipped in and out of them. Where Snow claimed that pa-tients feel no pain, the reviewer asked “who shall say through what vicissitudes ofvaried, and perhaps, fearfully exalted, though afterwards unremembered suffering,the apparently passive wretch is exposed while his stupefied faculties are graduallybecoming roused from the state of absolute insensibility?”89

But the LMG reviewer misread and misrepresented Snow’s book. Where Snowwrote, “It is not possible always to avoid having the breathing somewhat stertorous”(E, 39), the reviewer misquoted him as stating, “It is not possible to avoid. . . .”90

Both reviewers failed to mention the bench chemistry that formed the basis forSnow’s assertions, and the error in the LMG review tellingly reveals the kinds of skep-ticism that Snow’s certainty and precision about ether engendered. Snow saw a con-sistent pattern where others saw vicissitudes. He thought surgical procedures per-formed with ether tended to induce favorable terminations from hospital care,whereas others thought this questionable. He viewed the impact of ether as discretewhereas others were concerned about predisposing conditions.

In November 1847, not quite a year after Snow first learned of ether as an in-halation agent, news of chloroform as an anesthetic reached London. The emergence

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of this new agent confirmed Snow’s intuition that ether and, before that, nitrous ox-ide (whose anesthetic properties had been discovered in 1802) were part of a fam-ily of inhalants. He would continue the research project he had begun, extending itbeyond ether to a more general class of “narcotic” agents. He would soon come tobelieve “that other agents would be met with more eligible for causing anæsthesia byinhalation.”91

Notes

1. On 16 October 1846 the Boston dentist William Thomas Green Morton gave a success-ful ether demonstration at Massachusetts General Hospital. Several letters arrived in Englandbetween mid-November and mid-December 1846 communicating news of ether inhalation.The first was from a Boston lawyer who was assisting Morton in securing a patent; Ellis, “Earlyether anaesthesia,” 69–76. A letter describing Morton’s demonstration from Edward Everett,president of Harvard, to Henry Holland, a London physician, arrived on 2 December. Boottreceived a letter from Jacob Bigelow, professor of medicine at Harvard and also a witness ofMorton’s exhibition, with details and an article on experiments with ether on animals byBigelow’s son, Henry; see “Surgical operations performed during insensibility,” Lancet 1 (1847):5–9. On the dispute whether inhalation anesthesia began with Morton or his former partner,Horace Wells, who used nitrous oxide successfully in his dental practice as early as December1844, see Wolfe and Menczer, I awaken to glory.

2. James Robinson, letter to MT 15 (1847): 273–74. Surgeon–Dentist to the MetropolitanHospital, Robinson claimed to have been “the first in this country to employ the inhalationof ether as a means of rendering surgical operations painless.”

3. An alternative version is that Liston was present at the 11 November 1846 meeting of theMedical–Chirurgical Society where one of Morton’s assistants, on a visit to London, “dem-onstrated the anaesthetic properties of ether”; Merrington, University College Hospital, 31.

4. Lancet 1 (1847): 9, reprinted in J. Robinson, Treatise on Ether, 6.5. Zuck, “Dr. Nooth and his apparatus”; see also Merrington, University College Hospital,

31–33.6. Woolley, Bride of Science, 226–30, and Winter, Mesmerized, 165–74. For the argument that

opponents of mesmerism, including Wakley and Liston, hoped inhalation ether would scut-tle what they considered a medical fad, see Winter, 172–83.

7. Merrington University College Hospital, 32–33; Cock, “First major operation”; andReynolds, Essays and Addresses, 273–74. A description written shortly after the operation byListon’s assistant (“dresser”), Edward Palmer, makes no mention of Liston’s reaction to thesuccessful outcome; Liston, Casebooks, 11: 221, accurately transcribed by Merrington, Uni-versity College Hospital, 33. Winter reproduced the painting of Liston’s operation (181) com-missioned by Henry Wellcome in 1910, but Merrington says the Wellcome Foundation de-stroyed it in 1946 because they considered it inaccurate (33).

8. Nooth’s apparatus “had originally been designed for the domestic production of soda-water”; Zuck, “Physics of heat,” 88.

9. Robinson signed his letter “7 Gower Street, 28 December [1846]”; MT 15 (1847): 274.10. “Medical intelligence,” LMG 38 (1846): 1085; issue of 18 December.11. Ibid., 1089. A month later, LMG summarized a French editorial that warned unknowl-

edgeable practitioners undertaking surgery by candlelight that ether was not only inflamma-


ble but explosive. In addition, “operators should bear in mind that ether vapour is very heavy. . . compared with air. . . . Hence it follows, that, when the apparatus is above the level ofthe patient’s mouth, the respiration of the vapour is much facilitated by its density and itstendency to flow at once into the lungs”; LMG 39 (1847): 219.

12. “Surgical operations performed during insensibility,” Lancet 1 (1847): 5–9.13. For example, on 1 January 1847 Joseph Clover recorded in his diary that Mr. Squire was

unable to fully anesthetize two of Liston’s patients; K. Thomas, “Clover/Snow Collection,” 437.On skepticism among other London surgeons, see Ellis, CB, xviii. Another early skeptic wasNikolai Ivanovitch Pirogoff, professor of surgery at St. Petersburg, who noted that generationsof surgeons had learned to steel themselves to the patients’ screams; Researches on Etheriza-tion, 3. He changed his views after performing animal experiments designed to show the ef-fects of ether on nerves. He described four degrees of etherization and concluded that the bestroute to administer ether was via the rectum.

14. Pernick, Calculus of Suffering, 30; Rosenberg, “Therapeutic revolution,” 14–25. Gotfred-sen summarized the period from discovery in the United States to its European introductionin John Snow, 13–16.

15. “This new application of steam will be, indeed, a wide blessing; and . . . may lead toresults as new, whether in surgery, physiology, or psychology, as the steam of water and its ap-plication has been in the physical, domestic, and social existence of mankind”; “Letter fromMr. J. Robinson,” MT 15 (1847): 274, dated 28 December 1846.

16. Adams, “Scolding wives.”17. In the 29 January issue LMG believed “that Professor Simpson has the credit of having

first employed ether vapour in the practice of midwifery” in England. The journal then pub-lished an extract that noted that “whilst breathing the ether, the labour pains or throes con-tinued, and yet the mother (to speak paradoxically) felt no pains”; 39 (1847): 218.

18. Richardson, L, xiv. See also Ellis, CB, xviii–xix.19. Richardson, L, xiv.20. Pharmacology was still in a rudimentary state; see Caton, What a Blessing She Had Chlo-

roform, 59.21. Duncum discussed sixteen different inhalers produced in 1846 and 1847; Inhalation

Anesthesia, 130–57.22. Snow, “Circulation in the capillary blood-vessels” (1843), 813.23. Ibid. He refused to speculate about the forces involved: “I have nothing to advance re-

specting the intimate nature of the attractions and repulsions which accompany the changesof composition at the capillaries, and which tend to move the blood in a definite direction. Ihave carefully avoided such terms as chemical, electrical, and vital . . . . Our ignorance, how-ever, of the ultimate cause of these attractions is no argument against their existence; sincewe admit many laws in science of the causes of which we are ignorant” (813).

24. While there is some question as to where Snow conducted the bulk of his experiments,in “On narcotism,” which ran serially in LMG between 1848–1851, Snow makes several ex-plicit references to work done at home. It was common at this time to set up home labora-tories for chemical research. It is possible that Snow conducted some ether experiments at theAldersgate School of Medicine, where he was an instructor in forensic medicine during sum-mer sessions, but when the school dissolved in 1849, Snow’s pace of experimentation accel-erated, an unlikely outcome if the school’s chemistry laboratory had been his primary work-space.

25. Oliver Wendell Holmes is credited with the new usage (letter to Morton November 18,1846), although the word was used in a similar way by John B. Quistorp, De Anaesthesia in1718; see also E. Warren, Letheon, 79.

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26. In November 1846 Morton filed for U.S. patent a preparation of ether under the nameof Letheon in an attempt to control its commercial exploitation. This effort ultimately failed.

27. Charles Locock, Presidential address, Proceedings, RM-CS 3 (1858–61): 47.28. “Westminster Medical Society,” Lancet 1 (1847): 99.29. Gay-Lussac, “The expansion of gases by heat”; Dalton, “Experimental enquiry into the

proportion of the several gases or elastic fluids, constituting the atmosphere.”30. Snow, “Inhalation of the vapour of ether” (1847), 498; Ure, “New experimental re-

searches,” 359 (table 3). See Zuck, “Physics of heat,” on the English context for Snow’s re-searches, including Cullen, Robert Hooke, Ure, and a reproduction of Dalton’s table of satu-rated vapor pressures.

31. Snow, “Inhalation of the vapour of ether” (1847), 498.32. Ibid.33. Lancet 1 (1847): 99, containing an abstract of the table. The table was published in full

on 29 January; LMG 39 (1847): 219–20. See also Zuck, “Physics of heat,” 91–92.34. For the eudiometer-like instrument, see “Inhalation of the vapour of Ether” (1847),

498–99. “A table formed in this manner is the most correct way of exhibiting the subject, be-cause, since the vapour of ether is absorbed as fast as it arrives at the pulmonary cells, thequantity inhaled will be influenced rather by the volume of the air, than by that of the mix-ture of air and vapour, provided the patient’s respiration is not obstructed, and it never shouldbe, by the apparatus”; Ibid., 499.

35. Ibid., 498. These were the statements by Snow about ether printed in his own words,rather than as the transcript of a reporter at a society meeting.

36. Lancet 1 (1847): 99. The editor of PharJ missed Snow’s explicit mention of his indebt-edness to Jeffreys’ humidifier: “By a remarkable coincidence we find that an instrument iden-tical in principle with that invented by Dr. Snow, was invented some years ago by Mr. Jefferey[sic] as an inhaler”; “Apparatus for inhaling ether,” PharJ 6 (1846–47): 425. Snow clarified themisunderstanding in the following issue: “To the Editor . . . ,” PharJ 6 (1846–47): 474–75.

37. Lancet 1 (1847): 17.38. “Pharmaceutical Society—13 January 1847,” Lancet 1 (1847): 73.39. “Correspondence,” LMG 39 (1847): 218–19. Anticipating a modern phenomenon, “Mr.

Bell, the Chemist [and inventor of the inhaler] . . . was present, and assisted Mr. Tomes inits application”; Ibid., 219.

40. Lancet 1 (1847): 99.41. “Westminster Medical Society,” Lancet 1 (1847): 120–21.42. Jeffreys, “Artificial climates,” LMG 29 (1841–42): 821–22. According to Zuck, Jeffreys con-

sidered this humidifier “virtually a throwaway” in the mid-1830s on his path to devising a res-pirator that would constantly warm and humidify inspired air. Jeffreys patented the design of arespirator in 1836, then demonstrated it at the WMS in January 1837, three months before Snowfirst attended a meeting as a guest. See Zuck, “Jeffreys—Pioneer of humidification,” 4–6.

43. “Westminster Medical Society,” Lancet 1 (3 April 1847): 388.44. Ibid., 389.45. Ibid., 388.46. Snow, Inhalation of the Vapour of Ether in Surgical Operations, 16; hereafter cited par-

enthetically in the text as E.47. In all likelihood many unsatisfactory outcomes could be attributed to “cyanosis result-

ing from respiratory obstruction,” although most contemporaries did not recognize it as such;Zuck, “Cyanosis,” 1–2.

48. On 18 March Snow used an apparatus with wider tubes than before; “Operations with-out pain. St. George’s Hospital,” Lancet 1 (1847): 368.


49. “Operations without pain. University College Hospital,” Lancet 1 (1847): 546.50. “Hospital reports. St. George’s Hospital,” Lancet 2 (1847): 35.51. “Westminster Medical Society,” Lancet 1 (13 February 1847): 227. The paper was “Some

observations on the vapour of ether, and its application to prevent pain in surgical opera-tions.”

52. Ibid.53. In mentioning phosphorus Snow was referring to an observation made by Thomas Gra-

ham in 1829 that the presence of certain vapors (including sulfuric ether) would inhibit theslow oxidation of phosphorus in air. For a full discussion, see Zuck, “Thomas Graham,” 40.That Snow knew of this observation argues a close acquaintance with the literature of exper-imental chemistry. The reference to capillary action confirms that Snow’s mindset in ap-proaching ether inhalation involved the application of earlier research interests and experi-mentation. His reference to the “changes which take place in the capillaries” was to themetabolic processes, chemical reactions that involve the removal of oxygen from the bloodand the production of carbon dioxide, and were at that time thought to take place in the ter-minal capillaries, not, as was thought earlier, in the lungs. According to a contemporary text-book, “As it is now generally believed that the oxygen which enters into the blood combineswith the carbon, not in the lungs, but in all the extreme vessels, and in them forms carbonicacid, the evolution of heat throughout the body is thus at once explained—it is a mere in-stance of combustion in the extreme vessels, the union of carbon and oxygen being always at-tended by an increase in temperature.” Elliotson, Human Physiology, 238. It was demonstratedsome thirty years later that the site of this reaction was in the cells.

54. “Westminster Medical Society,” Lancet 1 (1847): 228. At this same meeting memberscommented on the effectiveness of different inhalers including Snow’s, which one member“had seen . . . used on many occasions . . . [to] great advantage . . . .”

55. Snow, “Pathological effects of atmospheres” (1846), 54.56. Snow, “Lecture on inhalation of vapour of ether” (1847), 551. Snow was not unusual in

experimenting with ether on animals. Early in 1847 a veterinarian did so on sheep and horses;“Medical intelligence: Painless operations on the lower animals,” LMG 39 (1847): 260–61. ADr. Gull read a paper at the South London Medical Society; “On the Effects of ether on thedifferent classes of animals,” LMG 39 (1847): 777–78. In Russia Pirogof introduced ether intothe bowels of various animals; “New method of etherization.” LMG 39 (1847): 950–51.

57. Snow, “Inhalation of the vapour of ether” (1847), 498.58. The United Service Institution had been founded in 1830 as a repository for objects,

books, and documents connected with the professional arts, science, and natural history andfor the delivery of lectures on appropriate subjects. Its premises were in Whitehall Yard, andit had on display, among many other things, such military relics as the swords of OliverCromwell and General Wolfe, part of the deck of the Victory, and the skeleton of the horseridden by Napoleon at Waterloo; Cunningham, Hand-Book of London, 517.

59. Snow, “Lecture on the inhalation of vapour of ether in surgical operations,” 551.60. Ibid.61. Snow the teetotler could not resist adding here that the ether and apparatus would not

add anything to the necessary baggage, for it would take the place of a far greater amount ofbrandy. He also avoided mention of a point that had been mentioned in some early French re-ports: that ether poses an explosive risk; “Westminster Medical Society,” LMG 39 (1847): 219.

62. Snow, “Lecture on the inhalation of vapour of ether in surgical operations,” 552.63. Ibid.64. Snow, E. Snow’s publisher, Churchill, still survives as a constituent of the medical pub-

lishing house Churchill-Livingstone.

Ether 137

65. Gotfredsen succinctly summarized Snow’s five stages in John Snow, 22–25.66. Longet, “Experiments on the effect of inhalation of ether on the nervous system of an-

imals,” Archives de Médecine (March 1847), cited by Snow, E., 13. A translation of an extractappeared in British and Foreign Medical Review 23 (April 1847), 570–72. Longet concludedthat narcotism was a form of asphyxia. Snow was unconvinced based on his own earlier stud-ies of asphyxia. In a hypotheticodeductive manner, he devised an experiment on mice to dis-prove Longet. Snow found that the effects of ether were not dependent on the amount of oxy-gen in the inspired air, that ether was unchanged when exhaled, and that it was possible thatthe amount of expired CO2 lessened during narcosis. His conclusion was that insensibility re-sulted from reduced tissue oxidation, especially in the nerves. See Snow, “Lecture on inhala-tion of vapour of ether” (1847), 553; and Gotfredsen, John Snow, 20–21.

67. Flourens, “On the effects of inhalation of ether on the nervous centres,” cited in Snow(E, 13). This extract was translated in British and Foreign Medical Review 23 (April 1847),572–73—the same number that carried extracts from the second of his LMG articles “On the inhalation of the vapour of ether” (March 1847). Gotfredsen noted that Snow’s early animal experimentation with ether was undertaken partially to confirm Flourens’s results;John Snow, 21.

68. Clinical classification, as well as case series development and monitoring, is consideredcentral to the practice of clinical epidemiology. It can therefore be argued that Snow’s etheranesthesia researches in 1847 laid some methodological groundwork for his later investiga-tions into the mode of transmission of cholera, now considered to be pioneering work in thefield of epidemiology.

69. Shephard, commenting on Snow’s work from the perspective of a modern anesthesiol-ogist, noted how Snow anesthetized a number of difficult patients, such as those with com-promised breathing, and stated that even today with modern equipment Snow’s safety recordwould be enviable; JS, 271.

70. Snow, “On the inhalation of chloroform and ether” (1848), 178.71. The attending surgeons whom Snow assisted included Richard Quain, Henry Charles

Johnson, Caesar Hawkins, Sir William Fergusson, Robert Liston, and Edward Cutler.72. Snow, “Lecture on inhalation of vapour of ether” (1847), 553. He did not mention two

operations at University Hospital on 3 May.73. “Operations without pain,” Lancet 1 (1847): 158.74. “Operations without pain. St. George’s Hospital,” Lancet 1 (1847): 184.75. Ibid. The apparatus was illustrated the next month in Snow, “Inhalation of the vapour

of ether” (1847), 501.76. “Operations without pain. University College Hospital,” Lancet 1 (1847): 546.77. “Operations without pain. St. George’s Hospital,” Lancet 1 (1847): 210.78. Zuck noted Snow’s silence about such mistakes in “Cyanosis.”79. “Hospital reports. University College Hospital,” Lancet 1 (1847): 639.80. “Reviews,” Lancet 2 (1847): 410–11. The five stages of etherization, the inhaler, and the

case reports were discussed at some length, and the reviewer concluded that “Dr. Snow’s lit-tle work . . . will prove valuable to all who undertake to administer the ether-vapour, by giv-ing them very useful rules for their guidance. . . . Some have rejected the employment ofetherization in surgery, because it annuls pain, which they deem necessary to success in op-erating, but we have seen no want of success where it has been resorted to, and if there hadbeen . . . we should be much rather disposed to attribute it to . . . bad surgery, than to thewant of pain”, Ibid., 411.

81. “Letter from Dr. Morton, of Boston, U.S.” Lancet 2 (1847): 81. Wakley added a foot-note—”the inhalation, by means of a sponge, had been recommended and practiced for some


time, in this country, by Dr. Smith, of Cheltenham.” The ether sponge replaced all appara-tuses, certainly in America, and was the method observed and described so vividly by CharlesTomes during his visit to the Massachusetts General Hospital in 1873. In Great Britain eventstook a different turn, but when ether was reintroduced at the end of the 1860s, administra-tion was by a sponge also, usually contained in a leather or even cardboard cone. Snow hadpioneered the first dosimetric technique for the administration of an anesthetic; the seconddosimetric movement, under the influence of the physiologist A. D. Waller, did not begin un-til the 1890s.

82. Reiser, Medicine and the Reign of Technology, 38–43. Anesthesia can be seen as one ele-ment in a line of historical argument that traces the depersonalization of medicine in thenineteenth century as clinical approaches and medical science developed. For analogous ar-guments, see Foucault, Birth of the Clinic; Jewson, “Disappearance of the sick-man from med-ical cosmology.”

83. Snow, “Inhalation of the vapour of ether” (1847), 541. Here Snow gives the first de-scription of the state of general analgesia, and this observation was the basis of the ether anal-gesia technique introduced by Artusio for cardiac surgery a century later; Artusio, “Ether analgesia.”

84. Snow, On Chloroform (1858), 36.85. Lancet 2 (16 October 1847): 410–11.86. LMG 40 (5 November 1847): 812–14.87. Ibid., 814.88. Ibid.89. Ibid., 813.90. Ibid. Snow called attention to this misstatement and its consequences for an under-

standing of his argument: “Dr. Snow on the effects of ether vapour,” LMG 40 (1847): 859.91. Snow, “On the vapour of amylene” (1857), 61.

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140

WHEN ANESTHESIOLOGISTS WITH A TASTE FOR the his-tory of their specialty read John Snow, they generally turn to On

the Inhalation of Ether or On Chloroform and discover comprehensive, albeit dated,accounts of these subjects, but reading Snow’s work from the white-hot years 1847 to1851 is a very different experience. He conducted research on the installment plan,and he was a serial and accumulative thinker in the golden age of serialization. As thenovel-reading public eagerly awaited the latest installment of David Copperfield inHousehold Words, the British medical world followed the latest developments chieflyvia Lancet and LMG. London had learned of ether through articles, bulletins, letters,and journals. Definitive reference works or compendiums were few and far between.Most of the real action was taking place in lectures, medical societies, and journals,and it is in the latter that one finds evidence of Snow’s furiously productive monthsof research in 1847 on the properties of ether and the risks of administering it, withinthe context of contemporary debates. Often writing in installments, repeating himselfto get new readers up to speed, and modifying as he went, he gradually developed hisviews on the subject. Then, as the workaholic Snow raced to keep pace with and aheadof developments, the ground shifted unexpectedly. Just as a serial novel might have it,an Edinburgh professor of obstetrics, James Young Simpson, directed the attention ofthe Medico–Chirurgical Society of Edinburgh to a new agent termed, with all thechemical nicety of the day, perchloride of formyle, or chloroform.

Chapter 6

Chloroform

Pharmaceutical Profiling

Ten days after Simpson’s announcement, Snow was at the Westminster Medical Societycomparing “the new letheon agent” (as the Lancet described it) to the old one, ether. Itwas 20 November 1847, only a year since ether’s discovery, but it seemed like an eternityhad passed.1 The early storm of excitement surrounding ether had lulled to a calm. Nowthe Scottish announcement created another storm. A local chemist had given Snow aquantity of chloroform rectified from calcium chloride (expense and ease of productionwere important factors that Snow never failed to consider). Snow placed this sample onthe table for the edification of his colleagues and gave them a favorable report. He hadtried chloroform himself and found that it made him no more wretched than ether did.In advance of his comments at the Westminster, he had placed his watch on a table, satdown, and begun to inhale. He felt a pleasant inebriation and thought nothing was outof the ordinary until he noticed that the second hand had disappeared. He found it againonly by pressing his nose up to the face of the watch (ON, 4: 334).2

He told the society that chloroform was preferable to ether in some respects. Chlo-roform affected the nervous system in the same way that ether did; animal experi-ments had confirmed this. Less pungent than ether, it was more easily inhaled, pro-ducing its effects “with great rapidity.” He also noted that it was more economical.“The quantity of it consumed was curiously small when compared with ether.”2a Pre-liminary surgical trials indicated superior efficiency. A few days before his presenta-tion, using his ether inhaler (water bath at 55°F.) he had administered chloroformfor a mastectomy at St. George’s Hospital. The third or fourth degree of “etheriza-tion” was induced in less than a minute, and the whole operation used one tenth ofwhat would have been necessary with ether. Snow felt that the speed of its actionmight even help to bypass the “preliminary excitement” (hysteria, spasms, or con-vulsions) commonly encountered in the first stages of ether inhalation. He then pre-sented a table, just as he had done with ether, that showed the quantity of chloro-form gas that air would hold in solution at various temperatures (Table 6.1).

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Table 6.1. Quantity of chloroform that 100 cubic inchesof air will take up

Temperature � F. Cubic inches

50 955 1160 1465 1970 2475 2980 3685 4490 55

Chloroform was almost twice as heavy as ether but took up one fourth the vol-ume, and for this reason it neither excluded as much air nor impeded respiration tothe extent that ether did. Simpson administered it by way of a sponge or handker-chief, but Snow preferred the precision and efficiency of his apparatus. With quietconfidence Snow proffered his judgment that chloroform, while not without dan-ger, was faster acting than ether and easier to use.

Discussion followed. Dr. E. W. Murphy (professor of midwifery, University Col-lege, with whom Snow would work on a number of deliveries in 1848–1849) re-mained unconvinced. He avoided using ether in labor whenever possible because ofthe nervous reactions it seemed to cause “both before and after insensibility,” in-cluding spasms that resembled “puerperal convulsions.” Murphy feared that the useof ether in labor might cause hemorrhaging. Did Snow think chloroform causedsimilar excitement? No, he replied, this kind of nervous excitement was caused bythe slowness with which it was necessary to give ether. The fast action of chloroformshould mitigate this problem during induction, but the nervous reactions wouldlikely occur as the patient recovered. He also suggested that patients do not die fromconvulsions while inhaling but from continuing to inhale after collapse had appearedand recommended that two practitioners be present for labor and delivery, one ded-icated to anesthesia. In other words, Snow admitted that chloroform did cause spasmssimilar to those seen with ether, but these were neither to be understood as convul-sions nor to be dreaded. His recommendation was not to avoid using these drugsbut to bring in a specialist.

Snow was quick to appreciate chloroform’s properties. It seemed to behave likea concentrated form of ether, generally acting like ether only faster. It fit what wasto Snow’s mind an emerging pharmaceutical profile. Simpson had been empiri-cally searching for other anesthetics when he hit upon chloroform, but Snow rec-ognized ether and chloroform as constituting a family of anesthetic agents inwhich similar chemical composition and properties indicated similar physiolog-ical action. It was a matter of calibrating safe dosages for the new drug. Therewere differences, but chloroform conformed to the pharmacokinetic model (howdrugs are absorbed, distributed, metabolized and excreted) that Snow had devel-oped for ether. There were undoubtedly other agents with similar properties wait-ing to be tested. As early as February of 1847 Jacob Bell, editor of Pharmaceuti-cal Journal, had tested chloric ether (which consists of chloroform in wine spirits)with some success.3 Snow and others returned with fresh eyes to Robert M.Glover’s Harvean Prize essay for 1842 that described bromoform, chloroform, andiodoform. According to Glover, “Great resemblance exists among the propertiesof this class of bodies, which appear to form a new order of poisonous substances,uniting in themselves physiological properties which are not found united in anyother known class of poisons.”4 Snow realized that the medical miracle ofether and chloroform was made possible by a beneficial side effect of a family oftoxins.


In a scant ten days chloroform had moved to the center of Snow’s research, whichmeant to the center of his life. The extant Case Books of his practice begin in July1848 (CB, 3), and they chart a widening circle of anesthesia from teaching hospi-tals and Soho environs to virtually every quarter of London and beyond. Chloro-form moved to the center of his thoughts about anesthesia, as he proceeded tomake it the basis of his pharmaceutical profile and to build a family of agentsaround it (as the title of his last work, On Chloroform and Other Anesthetics, indi-cates). Whatever risks chloroform presented were clearly outweighed, in Snow’smind, by its benefits. He believed that anyone who followed his methods couldwork with it safely. Although he would greatly amplify, complicate, and qualify hisunderstanding of chloroform in the ensuing decade, he remained within the par-adigm created in 1848. According to Richardson, Snow recalled a talk in which hestated that “in his opinion sulphuric ether was a safer narcotic than chloroform.Why, then, said a listener, do you not use ether? I use chloroform, he resumed, forthe same reason that you use phosphorous matches instead of the tinder box. Anoccasional risk never stands in the way of ready applicability.”5 Snow’s attitude wasrepresentative of British medical opinion at the time; according to Richardson,chloroform “was immediately used everywhere to a greater extent than ether hadbeen,” rapidly becoming the anesthetic of choice (OC, 22).6 In 1848 Snow wouldfollow Glover’s lead and expand the range of his investigations beyond one or twospecific agents toward a larger concept of a family of drugs that fit the same phar-maceutical profile. His approach was both bold and prudent—bold in its confi-dence, prudent in the way it controlled the dosage. Chloroform’s very virtues, itspower and convenience, made it dangerous, even though many doctors had theimpression (largely thanks to Simpson) that chloroform was safer than ether (OC,22). Within months of its discovery its risks would become all too real; the eu-phoria of national pride at the Scottish breakthrough that rivaled, perhaps evensurpassed American self-satisfaction at having “discovered” ether, gave way, like aserial novel, to death and doubt.

Hannah Greener

On 22 October 1847 a fifteen-year-old girl named Hannah Greener was admitted tothe Newcastle Infirmary suffering from an ingrown toenail on the big toe of her leftfoot. The big toe on her right foot was also affected, but less so. She had not hadmuch of an appetite lately but was otherwise healthy. A few days later the surgeonto the infirmary, H. G. Potter, operated to remove the left toenail. Ether was to beused, but the first two inhalers failed to produce the desired effect. A third inhaler(designed by Hooper) did the trick. According to Potter, the patient “screamed dur-ing the operation but did not feel any pain.” She had not cried or laughed or ex-hibited any “hysterical symptoms.” She never paled. Her pulse did weaken but then

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regained strength. Thirty minutes afterward, sans toenail, she was fine, said that shefelt no pain, and “was asleep the whole time.”7

On 28 January 1848 Greener’s feet were still giving her trouble, and her family de-cided to have another surgeon pay a visit to their home in Winlaton (near Newcas-tle) to have the other nail removed. Thomas Meggison and his assistant, Mr. Lloyd,arrived and found the girl in a fairly agitated state. She began crying from the mo-ment that they walked in and continued to weep as they seated her in a chair andbegan to administer chloroform.8 Meggison poured about a teaspoonful of chloro-form on a “tablecloth” and held it to her nose. After drawing two breaths she pulledhis hand down. He told her to keep her hands on her knees and breathe quietly. Thegirl complied, and in about thirty seconds he observed rigidity in her arm. Herbreathing quickened but was not stertorous. Her pulse was fainter than normal butsteady. Lloyd began the operation making a semicircular incision in the toe, andGreener’s leg gave a sudden jerk. Meggison thought she might need more chloro-form and was about to give her the cloth again when he lifted her eyelids and theystayed open. Then the patient’s face and lips turned white, and she moaned or splut-tered. The sound, he later explained, was “similar to the expiration in epilepsy orhysteria.” He dropped the cloth and dashed water in her face. It was no use. He gaveher some brandy, laid her down, and tried to bleed her. He opened a vein in her armbut nothing flowed. He tried her jugular with the same result. In total, about a fluiddrachm, or three and a half milliliters, of chloroform was used. The elapsed time ofthe entire process of inhalation, operation, venesection, and death: two to three minutes.9

The next day Sir John Fife and Dr. R. M. Glover conducted a postmortem exam-ination. They attributed the cause of death to “congestion in the lungs” caused bythe inhalation of chloroform in combination with the idiosyncrasy of the patient.Meggison and Lloyd were not held responsible for Greener’s death. Dr. Fife arguedthat “no human foresight, no human knowledge, no degree of science, could haveforewarned any man against the use of chloroform in this case.” The jury convenedat the coroner’s inquest unanimously agreed,10 but would juries continue to agree ifmore cases of sudden death occurred? This was both a crisis of medical knowledgeand a public relations nightmare for chloroform and doctors, like Snow, who pro-moted its use. Pain relief was a blessing, but it had its limits. Whatever went wronghad yet to be determined, but it was clear that a procedure to remove an ingrowntoenail should not result in the death of a fifteen-year-old girl. In the months thatfollowed the press was full of analyses of the case and soul-searching about the ben-efits and dangers of chloroform. The same page of the Lancet that carried a reportof the inquest into Greener’s death contained an account of Professor WilliamBrande’s lecture on the chemical properties of ether and chloroform. It ended, thereport tells us, with a demonstration of Snow’s inhaler and Brande’s endorsementof these chemicals as “of the greatest benefit to the medical profession and to hu-manity.” Following the account of this well-attended lecture, the Lancet chose to run


an editorial that scolded Brande for killing a guinea pig during his demonstrationof the effects of chloroform. The performance seemed to confirm chloroform’s dan-gers rather than to highlight its beneficent powers, and this was the last thing thegeneral public needed to see. There were ladies in the audience.11

Reports of other deaths from chloroform began to proliferate.12 In the generalpress there were calls for abandoning its use. In its “Medical News” column the Lancetreprinted an account from the Scotsman dated 12 February of a young man in hislate teens from Aberdeen who had been given to joy-popping chloroform and hadbeen found dead.13 A letter to the Lancet from a Robert Selby musing on the bene-fits and dangers of chloroform admitted to nearly killing a nine-year-old boy.13a InFebruary in a dental parlor in Cincinnati, Ohio, a thirty-five-year-old mother of sixdied under chloroform. A Boston man died in March. In May a thirty-year-oldwoman in Boulogne, France, succumbed. Snow, who assiduously collected and scru-tinized every case of death involving the medical use of chloroform, counted thir-teen fatal or allegedly fatal cases for 1848. By the end of his career in 1858, thesewould number more than fifty (OC, 120–222).

Doctors using ether and chloroform generally reacted defensively to these adversereactions and suggested that the proper stewardship of these drugs was the most press-ing issue. It was most commonly argued that the agents could be used safely but mustbe administered by informed, competent professionals. The letters in the Lancet werequick to remind readers that toenail surgery is intensely painful, fully mandating theuse of anesthetics despite the fatality that occurred. Simpson led the way with a de-fense of chloroform. Two weeks after Greener’s death he reviewed the facts of the caseand the autopsy as reported in the Lancet, concluding that she must have died of as-phyxia; he believed the dose was “so small as to render it exceedingly improbable thatit could have been the essential cause of the death of the patient.”14 She appeared tohave fainted (syncope) at a critical moment. The water and the brandy used to restoreher, Simpson argued, inadvertently caused her to choke and cut off her air, but he didnot blame Dr. Meggison for using these techniques, because he had no way of know-ing their dangers in the treatment of chloroformed patients.15

Reactions to Simpson’s analysis were generally sympathetic, with important dis-tinctions that reveal the uncertainty surrounding the chloroform-related emergen-cies. One correspondent agreed that the cause of death could not have been chloro-form but believed “that the girl Greener died from the shock of the surgicaloperation,” not efforts to revive her.16 David Davies, the house surgeon at Lough-borough Dispensary, disagreed with Simpson’s analysis. Simpson’s account did notjibe with his or Marshall Hall’s understanding of how anesthetic agents paralyze thenerves. “Would it not have been more physiological to have said,” he wondered, “thatthis poor woman’s death was owing to the power which anæsthetic agents have, insome very rare instances, of destroying the functions of the spinal and ganglionicsystems of nerves.”17 Davies felt that Simpson needed to be more critical of the agenthe had discovered.

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Like Davies, Snow disagreed with Simpson as to the cause of death, and he alsodisagreed with the coroner’s conclusion. Snow sent a letter to the Lancet, stating thatthe evidence did not support the thesis of syncope followed by asphyxia. While heagreed with Simpson that brandy and water were not wise in this case, he could notagree that they had asphyxiated the girl. Congestion of the lungs and heart, as wasfound with Greener, was not compatible with fainting prior to asphyxiation. Snow,who was lecturer on forensic medicine at Aldersgate School of Medicine, pointedout that “a certain number of those who are drowned” do not have congestion inthe heart and lungs, and it is believed that “those persons have fainted on falling intothe water.” The autopsy did not support Simpson’s account and pointed back towardthe chloroform and, to Snow’s thinking, toward Simpson’s preferred way of givingit, the hanky. There is a note of accusation in Snow’s critique. “For if anyone couldprevent his patient from getting into a state which cannot be looked on otherwisethan as one of imminent peril, it would be the authority who introduced that agent,and recommended this method of its administration.”18

Snow wrote Meggison seeking clarification on a number of points and then pub-lished his opinion in the LMG. He reasoned that if chloroform had caused death inthe manner concluded at the inquest, it “would necessarily invest the inhalation withsome degree of danger, however small, and would entail some anxiety on both theoperator and the patient. My view of the matter holds out more hope for the future.I look on the result as only what was to be apprehended from the over-rapid actionof chloroform when administered on a handkerchief.”19 He believed that the hand-kerchief had induced a much deeper degree of anesthesia than had been supposed,and the rapid action of the chloroform was carried too far too fast, to the point thatit put a stop to Greener’s respiration. Snow had found that the effects of chloroform,unlike ether, seemed to increase for twenty seconds or so after leaving off inhalation,and this would account for the acceleration into a lethal degree. He argued that ex-periments had shown that a teaspoonful of chloroform was sufficient to induce dan-gerous levels of anesthesia in a large man, and this would therefore also be possiblein a smaller, younger female, even if given in the inefficient handkerchief.

In his letter to Meggison Snow asked for details about time and Greener’s symp-toms in order to correlate them with the degrees of “etherization” he had establishedthe year before. What was “the nature of the breathing after the inhalation wasstopped?” “How long did the patient breathe after the removal of the cloth?” Whatwas the exact nature of the moan? From Meggison’s reply Snow reasoned that therigidity of the patient’s arm placed her in the third degree. From that position he in-terpreted all subsequent symptoms as acceleration to the fifth degree. He argued thatthe overdose stopped respiration and then the circulation, and this was the funda-mental cause of death. This was a key moment in the development of Snow’s thought.He noted that some of his more recent animal experiments indicated that in somecases “the respiration and circulation seem to cease together.”20 By October 1848 he would go even further and claim that chloroform at this strength “paralyzes the


action of the heart at the same time as the respiratory movements.”21 In the ten yearsof using chloroform that followed this investigation, Snow would elaborate on histheory, especially in response to the commentary of Francis Sibson, who pointed tothe heart as the key to the trouble and also mentioned fear as a factor.22 Snow woulddiscuss more cases and complications, but he would never essentially depart fromhis conclusions in the Greener case.

Concerns: On Narcotism

As he had done with ether, Snow looked to the mode of administration as the sourceof the problem. He concluded that with ether problems typically eventuated in anunderdose; with chloroform, however, the danger was an inadvertent overdose. Thisassessment would turn out to be only part of the story, but in 1848 there were toomany other basic questions that needed answering before subtler complications couldbe pinpointed. He needed to find a way to explain the effects of chloroform andether in general, and he needed to detail the emerging pharmaceutical profile. Whatwas the appropriate name for it? His former term, etherization, was obsolete. Anes-thesia was useful, but it placed the emphasis on the absence of sensation and dis-tracted attention from other phenomena associated with these agents that should bescrutinized. He settled on narcotism, because ether and chloroform closely resem-bled narcotico-irritants (the Greek narco encompassed both stupor and numbness).Strange as it may sound to modern ears, narcotism in the mid-nineteenth centuryreferred exclusively to narcotic vapors. In an era before the availability of nerve-blocking local anesthetics, anesthetists were using gases that produced unconscious-ness or stupor. Today, we tend to keep the pain relief derived from anesthetics sep-arate from that produced by narcotics like morphine and heroin, which carry anassociation with addiction. We also tend to distinguish the main property of a drugfrom its side effects, which frequently suggest more about a drug’s common appli-cation than its properties. For Snow, however, narcotism seemed the most compre-hensive term for the entire range of phenomena, and his usage resonates with theterm narcosis.

In February 1848, with the notes to fifty chloroform cases carefully logged, he an-nounced the next plank in his research agenda. Having established to his own satis-faction that chloroform conformed to the five degrees of etherization, he concludedthat there “can be no doubt that these degrees of narcotism correspond with differ-ent proportions of vapour which are dissolved in the blood at the time—propor-tions which I hope to be able to determine.”23 Narcotism was the total effect of thedrug on the system, and anesthesia was just one consequence.

These drugs could be measured against each other with respect to blood satura-tion levels, anesthetic and narcotic power, and various other effects. Snow usedFlourens’s theory of the cessation of neurological function as a working model of

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narcotism. “A certain quantity of vapour disturbs the functions of the cerebral hemi-spheres; an additional quantity appears altogether to suspend these functions, andto impair those of the spinal cord, and probably of the cerebellum; a still larger quan-tity to suspend their latter functions, but to leave the medulla oblongata more or lessunaffected.”24 As the gas escapes the lungs, the sequence is reversed.

With this model in mind, Snow began his pioneering study, “On narcotism by theinhalation of vapours,” published in eighteen installments by LMG between May1848 and December 1851. He completed twelve installments by August 1849, whenhe interrupted his research to develop his theory of cholera. He completed four moreinstallments between the spring of 1850 and the spring of 1851 and finished his se-rialization that December, just before LMG amalgamated with MT to become MTG.“On narcotism” (ON) placed his earlier work on ether in a broader context of nar-cotic and anesthetic phenomena. It is studded with examples of outstanding scien-tific observation and problem solving. Snow laid out the significance of saturatedvapor pressure. He expressed his rule of thumb that the amount of an agent neededto produce anesthesia was inversely related to its solubility in blood. He identified afamily of agents that worked in this way, gauging their potencies relative to one an-other. He added further considerations to his ether study on the mechanics of in-halation. He discussed oxidation, closed-circuit techniques, and tests to detect chlo-roform in air, blood, and tissues.25 It was an evolving study, written in periods ofgreat activity and energy and responsive to emerging controversies about deaths whilepatients were under chloroform. In sum, the installments of ON reveal the reach ofSnow’s mind, the patterns of his thinking, and his ability to incorporate develop-ments on practical, experimental, and theoretical levels.

His basic goal in ON was to determine the exact correspondence among precisedoses of ether or chloroform, degrees of narcotism, and quantity in the bloodstream,but first Snow needed to show experimentally what was already plain: ether and chlo-roform enter the blood via respiration. To show this he “passed a tame mouse”through a mercury trough and into a graduated jar containing a mixture of etherand air. After a short while he removed the mouse from the first jar and placed it ina second graduated container containing only air. He then removed the mouse fromthe second jar, let both jars return to the starting temperature, and observed that inthe first jar the mercury rose a good deal while in the second it fell somewhat (ON,1: 850). With relatively simple techniques of chemical analysis he had demonstratedthat the mouse had inhaled ether from the first jar and exhaled it into the second.

Even so, how could he determine the precise amount the mouse had inhaled andthe minimum required to induce the five degrees of narcotism? In 1847 Jean-LouisLassaigne and Andrew Buchanan had made crude estimates of how much ether wasrequired to fully anesthetize an adult. Snow was prepared to offer a more accuratemethod. Rehearsing the laws of proportion for gas mixtures and liquids that he hadconfirmed in 1847, he explained that when gases like ether or chloroform come incontact with a liquid like blood or water, the gas is absorbed into the liquid until


equilibrium is established. At a given temperature and pressure, equilibrium occurswhen both the gas and the liquid contain “the same relative proportion to the quan-tity which would be required to saturate them” (ON, 1: 850). If one knows the con-centration of the gas, the concentration at which that gas saturates air (at the tem-perature of the air in the alveoli), and the concentration at which that gas saturatesblood (at the same temperature), then one can calculate the concentration of the gasin the blood. He expected to find that, if one started with a three percent concen-tration of gas to air at equilibrium, the blood would contain a one per-cent concentration of the gas (assuming thirty percent was required for air satura-tion and ten percent for blood saturation). That is, the ratio of anesthetic gas to airwould be proportionate to the ratio of gas to blood. In Snow’s words, “As the pro-portion of vapour in the air breathed is to the proportion that the air, or the spaceoccupied by it, would contain if saturated at the temperature of the blood, so is theproportion of vapour absorbed into the blood to the proportion the blood woulddissolve” (ON, 1: 850). For the sake of clarity, this rule was perhaps best not con-densed into one sentence, but Snow’s formulation gives us a sense of how he saw theproblem. To regulate the dosage, he created an inhaler, which was a temperature-and volume-controlled environment for gas–air mixtures. To calculate the quantityabsorbed in the blood, the dosage had to be adjusted for alveolar temperature. Oncesaturation levels were established and concentrations known, determining theamount of the drug absorbed in the blood became a matter of solving for X. Snowhad come to see temperature, volume, and saturation as the keys to controlling con-centration and concentration as the key to understanding the physiology of narco-tism and the process of anesthesia.

The first series of experiments described in ON dealt with chloroform; he had de-cided to use the new drug, not ether, to build the database of narcotism. Using min-imal doses and allowing enough time to see that the drug’s effect no longer increased,Snow combined his acute powers of clinical observation with the numerical preci-sion of chemistry to determine the quantity of chloroform necessary to induce a par-ticular degree of narcotism. Working from a chemical and physiological perspective,Snow was practicing modern scientific medicine. He placed guinea pigs, mice,chaffinches, green linnets, and frogs in jars with different quantities of chloroform,allowed the effects to run their course, and monitored the animals for symptoms. Inthe course of the first sixteen experiments, Snow pinched the guinea pigs andchaffinches to see if they would flinch and made his notes. Table 6.2 summarizes hisfindings. The medical model enabled a new kind accuracy in his estimates. The se-lection of rodents, birds, and frogs afforded a variety of sizes and respiratory rates,allowing for a range of differences in reactions while supporting the general valid-ity of the blood concentration model.

To prove this last point, Snow concluded the first installment by recounting theexperiments he was invited to perform at the Royal College of Physicians for JamesArthur Wilson’s Lumleian Lectures (29 March 1848). In a very large jar (almost 1000

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cubic inches) Snow had placed a frog and a chaffinch (in a small cage) and then in-troduced five grains of chloroform. In less than ten minutes the frog was insensiblewhereas the bird was perfectly conscious. He inserted another frog and chaffinch ina much smaller jar (200 cubic inches) and added five grains of chloroform. In ninetyseconds the bird was insensible, but the frog was still very conscious (ON, 1: 854).These demonstrations showed how crucial dilution, respiration rate, and blood tem-perature were in the process of narcotism. In the first case the dilution was too greatfor the small, warm-blooded chaffinch to be affected despite its quick respiration,but the cold-blooded, slowly respiring frog was affected because the lower temper-ature of its blood meant that it did not require as high a concentration to achievesaturation. In the second case the greater concentration worked quickly on the bird,but ninety seconds was not long enough for the slow-breathing frog. Snow addedfurther confirmation by demonstrating that a warmed frog ceased to be affected bydiluted gases that would narcotize it at low temperatures.

The second installment of ON analyzed ether, using the same approach as he haddone with chloroform, and then compared the two agents. Snow found that the sec-ond degree of narcotism corresponded to .000875, or 1/1,142 proportion of ether inthe blood at 100° F., and that the fourth degree corresponded to .00175 or 1/572. Hecompared these results to his experience with human subjects. Working from GabrielValentin’s calculations of the weight of the blood in the adult human (about thirtypounds, equivalent to 410 fluid ounces), Snow calculated that the total quantity ofchloroform in the blood was 12 minims (.71 ml) for the second degree and 24 min-ims (1.42 ml) for the fourth. For ether, the corresponding numbers were 171.84 min-ims (10.17 ml) and 340.8 minims (20.17 ml). He found these to correspond verynearly with his experiences when administering both agents: “a considerable portionis not absorbed, being thrown out again when it has proceeded no further than thetrachea, the mouth and nostrils, or even the face-piece” (ON, 2: 895). He confirmedthis hypothesis by breathing chloroform over and over again from a balloon (as withnitrous oxide). Using this recycling technique, he found twelve minims sufficient toinduce the second degree.

He was particularly sensitive to the role temperature played in the administrationof vapors, both in the apparatus and the alveoli. He noted that birds “were found to


Table 6.2. Snow’s early experiments with chloroform

Chloroform/Degree of narcotism Quantity of chloroform/air blood concentration

2nd 1 grain (64.8 mg)/100 cubic inches air 1/16,285

3rd 1.5 grains (97.2 mg)/100 cubic inches air 1/10,857

4th 2 grains (129.6 mg) /100 cubic inches air 1/28

5th 2.5 grains (162 mg) /100 cubic inches air 1/22

require nearly twice as much” ether as were mice to render them insensible, whilethis was not the case with chloroform. Because these birds generally maintained atemperature of 110° F., he reasoned that the blood serum at that temperature woulddissolve much less ether than at 100° (the temperature of Snow’s mice), and there-fore the birds would require greater concentrations to achieve the same degree ofsaturation. Snow also began to consider the impact of ether and chloroform on an-imal temperature, not merely noting the difference between warm-blooded and cold-blooded creatures but as a physiological process. Snow came across Jean NicholasDemarquay and Auguste Dumeril’s statements that these agents lower body tem-perature during inhalation. Several ether experiments on linnets confirmed this, reg-istering drops of as much as eight degrees in fifteen minutes (ON, 2: 893–94).

This was John Snow in early 1848—poking guinea pigs, pinching chaffinches, pass-ing mice through quicksilver, and warming frogs near the fire in the name of med-ical science. His medical model focused on narcotic symptoms, concentration, volatil-ity, respiration, time, and temperature. Differences in species and individuals nowcame down to measurable differences of minutes, minims, cubic inches, degreesFahrenheit, degrees of saturation, and degrees of narcotism. Through the alembic ofthis medical model, he transformed a narcotized menagerie of experimental animalsinto reliable data on blood concentrations. To our knowledge no one else took sucha comprehensive numerical approach to these drugs, nor did anyone else wed chem-ical analysis to a physiological progression with such consistency.

After establishing a baseline with chloroform and ether, Snow concerned himselfwith broadening the spectrum of vapors that might have narcotic properties andmight be inhaled for anesthetic purposes. Through the spring and summer of 1848,when he published the third and fourth installments, he investigated six other agents:nitric ether (ethyl nitrate, C2H5ONO2), bisulphuret of carbon (carbon disulphideCS2), benzin (benzene C6H6 [Snow gives it as C12H6]), bromoform (HCBr3) ethylbromide (C2H5Br), and Dutch liquid (1,2-dichloroethane C2H4Cl2). He had begunto compile a systematic pharmacology of inhaled anesthetics. Whereas many wereengaged in the search for better anesthetic agents (Simpson and Thomas Nunnelyfrom Leeds, for example, experimented with many of the same agents), and medicaljournals were filled with suggestions for new agents, Snow established a method ofcomparison based on general principles of anesthetic and narcotic action.“His grandsearch,” according to Richardson, “was for a narcotic vapour which, having the phys-ical properties and practicability of chloroform, should, in its physiological effects,resemble ether in not producing, by any accident of administration, paralysis of theheart.”26 No doubt that would have been a desirable practical outcome from Snow’sresearch, but this was actually Richardson’s project.

For Snow, the grand search was for “the ‘perfect’ anaesthetic” as well as a generaltheory of narcotism itself.27 That was why he went to the trouble of calculating theblood saturation levels for substances like bisulphuret of carbon, when all of his ev-idence showed that it was too powerful, noxious, and dangerous; it caused convul-

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sive tremors in mice (ON, 3: 1076–77). He never really considered this agent a vi-able substitute for ether or chloroform, but he studied it because he wished to placeit on a continuum of inhaled agents that induced narcotism in the same way as didether and chloroform. In particular, he was looking for extremes to set the endpointson this continuum. He was careful to point out that not all narcotics functioned likeether and chloroform, and he mentioned hydrocyanic acid (prussic acid) as an ex-ample of one that did not. He was only interested in those narcotics “producing ef-fects analogous to what are produced by ether,” “and having . . . a similar mode ofaction.” However, he regretted that he was not “able at present to define them bet-ter than by calling them, that group of narcotics whose strength is inversely as theirsolubility in water (and consequently in the blood)” (ON, 4: 333). The analogical,deductive pattern of his thought is evident; similar substances producing analogouseffects implied similar pharmacodynamic mechanisms. In this manner he inventeda family of volatile liquids where formerly there had been only individual agents. Helinked blood solubility with the narcotic power, rated by the minimum concentra-tion in the blood, necessary to induce the second degree. He considered nitric ethera promising candidate, and he asked one of his regular chemists to make him a sam-ple. When he tried it on himself (“on two or three occasions”), a small amount“caused a disagreeable feeling of sickness each time” (ON, 3: 1075). In May 1848 heused it with encouraging results in a tooth extraction at St.George’s Hospital, but henever used it again, clinically, despite evidence that it was an effective painkiller. Hewas also interested in benzene, despite its tendency to cause convulsive tremors. Tri-als showed it to be nearly as efficient as chloroform, but its effects “are not so rap-idly produced as the effects of chloroform, on account of its lesser volatility.” He triedbenzene on human subjects at St. George’s Hospital, with success in minor opera-tions, but in an “amputation, where its effects were carried further, the patient hadviolent convulsive tremors for about a minute, which, although not followed by anyill consequences, were sufficiently disagreeable to deter me from using it again, orrecommending it in the larger operations” (ON, 3: 1078). Snow was a cautious prac-titioner, and it is admirable that he stopped using benzene. At the same time, givenhis reaction to the carbon compound, which also caused convulsions, one may won-der why he bothered to put benzene to clinical trial at all, or, for that matter, whyhe never pursued nitric ether, despite its promise. Convulsions alone would not havedissuaded him; both ether and chloroform could produce spasms.

He was deeply invested in the model of narcotism he had constructed aroundchloroform, and it shaped his theoretical and practical considerations of relatedagents. He probably did not pursue nitric ether because it was a weaker and moreexpensive agent than was chloroform.28 In the case of benzene, the potential of hav-ing a drug as economical and efficient as chloroform that acted less quickly (Snowconsidered gradual induction desirable) made it worth trying until convulsionsproved too violent. The sulfur–carbon compound was too fast acting to control ef-fectively, so it held no clinical interest for him. Snow synthesized his own bromo-


form, a substance with a molecular formula similar to chloroform and now knownto cause kidney and liver damage in animals. He found it “very pleasant to inhale”but too costly to produce (ON, 4: 330). He found ethyl bromide to be too volatile,requiring very high concentrations to be effective, so he never bothered to get an ex-perimental reading of its blood solubility. Dutch liquid tasted “at once sweet andhot,” and Simpson considered it too caustic to be inhaled by most patients (ON, 4:331). Snow determined that it required 46 minims (2.7 ml) of Dutch liquid to cre-ate 1/50th relative saturation of the blood to induce the second degree of narcotism.He was not particularly sanguine on its prospects as an anesthetic agent for addi-tional reasons: Two mice died after trials, and postmortem examinations revealedthat their lungs were congested, their hearts swollen, and the blood coagulated anddark.

Snow would continue for the rest of his life making trials of all kinds of hydro-carbon inhalants, but his main concern in 1848 was to confirm and reconfirm thatdegrees of narcotism corresponded to the quantity of the substance in the blood. Hebelieved that this quantity was a proportion of “what the blood would dissolve—aproportion that is almost exactly the same for all of” these substances. The actualdifferences in quantity were accounted for by differences in solubility: “When theamount of saturation of the blood is the same, then it follows that the quantity ofvapour required to produce the effect must increase with the solubility, and the ef-fect produced by a given quantity must be in the inverse ratio of the solubility” (ON,4: 332). Snow included acetone, pyroxilic spirit, and alcohol on his list, even thoughthey are infinitely soluble in blood, because they shared properties with the othervolatile liquids and were proportionately less potent, which seemed to prove his rule.In this fourth installment of ON, he again described the degrees of narcotism, usingchloroform as his model, began to make observations about chloroform and mid-wifery (a subject that would increasingly preoccupy him), and put forward an ideathat he had not previously mentioned: “The division into degrees is made accord-ing to symptoms, which, I believe, depend entirely on the state of the nervous cen-tres, and not according to the amount of anesthæsia, which I shall give good reasonfor believing depends very much on local narcotism of the nerves” (ON, 4: 334). Itturns out that Snow’s last opinion was incorrect, but it reveals the general pattern ofhis thought. Painlessness was, for Snow, a local epiphenomenon of narcotism.

Narcotism’s Reach

In these early installments Snow established the pharmacology of narcotism and amodel of how the body responds to relative quantities of narcotics. The fifth andsixth installments addressed the general physiological effects of chloroform, how thenerves were affected, how death could occur, and what autopsies on animals revealed.After reviewing the dangers of chloroform in part seven, he made a case for its safe

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use with a slightly modified version of the temperature-controlled chloroform in-haler (Fig. 6.1). In part eight he described the various conditions that influence theaction of chloroform such as age, strength, debility, disease, diet, hysteria, epilepsy,renal convulsions, and diseases of the heart, lungs, and brain. In parts nine and tenhe analyzed the data for amputation and other procedures under chloroform. Next(parts eleven and twelve), he considered various mixtures of chloroform and ether,and described an alternative mode of administration via a balloon and a valved facepiece. He made a few more trials of Dutch liquid and in 1849, as cholera raged inLondon, Snow evaluated it as a potential treatment. A seven-year-old girl was in thethroes of the disease, constantly vomiting and evacuating and in jactitation fromhorrific cramps. He had used chloroform in a number of cholera cases that year, andhe found that it offered some relief by inducing sleep free “from sickness and spasm.”For this girl, however, he administered Dutch liquid, which gave her only a few min-utes’ respite, although she did recover (ON, 12: 277). In June 1849 Snow continuedto experiment with his growing armamentarium of pain relievers in the face of


Figure 6.1. The modified chloroform inhaler and mouthpiece from November 1848

(Adapted from ON, 7: 843).

cholera. Sometimes he was able to give patients enough rest to make a recovery,sometimes he simply eased the suffering of the dying. In the process it must havebecome clear to him that giving chloroform and Dutch liquid to cholera victims wasonly a stop-gap measure.

Chlorophobia

On a night in early January 1850, a Lime Street solicitor named Frederick Hardy Jew-ett was walking along the bustling Whitechapel Road in the East End. Suddenly,someone put a felt rag or handkerchief over his mouth. The next thing he remem-bered was waking up the next morning in the filthy bed of a lodging house in ThrawlStreet, Spitalfields. When he attempted to leave, he found the door locked from theoutside. He was naked, covered with rags, and most of his valuables had been stolen.Two young women, Margaret Higgins and Elizabeth Smith, were arrested, tried, con-victed, and sentenced to fifteen years. At one of their hearings Catherine Donovan,the wife of a local grocer, testified that Higgins had confessed to the crime and toldher that the man with whom she lived had been operated on at a London hospital.They gave him “some stuff to send him to sleep,” and afterwards he had managed tosteal some of it. Higgins had used this “stuff” in the Whitechapel Road mugging.About the same time, a man was walking along the Borough Road, south of theThames, toward London Bridge when a woman passed a handkerchief across hisface. He immediately felt indisposed, and the woman helped him into a nearby pubfor a tumbler of brandy. Her name was Charlotte Wilson. Ten minutes later the manwas unconscious, and she left the pub with his hat and scarf in hand. Wilson wassoon apprehended. In the opinion of the court, she had used “some deleterious ar-ticle such as chloroform,” and she received ten years for robbery.29 It was not just aproblem of women attacking men. In April 1850 a young man named Charles Joplingand his girlfriend walked home from a pub dance near Marylebone. He beckonedher to follow him into a mews, where he poured the contents of a vial on a hankyand tried to smother her. Repulsed by the wet hanky and the pungent odor, she criedout for help. A policeman on his beat heard the screams and took the man into cus-tody. Jopling paid bail and married his girlfriend, and she dropped the charges againsthim.30 This was not exactly news. As early as November 1847, when Simpson’s newagent was first publicized, there had been reports of chloroform described as a rapedrug.31 There were a few reports of street robberies in 1849, but in the aftermath ofHannah Greener’s death the medical risks of chloroform received more press thanits criminal potential.32

In 1850 and 1851, however, chlorophobia swept the country, as the agent intendedfor medical purposes was increasingly perceived as an alleged agent of crime, rob-bery, rape, and murder. An old man asleep in a hotel room was attacked with chlo-roform by a man hiding under his bed. Prostitutes were charged with hocussing by

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way of chloroform, using it to lace the drinks of unsuspecting johns and then rob-bing them. In France a dentist raped a female patient while she was under its influ-ence.33 Chloroform’s fast action, incompletely reported in the press and experiencedby growing numbers of patients, led to a sensational misunderstanding of its pow-ers in the public and popular imagination. Long before the chloroformed handker-chief became a staple of fictional abductions—the kidnapper’s method of choice forsurreptitiously overpowering victims—the powers of chloroform were mythologizedon the streets and in the criminal courts.

Things came to a head in February 1851, when Lord Campbell, the recently ap-pointed chief justice of the Court of Queen’s Bench, proposed An Act for the BetterPrevention of Offences that called special attention to the use of chloroform for crim-inal purposes. Lord Campbell believed that British criminal law was too liberal andthat too many criminals were able to skirt whatever law did exist. He lobbied forstricter sentences as a deterrent. He wanted to make possession of tools of criminaltrades (e.g., picklocks) an offence for which the punishment was deportation. Aclause in Lord Campbell’s bill depicted chloroform as a potential tool in the crimi-nal’s trade: “And whereas it is expedient to make further provision for the punish-ment of persons using Chloroform, or other stupefying things, in order the betterto enable them to commit felonies: be it enacted, that if any person shall unlawfullyapply or administer, to any other person, any Chloroform, Laudanum, or other stu-pefying or overpowering drug . . . every such offender shall be guilty of felony, andbeing convicted thereof shall be liable, at the discretion of the Court, to be trans-ported [to Australia] for life, or for any term not less than seven years.”34

Snow believed Lord Campbell’s bill was unnecessary and unfairly targeted chlo-roform. In his opinion, “It ill becomes the gravity of the law, and is, I feel assured,far from your Lordship’s intention, that a legal enactment should be made on a falsealarm, or to meet a trivial and unsuccessful innovation in the mode of attemptinga crime: to legislate on this matter would revive the groundless fears of the public.”35

Snow was skeptical of public reporting on the purported uses of chloroform to com-mit crimes. Most descriptions did not conform to the known properties of the agent.The drug was far too pungent to be inhaled unawares. To force it upon someone re-quired smothering, or “burking”—a felony for which the law already provided. Per-haps Lord Campbell was cracking down in advance of the Great Exhibition of 1851,when tourists were expected in London. The bill had a distinct animus against theworking class, especially with its stiff sentencing. Snow thought social hypocrisy ex-plained much of the chlorophobia: “Persons who have been dead drunk are very un-willing to admit, even to themselves, that the result was the consequence of theirown voluntary potations, and still less willing to admit it to the world, when theyhave to complain of having been robbed whilst in bad company.”36 The editorial staffof the Pharmaceutical Journal concurred, stating that, “It may be a convenient sub-terfuge for a man who finds himself in a scrape . . . to conjure up a mysteriousand exciting story about chloroform and a handkerchief, for the purpose of throw-


ing dust in the eyes of the magistrate, and working upon the prejudices of the jury.[This act] may be the means of entailing an unjustly severe punishment for a com-paratively trifling offence.”37 Snow’s letter was discussed in the House of Lords. TheTimes reported that “a most respectable physician” had done Lord Campbell thehonor of writing him a letter, stating that the fear of using chloroform in this waywas “altogether imaginary.” Nonetheless, Campbell kept the provision and hoped thatanyone convicted would “be guilty of a felony, and liable to be transported beyondthe seas.” To which his fellow lords replied, “Hear! Hear!”38 The act passed in June1851.

Narcotism’s MO

When Snow resumed publication of ON in April of 1850, he apologized for the in-terruption. He justified it on the grounds that he needed to “repeat many experi-ments and institute fresh ones,” but his study of cholera in 1849 may have been anadditional factor (ON, 13: 622). The new installments reflect a shift in thinking. Ear-lier, his goal was to establish a pharmaceutical profile of narcotism, to measure in-verse ratios of solubility, and to describe the benefits of various agents in amputa-tion and dentistry. Now, in 1850, he concerned himself with the underlyingphysiological mechanisms, or, as he called it, “the modus operandi of ether and chlo-roform” (ON, 13: 622). He began to tackle complex questions involving the bio-transformation of these drugs as they circulated in the body.39 This approach wouldpush him beyond the pharmacokinetics of narcotic agents into thornier issues ofpharmacodynamics (how drugs interact at cellular and molecular levels). It was terraincognita. Where to begin? His cholera research had led him deeper into patho-physiology to Liebig’s Animal Chemistry, especially Liebig’s descriptions of how car-bon and hydrogen in fat, starch, sugar and gum “combine with oxygen in the blood,and are given off as carbonic acid gas and water” (ON, 13: 627). Based on this gen-eral model, Liebig also offered an “explanation of the physiological action of alco-hol,” that is, how it was metabolized in the system (ON, 13: 626). When ether camealong, Snow observed, “many persons were inclined to extend” Liebig’s alcohol the-sis to ether (because of its chemical similarity to alcohol). Snow would begin by test-ing the validity of Liebig’s theory of the physiology of alcohol to see what he mightlearn about the physiology of narcotism.

Snow began by reconfirming what his blood solubility table had shown: a familyrelation between alcohol, chloroform, and ether.40 He showed that alcohol did, in-deed, correspond to the pharmaceutical profile he had set up for narcotism. It obeyedthe inverse ratio rule of blood solubility. He also extended his analysis by confirm-ing that its clinical effects corresponded to his model of degrees. This was not easyto do because the effects of alcohol last so much longer than those of chloroform orether. He concluded that “ordinary drunkenness does not exceed the second degree

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of narcotism; the popular term of dead drunk being often applied to a state of sleepfrom which an individual is still capable of being roused to a state of incoherent con-sciousness.” He calculated the blood-alcohol level for this condition (fifteen ouncesof proof spirit) and asserted that less than twice this amount taken all at once on anempty stomach ought “to prove fatal” (ON, 13: 625). The result corresponded wellwith common experience and his established degrees of narcotism (and today’sblood-alcohol standards). Snow concluded that the “amount of anesthesia from al-cohol is apparently as great, in proportion to the narcotism, of the nervous centresattending it, as from chloroform and ether,” but it does not yield enough vapor atroom temperature to cause insensibility in a reasonable amount of time (ON, 13:626). Were it a more practical anesthetic, the teetotaler Snow mused, alcohol wouldbe in public opinion “as praiseworthy as it is disgraceful when resorted to for thepurpose of supposed enjoyment, or to satisfy a craving which has resulted from apernicious habit” (ON, 13: 626). Alcohol, a substance he had opposed his entire adultlife, was actually a cousin to ether and chloroform, substances he championed andsources of his livelihood.

Snow concluded that alcohol was a narcotic, for which Liebig had supplied a thickdescription of its physiological action. According to Snow, Liebig argued that obser-vation had led him to conclude that “neither the expired air, nor the pers-piration, nor the urine, contains any trace of alcohol after indulgence in spiritousliquors . . . ; that the elements of alcohol combine with oxygen in the body, andthat its carbon and hydrogen are given off as carbonic acid and water; that the ele-ments of alcohol appropriate the oxygen of the arterial blood, which would other-wise have combined with the matter of the tissues, or with that formed by the meta-morphosis of the tissues: and that thus the change of the tissues . . . are diminished”(ON, 13: 626). Snow believed this description was largely incorrect and, as any Breath-alyzer will reveal, he was right, and Liebig was wrong. Whereas Snow concurred thatalcohol and other narcotic vapors diminish or suspend “molecular change” (Liebig’scatchall for chemical and biochemical interactions) of the affected tissues, it was notthe result of “appropriating the oxygen in the blood” (ON, 13: 626–27). While oxy-gen may combine with hydrocarbons in fat, starch, sugar, and gum, yielding carbondioxide and water, none of these substances were in any degree narcotic. Second, theamount of carbon and hydrogen present in enough chloroform to render someonecompletely insensible was “totally insignificant” compared to the amount of oxygenabsorbed in the lungs (ON, 13: 627). Alcohol has a very similar action to chloroformand therefore could not, as Liebig argues, appropriate very much oxygen in the blood-stream. Third, if alcohol did indeed create its narcotic effect by appropriating oxygen,then supplying more oxygen should prevent or diminish the narcotic effect, but thiswas not the case. Snow had observed patients in states of complete insensibility whoseskin turned “bright vermillion” with excess oxygen coursing through their arteries.

Through the summer of 1850 Snow demonstrated how to detect the presence ofchloroform, ether, and alcohol excreted in the breath. Consulting with Dr. Alfred


Taylor of Guy’s Hospital, he refined a test for the presence of chloroform in the bloodin the Journal de Chemie Medicale (March 1849). By inhaling chloroform and breath-ing into a heated tube lined with silver nitrate, Snow obtained precipitates of silverchloride crystals that corresponded to the amount of chloroform taken. He showedhow this method could detect chlorine in urine and tissue samples as well. Snow wascareful to qualify his analysis, reminding his readers that the process did not “provethe presence of chloroform itself, but only that of a volatile [at the heat of boilingwater] compound containing chlorine” (ON, 14: 326).41 This meant that only thecompounds in the family he had been studying were likely candidates, of which onlychloroform was commonly used.

Snow devised a parallel series of experiments to detect traces of ether and alco-hol in the breath. He had smelled ether on the breath of patients in the same wayone smells alcohol on the breath, but, as with chloroform, he sought quantitativechemical confirmation. In both cases he took the drugs himself, trapped his respi-ration in a balloon, and was able to rectify pure ether and alcohol from the breath.Braving the perils of intoxication in the name of science, the temperance advocatemanfully took his measured dose of spirits with bread and butter, became mildly in-toxicated, and breathed into a spiral tube connected to a small bath of sulfuric acid.Trapping the alcohol vapor in the acid, he developed a process of heating the mix-ture to obtain alcohol in a pure state (ON, 15: 751–53).

This was classic Snow. The implications of his research spun off, like a serial novel,in social and medical directions. He wished to demonstrate that Liebig was wrongabout alcohol. He had also devised tests for detecting both alcohol and ether thatwere more conclusive than was the test he devised for chloroform, yet he began thediscussion with chloroform because it had become the baseline for all his researchon narcotism. He was also highly sensitive to the social uproar surrounding chloro-form in 1850. Snow’s test would be very useful in forensic investigations in whichchloroform was suspected. There was no pressing social need to detect alcohol orether on the breath, so he did not bother to develop a socially useful test for them.He continued to investigate alcohol and ether in order to solidify his claim of thefamily relations of narcotic agents, to further his physiological theory, and to proveLiebig wrong.

The detection of chloroform, ether, and alcohol yielded a key physiological insightrather than the modus operandi of narcotism per se. “I have assumed from the first,”he explained, “that the speedy subsidence of chloroform and ether, in comparisonwith that from alcohol and other narcotics, depends on the volatility of the formersubstances, which allows of their ready exit by the expired air. Indeed, the effects ofthese medicines usually subside in the period which a calculation founded on thisview would assign to them” (ON, 15: 753). Snow preferred the term degrees of nar-cotism to stages because degrees suggested the passage of time on the face of a clock.The duration of the effects of narcotism were determined by solubility and volatil-ity: how much of the narcotic gas was absorbed by the blood, how fast the blood

Chloroform 159

circulated, and, once the narcotic gas was left off, how quickly the air removed thegas from the blood. With their quicker circulation and respiration, children went un-der and came out more quickly than did the slow-breathing elderly. He suggestedthat diffusion of the agent to smaller vessels and tissues could play an ancillary rolein “allowing the brain to resume its functions” (ON, 15: 753). Ether was more volatilethan was chloroform but much more soluble, so the quantity absorbed by the bloodwas much greater. Greater solubility compensated for the lesser volatility, Snow rea-soned, and therefore ether wore off more slowly than did chloroform. It followedthat alcohol, with even greater solubility and less volatility than ether, lasted evenlonger.

It also followed that one could prolong the effects of a narcotic by recirculatingthe expired breath. Snow devised an autoexperiment, based on an attempt to relievethe sufferings of a cholera victim in 1849, in which he first filled a balloon with pureoxygen. Using a glass condensing coil, he connected the balloon to his ether inhaler,which was filled with a “solution of potassa” (potassium monoxide) and attachedthis setup to a valveless mouthpiece.42 After inhaling as much chloroform as possi-ble without passing out, he breathed and rebreathed from the balloon–inhaler de-vice; the oxygen he inhaled became mixed with the air already present in the inhaler,while the potassium solution absorbed his CO2. He reported that the narcotism,which ordinarily would have passed off in three to four minutes, lasted a full tenminutes, with feelings persisting for approximately thirty minutes afterwards. Itworked for ether as well (ON, 15: 754). The potassium solution permitted him toquantify the amount of CO2 produced while he was under the influence of narcoticgasses.43

Oxidation–Asphyxia Theory

In April 1851 Snow presented a theory that explained how narcotic vapors worked.It was based on two fundamental observations: The inhalation of narcotic gases re-duces “the amount of carbonic acid formed in the system,” and “chloroform andether are exhaled unchanged from the blood” (ON, 16: 626). These agents, definedas “the volatile narcotic substances not containing nitrogen, or those subsances whosepower was found to be in the inverse ratio of their solubility in water and the serumof the blood,” have “the effect of limiting those combinations between the oxygen ofthe arterial blood and the tissues of the body which are essential to sensation, voli-tion, and, in short, all the animal functions” (ON, 16: 626). They “modify, and inlarger quantities arrest, the animal functions, in the same way, and by the same power,that they modify and arrest combustion, the slow oxidation of phosphorous, andother kinds of oxidation unconnected with the living body” (ON, 16: 626). He ar-ticulated his theory of narcotism in the form of twelve propositions. The first wasan assumption that the life force is a variation of basic laws of physics: “Sensation,


motion, thought, and indeed all the strictly animal functions, are as closely con-nected with certain processes of oxidation going on in the body, as the light and heatof flame are connected with the oxidation of the burning materials” (ON, 16: 626).

Propositions two through six summarized the clinical and experimental findingsdetailed in earlier installments. The seventh was a conclusion drawn from his long-standing research into respiration: “The different parts of the nervous system losetheir power under the influence of the narcotics we are considering, in the same or-der as in asphyxia—the privation of oxygen, as was observed by M. Flourens withrespect to ether, in 1847” (ON, 16: 627). The last five propositions summarized ear-lier comments on the effects of narcotic vapors on muscular irritability, ordinarycombustion and oxidation, and putrefaction, as well as the narcotic parallel pro-duced by a reduction in body temperature.

In Snow’s theory narcotic gases were an unusual kind of antioxidant that sloweddown the body’s oxidizing processes without combining with the blood’s oxygen. Inother words, the narcotized body behaved as if it were being asphyxiated; the bodycould not make use of the oxygen present. Asphyxia and narcotism enjoyed a par-allel relationship with respect to the molecular action of oxygen: “The relation be-tween asphyxia and narcotism is this—that in asphyxia there is an absence of oxy-gen, whilst in narcotism the oxygen is present, but is prevented from acting by theinfluence of the narcotic” (ON, 17: 1053). In both conditions body temperaturedropped, nervous centers lost power in the same sequence, and the heart continuedto beat after breathing had stopped. When robust athletic individuals were narco-tized or asphyxiated suddenly, convulsions or rigidity frequently occurred. When ei-ther occurred gradually, convulsions tended not to take place. Both states were ac-companied by delirium and languor. He noted that acute bronchitis, in which thepatient could not breathe, often produced delirium, strange visions, and dreams. Hespeculated that the languid movement of the fetus in utero was due to the reducedlevel of oxygen available via the placenta. And, as Snow had long known from hisefforts to resuscitate guinea pigs, muscular irritability was reduced by asphyxia andsuspended by narcotics.

In the final part of ON, he suggested that the antiseptic power of chloroform,ether, and alcohol could result from their antioxidant properties. In those pre–germtheory days, Snow reasoned that preventing oxidation functioned to prevent, or atleast inhibit, putrefaction. Essential oils, like lemon and peppermint oil, that pos-sessed narcotic properties might be used to preserve meat. A dead rabbit that he in-jected with lemon oil “kept very well for seventeen days” (ON, 18: 1091). Oxidationwas the key for Snow, and he considered biochemical oxidation similar to what tookplace outside the body. According to Richardson, Snow believed he “could illustrateall the meaning of this great practical discovery of narcotism on a farthing candle”by showing the flame subdued but glowing under the influence of chloroform.44 InSnow’s metaphor, narcotic vapors did not only inhibit combustion (oxidation) of acandle flame, they inhibited the oxidation of bodily tissues. It was an analogy born

Chloroform 161

of experience and theory. In his 1841 paper “On asphyxia and the resuscitation ofstill-born children” he had compared respiration with combustion and the lungs toa furnace: “The whole body ought to be compared to the furnace, and the lungs tothe draught and chimney department—a view which better explains the uniformdiffusion of warmth throughout the body.”45 Respiration was combustion fueled byoxygen, whereas asphyxia was deoxygenation of the blood. Years before he everlearned of the properties of ether or chloroform, he had formulated the basics of ox-idation and asphyxia that would inform the physiological model in his theory of nar-cotism. He had witnessed, time and again, the incandescence of respiration underchloroform. He had seen his patients’ breathing grow stertorous and sputter. He hadseen their skin glow red with unignited oxygen. Small wonder that most of the agentshe experimented with were potential fuels or coolants. Keeping someone under dur-ing anesthesia was like knowing how to stoke a fire or run a combustion engine.

Chemical Affinity/A Balance of Forces

After four years of research, Snow had found the handle to a complex process, buta fundamental question remained unsolved. “Having traced the narcotic action ofether and other bodies to the more general law of their power of preventing oxida-tion under a great variety of circumstances,” his “mind naturally inquire[d] by whatkind of power oxidation is thus prevented” (ON, 18: 1092). His hypothesis, offeredwith “considerable diffidence,” was that

chemical attraction or affinity is a constantly acting force, by which each atomof matter exerts an influence on all other atoms within the sphere of its attrac-tion, . . . varying with the respective nature of the substances, and the physicalconditions in which they are placed. In this point of view, it will be seen that anytwo substances in a condition to unite together might be prevented from doingso by the intervention of a third body possessing a sufficient attraction for ei-ther of the others; and it would not be necessary that this third body should en-ter into chemical combination; for a balance of forces might be established, sothat the three substances would remain exerting reciprocal attractions for eachother, but unable to enter into more intimate union.

ON, 18: 1092

Snow reasoned that narcotic gases entered into the bloodstream and attracted theoxygen with a force insufficient to bond with it. Even so, the force was strong enoughto counter the attraction between oxygen and “certain constituents of the blood andtissues of the organs,” thereby inhibiting or preventing (depending on the dosage)“those changes which are, in a manner, the essence of all the animal functions” (ON,18: 1093). Although this hypothesis did not pan out, Snow proposed that chemicalaffinity explained the stalemate he considered characteristic of narcotism: oxygen,


chloroform (or any other narcotic gas), and the materials of the body were coursingthrough the bloodstream in a state of suspended molecular animation. He consid-ered it possible that counteraffinity was a form of molecular anesthesia in which theforces that explain normal oxygenation were neutralized.

He was pushing his theory of narcotism into a speculative realm well beyond whatanyone at the time could demonstrate in the laboratory. The Medical Society of Lon-don (successor to the Westminster) would select him as their orator for 1853. Theaddress he delivered, entitled On Continuous Molecular Changes, contained a grandtheory of biochemistry that included speculations on the basic mechanisms of nar-cotic vapors and the nature of epidemic diseases, chiefly cholera. Since the fall of1848, an understanding of that dreaded disease and how to prevent its communica-tion had rivaled inhalation anesthesia as major medical concerns in London.

Notes

1. Simpson’s announcement took place at a meeting on 10 November 1847; LMG 40 (19November 1847): 906 contained a brief notice, but Snow already knew about it. During a mas-tectomy at St. George’s Hospital on November 18, “The chloroform was administered by Dr.Snow with his ether apparatus”; “Operations without Pain,” Lancet 2 (1847): 661. For Snow’sremarks at the Westminster Medical Society on 20 November 1847, see LMG 40 (1847):1030–31; and Lancet 2 (1847): 575–76.

2. Snow, “On narcotism by the inhalation of vapours,” 4: 334. Citations to the original se-ries in LMG are placed parenthetically in the text as ON, indicating part number and pages.

2a. Lancet 2 (1847): 575. Subsequent quotations from this meeting taken from Ibid., 575–76.3. PharJ 6 (1847): 357. Snow contributed a version of his ether saturation table to this is-

sue and made mention of Bell’s experimentation in OC, 20.4. R. M. Glover, “On the properties of bromide and chloride of olefiant gas of bromoform,

chloroform, iodoform,” Edinburgh Medical and Surgical Journal 58 (1842). The essay was ex-cerpted in PharJ 7 (1848): 348–49. For Snow’s citation, see OC, 112.

5. Richardson, L, xxxv.6. For support of Snow’s observation, see Duncum, Inhalation Anesthesia, 178–81; Davi-

son, Evolution of Anesthesia, 137.7. Potter, “Late fatal case at Newcastle,” Lancet 1 (1848): 214.8. Although this detail does not appear in the inquest, it does appear in Snow’s definitive

account; see OC, 124.9. This account is drawn from several sources: “Fatal application of chloroform,” Lancet 1

(1848): 161–62; J. Y. Simpson, “Remarks on the alleged case of death from the action of chlo-roform,” Lancet 1 (1848): 175–76; “Fatal case of inhalation of chloroform,” LMG 41 (1848):255. Snow, “Fatal chloroform case at Newcastle”(1848); “Remarks on the fatal case of inhala-tion of chloroform (1848); and OC, 124.

10. “Fatal application of chloroform,” Lancet 1 (1848): 161–62.11. “Royal Institution,” and “Experiment with chloroform at the Royal Institution,” Lancet

1 (1848): 162–63. Quotation from 163.12. Times (3 February 1848) reprinted the report from the inquest.13. “Medical news—another death from chloroform,” Lancet 1 (1848): 218–19. See also

“Fatal effects of chloroform,” Times (14 February 1848), 6.13a. “Chloroform—its benefits and its dangers,” Lancet 1 (1848): 190.

Chloroform 163

14. “Remarks on the alleged case of death from the action of chloroform,” Lancet 1 (12February 1848): 176.

15. Ibid., 175–76.16. “The alleged death from chloroform at Newcastle,” Lancet 1 (1848): 240.17. “The Fatal Chloroform Case at Newcastle,” Lancet 1 (1848): 296.18. Snow, “Fatal chloroform case at Newcastle” (1848).19. Snow, “Remarks on the fatal case of inhalation of chloroform” (1848), 277. See also

“Westminster Medical Society,” Lancet 1 (1848): 312.20. Ibid., 277–78.21. Snow, “On the discussion respecting chloroform in the Académie de Médecine of Paris”

(1849), 324. See also Snow, ON, 6: 614–19.22. For example, see OC, 120–27.23. Snow, “On the inhalation of chloroform and ether, with description of an apparatus”

(1848), 178.24. Ibid.25. For a longer summary and interpetation, see Ellis, introduction to reprint of ON.26. Richardson, L, xxviii.27. Duncum, Inhalation Anesthesia, 208.28. Nitric ether was apparently difficult to obtain and required 1.5 drachms (5.3 ml) to

reach the second degree, whereas chloroform required only .71 ml to reach the same state.Snow was quick to suggest that the anesthetic power of nitric ether was not unique: “I do notlook on [it] as a peculiarity of nitric ether, for I have met with it occasionally from chloro-form and sulphuric ether when the vapour was introduced slowly” (ON, 3: 1076).

29. For accounts of the case, see “Police—Higgins, Margaret, and another, for stealing,”Times (25 January 1850); Times (1 February 1850); and “Criminal trials—Higgins, Margaret,and another, for robbery,” Times (9 February 1850).

30. “Police—Jopling, Chas., for attempted rape,” Times (1 May 1850).31. “New crime, rape on young girls under chloroform,” Times (5 November 1847).32. “Chloroform, use of, by thieves,” Times (5 October 1849).33. Snow, “A letter to Lord Campbell” (1851), 13.34. Quoted in Ibid., 14.35. Ibid., 4.36. Ibid., 14–15.37. “The use of chloroform for criminal purposes,” PharJ 10 (1851): 488–89.38. “Parliamentary proceedings—Prevention of Offences Bill,” Times (15 March 1851).39. Shephard, JS, 136.40. Snow included the other two agents from his table in this series of experiments, py-

roxilic spirit (methyl, or wood, alcohol) and acetone, but his main focus was on ethyl alcohol(ON, 13).

41. See also the description in A. Taylor, Medical Jurisprudence, 320.42. ON, 15: 753–54. In a footnote Snow wrote, “I used the same arrangement in giving

oxygen gas last year, at the request of Dr. Wilson, to a cholera patient in St.George’s Hospital.The patient, who was in a state of collapse, was not saved or relieved by it.”

43. In 1851, using an apparatus devised by Regnault and Reiset described in the Annalesde Chemie et de Physique (1849), he confirmed his findings from autoexperiments on chlo-roform, ether, and alcohol with extensive animal experimentation; ON, 16: 622–26.

44. Richardson, L, xvii.45. Snow, “On asphyxia and the resuscitation of still-born children,”(1841), 223–24.


AS LATE SUMMER TURNED TO AUTUMN in the year 1848,Snow occupied himself with narcotism research and his growing

anesthesia practice. No other British physician or scientist was engaged in the proj-ect he had undertaken: to study ether and chloroform as members of a family ofvolatile narcotic agents related by common chemical and physical properties and todetermine the physiological mechanisms by which members of the family exertedtheir effects. In addition, following the initial reports from Flourens’s laboratory, nowork on the basic physiology of anesthesia was underway in France. Occasional reports of deaths under chloroform continued to appear in the medical liter-ature. These deaths demanded Snow’s analysis because, as an advocate of inhalationanesthesia, he needed to determine whether they were due to the chloroform itselfor (as he had stated on many occasions) defects in the apparatus and improper administration.

In October 1848, however, articles advocating chloroform as a treatment forcholera began appearing in the medical journals. Henry Clutterbuck, former presi-dent of the Westminster Medical Society and Snow’s superior at the Aldersgate StreetSchool, endorsed such treatment at a meeting of the Medical Society of London. Avisiting physician to a poorhouse, he had observed the resident surgeon includingchloroform in a new method of treating cholera victims. The treatment involvedputting the patient to bed wrapped in warm blankets, followed by “a glass of brandy

165

Chapter 7

Cholera Theories:Controversy and

Confusion

in hot water, with sugar, and spice”; briskly rubbing the body and applying a heat-ing liniment; and placing “the patient under the influence of chloroform by inhala-tion” for as long as “the bad symptoms recur.” Discussion of this procedure, as wellas other ways of administering inhaled chloroform for cholera, continued at theweekly meetings of the Medical Society of London into December.1 Snow was not amember of this society, but he could have read summaries of the meetings in thejournals he regularly consulted. These journals also carried articles and letters in No-vember and December 1848 from medical men who had found that chloroformworked best when given internally or who preferred other anesthetic agents as treat-ments for cholera.2

Epidemic cholera, after dying away in England in 1832, soon after Snow had at-tended to the Killingworth miners, had been mercifully absent for sixteen years. Itreturned to England in the summer of 1848, with the first cases appearing in Lon-don in October. In the interim no consensus had been reached about efficacioustherapeutics. Virtually every known treatment had been tried during the first epi-demic. The three medical corporations had not agreed on what to recommend, andguidance received from the Board of Health was too inclusive to be useful. The rangeof disagreement was even broader in 1848, because anesthetics could be added tothe mix,3 and the situation remained unchanged when the third major epidemiccame to England in the mid-1850s.

Just as no consensus existed about how to cure cholera, there were continuing dis-agreements about its pathology and cause; between 1845 and 1856 some 700 workson cholera were published in London alone.4 The Medical Times noted in an edito-rial at the end of 1847, “It must be acknowledged that scientific investigations havedone but little in advancing sound knowledge upon some most important pointsconnected with the disease.”5 Six years later, at the onset of the third epidemic, aneditorial in the Lancet emphasized continuing uncertainties: “The question, What ischolera? is left unsolved. Concerning this, the fundamental point, all is darkness andconfusion, vague theory, and a vain speculation. Is it a fungus, an insect, a miasm,an electrical disturbance, a deficiency of ozone, a morbid offscouring from the in-testinal canal? We know nothing; we are at sea, in a whirlpool of conjecture.”6 Con-troversy was endemic in the midst of so much confusion.7 But the disputants hadcoalesced into several camps depending on whether they believed the “exciting cause”was a contagious “virus” generated in the bodies of the sick, a noncontagious atmo-spheric principle, or some amalgam of the two.

Pure contagionist opinion was dominant early in the 1831–1832 epidemic but lostground to modified versions and noncontagion by the second and third epidemics.To acquire cholera the purely contagionist perspective required contact either witha sick person’s body or with the fomites from infected bedding and clothing; small-pox was often cited as a model. A third variation of contagion, the idea of infection,became increasingly prevalent among medical men in the 1840s: according to thisnotion, the bodies of cholera victims produced an infectious “virus” that, in vola-


tized form, emanated into the immediate atmosphere and was inhaled by the healthy.A few contagionists believed that a person must swallow the cholera matter or itsgerms.8

Adherents of pure noncontagiousness believed that epidemic cholera was betterexplained by Sydenham’s theory of the epidemic constitution, in which general atmo-spheric changes occasioned by seasonal fluctuations produced diseases in suscepti-ble individuals.9 Each disease was associated with a particular seasonal–atmosphericcondition, but only people with physiological predispositions unfavorable to the con-dition actually became ill. Once cholera had spread westward from the Indian sub-continent during the first pandemic, climatologists thereafter looked for patterns intemperature, humidity, barometric pressure, wind, and so on that would permit pre-diction about the extent and duration of the next one. However, some critics of atmo-spheric causation believed the evidence about cholera transmission pointed to localcircumstances, in which “a poison formed by the decomposition of organic matter[miasma] . . . , when applied to the human body, produces the phenomenon con-stituting fever.”10 For some local miasmatists what appeared to be distinct diseaseswere variations of one pathological state, fever. Others believed in specific diseasesassociated with particular conditions, so that ague was common near malarialmarshes, whereas cholera was prevalent in areas of concentrated animal putrefac-tion. Most miasmatists (whether general or local) believed that the primary cause ofepidemic disease was inhaling poisons generated by a chemical reaction during pu-trefaction; this view was so pervasive that the name epidemic was often associatedwith it.

Some local miasmatists, however, grudgingly acknowledged that person-to-per-son transmission of cholera by infection did occur in rare circumstances of unusualovercrowding and filth. That is, particular environmental “contingencies” could pre-dispose people to become ill.11 This contingent contagion perspective offered a con-genial middle ground for miasmatists who considered individual predisposition anoutmoded explanation, and for contagionists who could not find evidence ofcholera’s progress in every local outbreak. Unsanitary environments could transforma normally noncontagious disease into a contagious one, or vice versa. By the mid-1840s local miasmatists, infection contagionists, and contingent contagionists in-creasingly downplayed theoretical disputes in order to unite behind practical sani-tary reform measures directed at eliminating nests of cholera fever. Snow appears tohave been an interested listener rather than an active participant in professional de-bates about the nature of cholera during this period.

The Horror from the East

Concern about epidemic cholera began appearing in the London medical press in1817, when British physicians in India reported that an endemic native disease was

Cholera Theories: Controversy and Confusion 167

spreading widely and with great virulence.12 The symptoms of this disease were strik-ing. In the first, or premonitory, stage the sufferer might experience nothing but avague unease and perhaps a mild diarrhea, as if having eaten spoiled food. The sec-ond stage was characterized by vomiting, muscular spasms, and pains in the lowerchest and upper abdomen, accompanied by a profuse diarrhea. The diarrhea, widelyaccepted as the signature symptom of the disease, was of a peculiar type—there wasvirtually no fecal color or smell to the stool, which instead appeared watery withsmall white particles suspended in it. Because it looked like water in which rice hadbeen boiled, it was dubbed “rice-water stool” and considered a hallmark indicationof second-stage cholera.13 The third stage was one of profound collapse. Victims re-tained mental function until near the end, but the body became cold, a pulse couldscarcely be felt, and the face and extremities often turned dusky.14 Blue, corrugatedskin made even young patients seem aged (Fig. 7.1).15

The conceptual and therapeutic confusion regarding cholera was reflected in itsname. Searching about for something to call this epidemic disease, surgeons andphysicians with the East India Company chose cholera, a name already in use forquite a different condition. “Cholera,” or “cholera morbus,” was well known in En-gland as an endemic diarrheal disease most common during the summer months.It got its name from the yellow–brown color of the diarrhea and vomit, suggestingthat it was caused by an excess of “choler” (the humor yellow bile).16 Relatively few


Figure 7.1. “Blue Stage of the Spasmodic Cholera,” showing blue coloration of face, neck,

hands, and feet as well as the abnormally aged appearance of cholera victims (Lancet 1

[1831–32]: between 538 and 539).

died of English cholera, and those that did tended to be infants or the debilitated.By contrast, the disease spreading out of India was marked by an absence of yellowbile and often struck those in the prime of life with a mortality rate of up to fiftypercent.17

To avoid confusing this emerging epidemic disease with English cholera, authorsoften added a qualifying term such as malignant, Asiatica, or Indica (Table 7.1),but the profusion of terms impeded medical and popular understanding of thenew disease.18 The language dispute suggests some of the conceptual issues—a per-son who elected to use the term spasmodic cholera probably favored a view of thedisease as essentially involving the nervous system, for example. A disease that couldseize a British soldier in perfect health, reduce him six hours later to a whimper-ing infant unable to control the discharge from his bowels, and lay him out a corpsesix hours after that inspired horror even in supposedly objective medical ob-servers.19 One account from an official Indian report seemed to depict cholera asa man-eating tiger: “It was [in an army camp near the banks of the Sinde inBundlekund] that the disease put forth all its strength, and assumed its most deadlyand appalling form. . . . After creeping about . . . in its wonted insidious man-ner, for several days among the lower classes of camp followers; it, as it were in aninstant, gained fresh vigor, and at once burst forth with irresistible violence in everydirection.”20

British medical practitioners became more anxious over the next fourteen yearsas the tiger progressed westward. In 1821 the disease spread northwest from Indiainto Persia and the Middle East, eventually reaching the city of Astrakhan on theCaspian Sea in 1823. It then died out but retraced these same steps in 1829–1830,this time continuing northward through Russia. It had spread westward to the Balticports in the spring of 1831 and from there hopped to Sunderland, a British port justsouth of Newcastle, that fall before petering out by the turn of the year.21 It reap-peared the following summer, spread north to Edinburgh and south to London. New-castle was hard hit once again, including outlying mining villages like Killingworth,where Snow was sent to treat its victims.


Table 7.1. Alternative terms forcholera morbus, 1831–1855a

Algideb IndianAsiatic MalignantAsphyxial PestilentialEpidemic Spasmodic

a Only one term is shown when theterm was often used in either an En-glish or a Latin variant, e.g., “Asiaticcholera” and “cholera Asiatica.”b From Latin algor, “cold.”

With cholera on their very doorstep, British physicians felt called upon to take de-cisive action—but what should one do? It was difficult to make any sense of the ac-cumulating literature. Regarding the spread of cholera, for example, E. O. Spoonerstated that from 1817 cholera had followed well-established trade and travel routes,always attacking a port city, for example, before spreading inland and never movingfrom one location to another faster than human beings traveled,22 but G. H. Bell of-fered contrary evidence that the disease usually moved about in ways totally un-connected to human trade and travel.23

Social Upheaval and Sanitary Reform

Cholera arrived in England at a time of social upheaval as well as medical contro-versy. The first epidemic struck shortly after the opening of the first steam-poweredpublic railway in 1830. Manufacturing interests began to flex their political muscleswhile many workers, especially in the new industrial towns, lived in horribly crowded,unsanitary, and dangerous housing. The Reform Bill of 1832 shifted the power struc-ture within Parliament by expanding the franchise to include small property own-ers, but radical democrats considered these measures incomplete because the work-ing classes were still excluded. Unemployment, poverty, hunger, and unmetexpectations spawned the Chartist Movement, riots, and unrest of the mid-1830’s.

Cholera seemingly took advantage of the new conditions of industrialized En-gland—entering through the seaports, traveling inland along the new highways andrailroads, and attacking first the most densely populated and unsanitary abodes ofthe desperately poor. To many contemporaries epidemic cholera was just anothersymptom of the social unrest and upheavals that plagued Great Britain. Radical de-mocrats among medical men, such as the physician James Phillips Kay-Shuttleworth,thought the epidemic was an opportunity to “follow the footsteps of this messengerof death” into “the abodes of poverty . . . the close alleys, the crowded courts, theoverpeopled habitations of wretchedness, where pauperism and disease congregateround the source of social discontent and political disorder in the centre of our largetowns, and behold with alarm, in the hot-bed of pestilence, ills that fester in secret,at the very heart of society.”24 Radical reform meant the expansion of liberal valuesto the entire population. Everyone should share the new wealth generated by indus-trial and commercial capitalism. Epidemics were just proof of this for medical rad-icals: Eliminate the environmental conditions that permit these diseases to “fester .. . at the very heart of society,” or they will soon spread to the middling and upperclasses. Just as an expansion of the franchise was fair in a democratic society, med-ical radicals argued that good public policy required the state to undertake positive(in the sense of legislative) sanitary measures. Yet another divide had emerged in themedical profession; many medical men believed reform was uncalled for or too incendiary.


Not everyone shared Kay-Shuttleworth’s view that disease and social conditionswere intimately connected. Edwin Chadwick, a barrister who had been secretary tothe utilitarian philosopher Jeremy Bentham, was instrumental in designing the NewPoor Law of 1834. His initial goal was efficiency, seeking both to centralize the re-sponse to poverty and to create systems that discouraged pauperism and reduced total state expenditures. The previous system had focused on “out-door relief”—assistance provided to the poor mostly in their own homes—and was administeredby 15,000 individual parishes. The New Poor Law shifted some responsibilities toBoards of Guardians of about 600 unions, thereby creating another administrativelevel of geographical units with the financial base to construct and maintain largeworkhouses. Workhouses were supposed to provide “in-door relief” for paupers only;“least eligibility” requirements were restrictive by design and conditions within theworkhouses repellent to encourage the population to seek gainful employment ratherthan welfare. The New Poor Law was an example of the intent of liberal social en-gineering. Benthamites believed that effective government should actively promotethe work ethic necessary for capitalism to function and promote the wealth of na-tions. In addition to deciding who was eligible for admission, Boards of Guardiansappointed surgeons to attend sick inmates in the infirmaries attached to the work-houses; managed paving, sewer construction, and local water pumps; and supervisedall sanitary and medical measures undertaken during epidemics.

Only after the new system began to operate did Chadwick realize that the incen-tives were not working as he had planned and that many of the poor became pau-pers not because they were lazy, but because they were often too sick to be employ-able. With workhouses choked by the sick poor, the infirmaries turned out to be themost rapidly expanding and expensive part of the entire system.25 By 1837 Chad-wick shifted direction and began to focus more on the goal of preventing disease asa means to reduce the burden of poverty on the nation. He sought the help of med-ical advisers, most notably Thomas Southwood Smith, another close associate of Ben-tham’s.26 In the Benthamite spirit they believed a compilation of statistics on a na-tional scale would illuminate the precise relationship between poverty and illness,after which Parliament could design sound public policy. A General Register Officewas formed in 1837, and the Report on the Sanitary Condition of the Labouring Pop-ulation followed in 1842, based in part on the reports submitted by the New PoorLaw medical officers.27 A Royal Commission on the Health of Towns was establishedin 1843, and various items of sanitary reform legislation followed.28

Chadwick’s and Southwood Smith’s efforts culminated in the Public Health Act of 1848, the year the second great cholera epidemic reached England. A three-member General Board of Health was created as a strong central authority. MedicalOfficers of Health were appointed to oversee local sanitary conditions in each dis-trict, regulate offensive trades such as slaughterhouses and tanneries, condemnhouses unfit for human habitation, and supervise burial grounds, sewers, water sup-plies, and waste disposal. In short, this new medical arm of the state was given


primary responsibility for ensuring a healthy population and a productive workforce.By 1853 103 towns had come under the Public Health Act.29

Champions of local control, however, mounted considerable opposition to the na-tional sanitary policy advocated by Chadwick and his allies. According to Baldwinthe Benthamite version of sanitary reform was “a totalizing worldview resting on cer-tain presuppositions concerning the balance of nature and the role of illness and dis-ease in the divine harmony of the universe. . . . Sanitationism was a remarkablyconsistent and unified vision that combined social reform and public hygiene in aseamless whole. All epidemic diseases were to be prevented, or at least ameliorated,in one fell swoop while at the same time social problems were addressed. . . . Hous-ing reform and disease prevention, for example, went hand in hand, part and par-cel of the same grand vision of a society that through its concern with public healthalso improved the lives of its poorest.”30 Baldwin has contrasted sanitarianism withthe “quarantinist” posture, which was narrowly concerned with preventing the spreadof disease. Advocates of quarantine saw no link between preventing disease and bet-tering the lives of the potential disease sufferers.31 Comprehensive sanitarianism, onthe other hand, was a central plank in the radical reform agenda and suited the me-liorist attitudes of those in the middle and upper classes, both moderate Whigs andTory Democrats, whose social conscience was piqued by altruism, worry about epi-demic diseases, or fear of social revolution.

Sanitary Reform and Anticontagion

As disciples of Bentham, the sanitarians embraced the most up-to-date methods ofstatistical analysis, which they believed would identify the environmental sourcesconsidered predispositions to constitutional or epidemic diseases. The common viewamong sanitarians was that epidemics were caused by inhalation of agents in theatmosphere. Once inhaled, the causative agent acted upon the blood to disrupt thebody’s internal balance, resulting in fever and other symptoms of each epidemic disease.

The lineage of atmospheric causation was ancient, with origins in the Hippocraticcorpus that was updated in England by Thomas Sydenham. He attributed the “ex-citing cause” of each epidemic disease to particular atmospheric conditions affect-ing large areas. The required elements for disease were peculiar vagaries of climateand season—the “epidemic constitutions.” Whether one became depended ill on thesituation of one’s “internal constitution.” People in whom seasonal changes producedsignificant humoral imbalances were particularly susceptible to epidemic diseases;those whose humors remained in balance were not normally afflicted. No person-to-person transmission was invoked. Sydenham’s followers retained the notion of“epidemic constitution” but replaced the humoral framework with chemical imbal-ances. For example, a correspondent to the Lancet in 1837 compared influenza and


cholera: “both are of an epidemic nature, arising, passing over the face of the earth,and disappearing, in a mysterious manner. Both seem to be influenced by the sea-son of the year, or by the state of the atmosphere as regards heat and moisture. Thecourse of both is, mostly, from east to west. . . .”32 John Snow himself seemed toemploy this line of thinking in 1842, when he commented to the Westminster Med-ical Society about an outbreak of influenza he had seen during his first year as anassistant: “The epidemic in April, 1833, occurred immediately after a continuance ofcold wet weather had been succeeded by that which was warm and dry; and the epi-demic in the winter of 1837 took place after a frost had yielded to weather consid-erably warmer.”33 By Snow’s day, however, the appearance of Asiatic cholera hadsharpened disagreements about the causes of epidemic disease, and Sydenham’s the-ory had been relabeled as general anticontagionism.34

The appearance of cholera in the west also resurrected an eighteenth-century vari-ant of the theory of “epidemic constitution,” atmospheric corruption by local mias-matic sources.35 Thomas Southwood Smith, a visiting physician to the London FeverHospital, advocated this version of anticontagionism, which explained why epidemicdisease appeared in one locality while leaving nearby areas untouched. No longerwas it sufficient to state, for instance, that a spell of cold weather had been super-seded by a period of warm weather. To local anticontagionists concentrated amountsof rotting vegetable matter generated “a principal, or give origin to a new compound,”that was emitted into the surrounding atmosphere by gaslike miasmas that were poi-sonous to humans.36 Southwood Smith’s theory of local miasmas adopted Syden-ham’s assumption that disease took its character, in part, from the geography, cli-mate, and the individual histories of the people in the places where it occurred: “Thefever of one country is not the same as the fever of any other country; in the samecountry, the fever of one season is not the same as the fever of any other season; andeven the fever of the same season is not the same in any two individuals.”37 Manylocal miasmatists believed that diseases such as typhoid fever, dysentery, and cholerawere variants of one basic form of fever and that local changes in atmospheric con-ditions would determine which variant one might contract. It was also taught thatwhen a particular epidemic disease (such as influenza) was raging in an area, otherdiseases that happened to occur there (such as diarrhea) would be modified by theprevailing epidemic influence and bear the “impress” of the epidemic disease.38

Local miasmatists assumed that putrefying animal matter produced the most lethalconcentrations of poisonous agents, sometimes distinguished as effluvia. SouthwoodSmith regarded the noxious effluvia given off by fever sufferers in closely confinedspaces as “by far the most potent febrile poison.”39 He cited a case report that sug-gested how locally generated miasmas could be transformed into effluvial poisons:

The suddenness with which a fever sometimes attacks individuals on board aship, or even an entire ship’s crew, on the approach of a vessel to a shore wherethe poison is generated in large quantity, and in a high state of concentration,


illustrates its operation, perhaps, in a still more striking manner. Dr. Maculloch. . . relates an instance of some men on board a ship, who were seized, whilethe vessel was five miles from shore with fatal cholera, the very instant the land-smell first became perceptible. Several of these men, who were unavoidably em-ployed on deck, died of the disease in a few hours. The armourer of the ship,who, before he could protect himself from the noxious blast, was accidentallydelayed on deck a few minutes, to clear an obstruction in the chain cable, wasseized with the malady while in that act, and was dead in a few hours.40

Unlike the weaker miasmas, to which only predisposed individuals were susceptible,some effluvia killed everyone who inhaled them.

Like Sydenham, local miasmatists resorted to the long-standing doctrine of con-stitutional predisposition to explain why, although many people breathed the air con-taining a miasma, only some became sick. This is what Southwood Smith meantwhen he wrote, “even the fever of the same season is not the same in any two indi-viduals.” Unlike Sydenham, nineteenth-century local miasmatists generally cited personal characteristics and environmental conditions rather than humors as pre-disposing factors. For example, W. Lauder Lindsay of Edinburgh argued in the 1850s that strong emotions, especially fear, rendered one susceptible to epidemic diseases like cholera. He had “full faith in the Board of Health views on the non-contagiousness of the disease,” so he felt no fear when he attended its victims at theSurgeon’s Square Cholera Hospital in Edinburgh and did not render himself sus-ceptible.41 Immorality (specifically, overindulgence in alcohol and sex) also predis-posed people to contracting cholera, especially when the “epidemic constitution” wasmost conducive: “The probability of an outburst or increase during [calm, mild]weather, I believed to be heightened on holidays, Saturdays, Sundays, and any otheroccasions where opportunities were afforded the lower classes for dissipation anddebauchery.”42 Improper nutrition, overcrowding, and inadequate ventilation couldalso make one unusually susceptible to cholera.

The inclusion of certain environmental circumstances among the predisposingfactors for epidemic diseases allied local miasmatists with Benthamite sanitary re-formers, who believed only a governmental agency could undertake the sophisticatedstatistical analyses necessary to prevent the spread of disease in the first place (Fig.7.2). In general, the sanitarians believed that many diseases were caused by “filth.”Filth could be detected by the unaided senses, and the major way to prevent diseasein urban settings was to clean up accumulations of garbage and sewage or whateverelse produced foul odors.43 Careful statistical studies could identify where concen-trated pockets of disease existed and then trace the hoped-for decline in disease ratesas the filth was cleaned up. By this reasoning one should focus on removing fevernests within one’s own land rather than worry about threats from without. Sani-tarians and local miasmatists, therefore, opposed quarantine measures during pandemics. In an island nation that depended heavily on trade, this position won


them support among the mercantile and manufacturing classes, who wished to avoidany major impediment to the flow of ships and goods.44 Miasmatists also arguedthat their position was good public policy because it would not result in public panicor abandonment of the sick, as a belief in contagious properties of cholera might.45

The General Board of Health (GBH), established by Parliament during the sec-ond cholera epidemic and in place until 1853, was sanitarian and local miasmatic inorientation. Chaired by Chadwick, its only medical member was Southwood Smith.Its reincarnation during the third cholera epidemic of 1854–1855 maintained thisdouble orientation, albeit even more aggressively critical of contagionism than wasits predecessor.46 In retrospect, the advice given by the sanitary reform movementcould hardly fail to be helpful. In a day when one could hardly walk the streets ofthe working-class section of any English city without tripping over piles of decayinggarbage and landing in pools of human excrement, cleaning up whatever smelledbad seemed certain to improve the overall public health.47

Contagion

Although official pronouncements during the second and third cholera epidemicsleaned toward local miasmatic and sanitarian views, most government officials at the


Anticontagionist(Miasma) Theory

lungs

miasmadecomposingorganic matter

humoraldisruption

noxious effluviaexhaled

(via skin, sweat)

disease state

new cases ofdisease

IMPORTANT:humoral/

constitutionalpredisposition

atmosphericinfluences?(mild)

under certainconditions

lungs

Figure 7.2. Anticontagionist theory according to sanitarians such as Southwood Smith.

time of the 1831–1832 epidemic believed cholera was a contagious disease.48 Thecontagionist position had been little modified since propounded by Fracastorius in1546.49 In essence, contagionists viewed the causative agent of epidemic diseases asa particle, often described as a “virus”; Fracastorius’s phraseology suggested an anal-ogy to a seed.50 In the following century Athanasius Kircher (1602–1680) proposedthat animalculae (microscopic animals) might be the causative agents of infectiousdiseases,51 but like the undetectable “principal” or “compound” of the local mias-matists, the structure of the contagious particle remained unknown during Snow’slifetime, so contagionists were primarily concerned with the effects that could be at-tributed to it.

Significant subdivisions existed within the contagionist camp (Fig. 7.3), but allwere in agreement that in some diseases the bodies of sick persons produced“viruses,” or seeds, that could cause the same disease in a previously healthy person.The contagious particles could be transmitted in several ways. In smallpox, for in-stance, there was general consensus that spread could occur by simple touch. Fol-


ANTICONTAGIONISM

Disease-causing matter inatmosphere and physicalenvironment, inhaled throughlungs, enters blood and disruptsphysiological balance

Local

Anomalous factsunexplained by

theory

Miasma due toputrefaction ofvegetable oranimal material

General

Widespreadatmosphericconditions, etc.(Sydenham:epidemicconstitution)

Anomalous factsunexplained by

theory

In closelyconfined spaces,effluvia from sick

may infect thehealthy via lungs

CONTAGIONISM

Infection Fomites Touch

Virus givenoff by sick inexhalations;inhaled byhealthy

Disease-causing matter (virus)produced in bodies of sickpersons and transmitted by:

CONTINGENTCONTAGIONISM

Disease may be contagious or notdepending on factors such as:individual susceptibility,filth/poverty, diet, habits,elevation, virus dosage, weather.

Figure 7.3. Three theories of cholera transmission, 1830–1850.

lowing the development of smallpox inoculation (and later vaccination), inocula-tion directly into the body or the blood became recognized as a mode of transmis-sion under the general category of contagion. A form of indirect contact was throughfomites—articles such as clothing and bedding used by the sick that harbored theshed “virus” and preserved its capacity to transmit disease for some period of time.52

Another route was “infection,” in which healthy people inhaled the “virus” after itwas given off in the exhaled breath or from the skin pores of the sick person.53 Somemedical men distinguished infection from “true” contagion, which they limited totransmission by touch.54 James Copland, a physician colleague of Snow’s, was rep-resentative of those who believed in “the infectious nature of pestilential cholera”rather than contact contagion: “It was not caused or propagated by immediate ormediate contact—by a consistent, manifest, or palpable virus or matter; but by aneffluvium, or miasm, which, emanating from the body of the affected, and contam-inating the air more immediately surrounding the affected person, infected thehealthy who inspired the air thus contaminated. . . .” He believed that “this mor-bid effluvium or seminium of the distemper—this animal poison emanating fromthe infected—was often made manifest to the senses of smell and even of taste; itattached itself to the body and bed-clothes; . . . and reproduced the disease whenthe air respired by predisposed persons was contaminated or infected by the clothesimbued by the effluvium or poison.”55 Whether Snow accepted Copland’s notion ofan infectious effluvium is unclear. He may have, because according to the minutesfrom an 1838 meeting of the Westminster Medical Society, “Mr. Snow believed thattyphus fever was contagious, and related a case in which a servant girl was attackedwith the disease, and sent home, a distance of many miles; there had been no typhusfever in the place; the whole of her family suffered from the complaint, and severalof the members died.”56 One cannot determine from such a cryptic synopsis if hebelieved the contagion had occurred by touch, fomites, or infection.

Contingent Contagion

Occasionally the dispute between contagionists and anticontagionists could be de-cisively settled by the characteristics of the disease itself. Very few British physi-cians in the nineteenth century denied the contagiousness of smallpox. It seemedobvious to all that susceptible people coming into close contact with a smallpoxsufferer frequently contracted the disease and that smallpox cases occurred se-quentially in a manner consistent with person-to-person spread.57 Influenza, onthe other hand, was most often thought to be an exemplary miasmatic epidemic,appearing to break out within a local region with numerous cases simultaneously.After the clear-cut diseases were addressed, medical men were left with a numberof diseases, including plague, cholera, typhus, and yellow fever, for which the factswere less decisive.58


When it came to cholera, the problem was that while some outbreaks and individual cases of cholera followed anticontagionist criteria, others seemed to fitcontagion (Table 7.2). Observers in India reported that surgeons and others caringfor the sick seldom if ever contracted cholera, but reports from Russia indicated thatphysicians fell ill in substantial numbers.59 Each camp put forth explanations de-signed to cover the anomalous cases. Fomites (infected articles such as clothing)helped the contagionists to explain an outbreak of cholera in a vicinity as yet un-visited by any known cholera sufferer, while anticontagionists appealed to individ-ual predisposition to explain why some who inhaled noxious miasmas and effluvianevertheless failed to develop the disease. Autoexperiments in which researchers in-gested fluid from cholera victims without contracting cholera themselves seemed todisprove the contagionist claim that the stomach could be a portal of entry for the“virus.”60 In general, each side of the dispute was more skilled at pointing out theanomalies left unexplained by their opponents than at repairing the chinks in theirown arguments,61 but contagionist ranks suffered the greatest number of defectionsafter the 1831–32 epidemic. “As it became increasingly clear that cholera was not asdirectly contagious as the plague, as experience showed that the medical personnelin closest contact were not necessarily more afflicted than others, that its incidencevaried by class, season, region, neighborhood and person, the evidence seemed tomount that something other than a contagion was at work. . . .”62

Although theoretical purists reviled it, contingent contagionism became increas-ingly popular with the accumulation of anecdotal evidence about cholera outbreaksthat could not be explained by either of the extreme perspectives. Its initial Londonproponent was James Johnson, former naval surgeon and editor of theMedico–Chirurgical Review.63 During the Napoleonic Wars he had observed a choleraepidemic in India. About a quarter century later, during the first “visitation” of Asi-atic cholera to England, he offered readers of his journal a definition that spannedthe contagionist–miasmatic divide: “In epidemic cholera, as in most other epidemics,


Table 7.2. Characteristics of outbreak favoring competing theories

Anticontagionism Contagionism

Instantaneous; greatest number of Propagates gradually; number of casesvictims in first few days builds

Not traceable to human contact Traceable to human contact

Medical attendants spared Medical attendants often contract disease

Apparent spontaneous initiation Often brought to a previously unaffectedin locations without obvious place from an affected locality by acontact among sick individuals sick visitor

Previous case of disease creates immunity(follows smallpox inoculation model)

a poison or sedative principle, whether emanating from the earth, from animal orvegetable bodies on the earth, or engendered in the air, strikes a predisposing indi-vidual, and after an uncertain period of incubation, . . .” produces the visible symp-toms of the disease.64 Local miasmatists could agree with Johnson’s assumption thatthe causative agent was a chemical produced by decomposing vegetable and animalmatter, and Johnson’s multicausal definition could satisfy moderate contagionists,who accepted transmission by an infectious “virus” produced in the bodies of thesick. However, his qualification that the predisposing factors (“contingencies”) wereenvironmental rather than constitutional ruled out an alliance with general mias-matists. In his view most diseases required particular contingencies to render themepidemic: “diseases arising from aerial or terrestrial influences, far beyond our con-trol, have, in the hovels of the indigent, in crowded populations, in concentratedfilth, and in the absence of ventilation, taken on a character of infection or com-municability which they did not originally possess, and of which they are quicklydeprived under opposite and favourable circumstances.”65 For example, filth andovercrowding were essential for typhus.66 Johnson considered cholera analogous totyphus; both were contingent–contagious diseases and easily controlled by remov-ing filth and improving ventilation (Fig. 7.4). Smallpox was the exception that provedthe rule. Unlike the majority of epidemic diseases, it was a purely contagious diseasebecause it could develop and be transmitted in all environmental circumstances.

Thus, contingent contagionists could actively join local miasmatists in recom-mending sanitary reform as the most effective preventive against Asiatic cholera. Byand large, Johnson’s theory became the refuge of perplexed miasmatists: “we are in-finitely more favourable to the views of the exclusive anti-contagionists than to thoseof their opponents . . . because we are convinced that their [sanitary] doctrines,on the whole, are infinitely more beneficial to society and to the sick, even if theyare wrong, than are those of the opposite sect.”67 Filth should be removed, regard-less of whether one believed it was a necessary environmental contingency or just apredisposing factor for cholera.68 Their preference for anticontagionist allies notwith-standing, Johnson and his followers had staked out the basis for theoretical overlapwith moderate contagionists, who admitted cholera could be transmitted by the in-halation of bodily effluvia generated in its victims (“infection” in contagionist parl-ance). By the mid-1830s most local miasmatists were prepared to admit disease cau-sation by bodily effluvia in rare circumstances such as close confinement with poorventilation. Their concession that cholera was occasionally contagious reduced thecontroversy considerably thereafter.69 Consensus was emerging on one key point:The agent that caused cholera was inhaled. Miasmatists felt vindicated. Most conta-gionists by the mid-1830s, with the exception of a minority who cited etymology(con + tangere, “to touch”), believed that infection (inhalation) was as likely a modeof transmission as contact for a disease like cholera.70

An example of a contagionist strongly committed to the infection theory was E. O. Spooner of Blandford.71 In 1849 he ridiculed the local miasmatic stance of the


GBH. There had been rotting garbage and other evil smells in the streets for decades,but cholera epidemics occurred only in 1831–1832 and 1848–1849. He claimed thatmiasmatists had gained unwarranted support by demanding unrealistic standards ofproof: “The difficulty sometimes found in tracing an infectious disease up to its truesource, does no more invalidate the doctrine of contagionism than would a hundredundetected larcenies lead us to suppose that they could be committed without thethief.”72 Contagionists had identified three different routes of possible transmission:touch (whether direct or via fomites), infection (inhalation), and deliberate inocu-lation. Spooner believed the presence of a specific rash or exanthem suggested in-fection as the most likely route: The substance causing smallpox was inhaled intothe lungs, transmitted to the blood, and from there caused an eruption of the skin


Contingent Contagionism

lungs lungs

miasmadecomposingorganic matter

"contingencies"

humoraldisruption

effluvia

J. Johnson, 1831(per Durey)

humoraldisruption

individualdisease state

individualdisease state

X

no spreadto others

spread to otherpersons

environmentalfactors: filth &overcrowding

Figure 7.4. Contingent contagionism theory according to James Johnson.

that eventually caused the skin to peel. The same model applied to scarlatina.73 Byanalogy, the substance that caused cholera should be inhaled, transmitted to theblood, and cause similar changes—only to the inner lining of the bowel instead ofthe skin.74 Spooner relied heavily on the pathological investigations of Ludvik Böhmof Berlin, who had claimed that the desquamation of the inner lining of the mucousmembrane of the intestinal canal was a hallmark of cholera.75 Spooner assumed thatthis peeling away of the intestinal mucous membrane was, in effect, the “rash” ofcholera, making the analogy with smallpox complete. Perhaps Snow had a similarmodel in mind when discussing a case of smallpox he had treated: “The row of smalldwellings, in one of which this boy lived, are damp and ill ventilated, and all the ill-ness I have seen in them has been more severe and intractable than in the rest of theneighbourhood. I have treated two cases of sporadic cholera [English cholera, orcholera morbus] there, as bad as any cases of the epidemic disease [Asiatic cholera]which I have known to end in recovery. . . .”76 The reference to local circumstances(dampness and poor ventilation) producing diseases equivalent in severity to epi-demic cholera parallels the reasoning of contingent contagionists.

Farr and Zymotic Disease

While some sanitary reformers seemed wedded to the older bedside medicine withvestiges of the humoral paradigm, others incorporated new ideas from hospital andlaboratory medicine that accommodated the infection model with its emphasis onspread by the respiratory route. William Farr (1807–1883), Benthamite radical andsanitary reformer, regular contributor to the Lancet, and compiler of health and mor-tality reports at the General Register Office, was a master disease statistician (Fig.7.5).77 When Farr began classifying diseases for statistical purposes in 1837, he em-ployed the categories “endemic, epidemic, and contagious diseases.” His scheme’s in-clusiveness appealed to contingent contagionists, and Farr’s weekly disease reportswere reprinted in medical journals and the lay press. In the early 1840s he replacedthe tripartite categories with “zymotic diseases,” by which he meant diseases causedby a chemical process similar to, if not identical to, fermentation.78

Farr adopted his ideas on fermentation and allied processes from the work of theGerman chemist Justus Liebig (1803–1873).79 Liebig argued that yeast was an “ex-citer,” a nonliving organic material that, when in a state of decomposition and placedin a fluid with the proper chemical constituents, was capable of reproducing itselfwithin the fluid. He rejected the notion that yeast was a living organism that livedon sugar and excreted alcohol and carbon dioxide. The blood, which Liebig consid-ered one of the most dynamic and unstable components of the body, was a primetarget for an externally introduced exciter capable of reproducing in the blood. Whenthis happened the outcome was an internal state of decomposition because the ex-citer, in order to reproduce itself, absorbed the chemical constituents normally used


to maintain the blood in a healthy state. Liebig thought that two distinct types ofexciters caused the blood decomposition symptomatic of all diseases. In smallpox,syphilis, and plague the exciters initiated a process of decomposition in the blood ofthe victim that both reproduced (“propagated”) the exciter substance and also pro-duced the disease symptoms. The new generation of exciter particles produced byinternal propagation explained the disease’s capacity to spread from person to per-son. Miasmata, by contrast, caused blood to decompose and produced disease, butthese exciters could not reproduce within the body and, therefore, could not be trans-mitted to another person.80

Besides borrowing Liebig’s notion of fermentation, Farr relied on an analogy be-tween the exciters and chemical poisons in classifying zymotic diseases. If one sawin the body the specific set of symptoms and signs that were consistent with arsenicpoisoning, one was entitled to infer that arsenic had been taken into the body andwas the exciting cause. Similarly, zymotic diseases arose when a poison specific forthat disease entered the body and became seated in the blood. Like chemical


Figure 7.5. William Farr (1807–1883).

poisons, zymotic poisons affected some organs more than others, and such localpathological changes accounted for the specific characteristics of different diseases.Farr assigned names for the unseen but hypothesized exciting causes, so that small-pox (variola) was caused by the poison “varioline,” cholera by “cholerine,” and so on.These names were placeholders until investigations in the collateral sciences coulduncover the specific nature of the causative agents.81

Although Farr was unsure about the precise features of the agents that producedzymotic diseases, the data he collected suggested that they were small particles ofnonliving organic matter rather than gases. The spread of contagious diseases didnot match the predicted pattern for the diffusion of gaseous vapors alone (Fig. 7.6).


atmosphericconditions,

altitude, etc.

Farrcirca 1840s—1850s

lungs lungs

cholerine(specificorganic

nonlivingparticle)

decomposingorganic matter

occasionally

exciteschemical

reaction inblood akin tofermentation

diseasesymptoms

reproductionof cholerine

particle

exciteschemical

reaction inblood akin tofermentation

usually

person-to-personspread

Figure 7.6. Farr’s contingent contagionism theory.

By 1852 his analysis of two cholera epidemics in England suggested that the primaryfactor was elevation above sea level; the lower the elevation, the higher the mortal-ity (Fig. 7.7). It made sense to him that cholerine, the particulate matter that causedcholera, would be concentrated in the air at lower elevations and that cholera wouldtherefore be more prevalent along the seacoasts and tidal rivers than in the interior.


Figure 7.7. Farr’s graph of cholera incidence related to elevation

([Farr], Cholera in England, 1848–1849, lxv).

Farr remained uncommitted at this point on whether cholerine was also producedinside the human body and propagated by infection, ingestion of impure water, orby multiple channels.82 His “zymes,” like Liebig’s exciters, spanned the contagionistand anticontagionist divide. No matter how the disease might be spread, one couldstill claim that its underlying process was explainable in chemical terms as a sort offerment.83 By 1854 Farr had extended his theory to embrace four subcategories ofdisease—the miasmatic (which included smallpox as an infectious disease); the en-thetic or contagious (limited to those spread only by direct contact, such as syphilis),the dietetic (such as scurvy), and the parasitic.84

Infection, Pathology, and Treatment

In the London-based medical journals at midcentury, disagreement about the causeand mode of transmission of cholera was often overshadowed by uncertainty aboutits pathology and the continuing controversy over how to treat it. Theories of cholerapathology sought to incorporate information taken from research in the collateralsciences, which proved frustrating. Autopsy was the dominant tool of the day in ap-plying hospital medicine to the problems of epidemic disease, and most experts re-ported that autopsies of cholera patients revealed few consistent or characteristicfindings.85 Those who thought that massive diarrhea was the cardinal symptom ofthe disease developed pathological theories that implicated the intestines. Spoonerassumed that Böhm’s idea of desquamation of the intestinal lining effectively linkedthe theoretical model to the final result, diarrhea. Others were more impressed withthe spasms and the symptoms during the third stage (collapse), which seemed topredict a fatal outcome, and postulated the nervous system as the “seat” of cholera.86

The local miasmatist Southwood Smith believed putrefactive poisons first attackedthe central nervous system. The fevers characteristic of epidemic diseases were merelysymptomatic of the body’s loss of regulatory control, after which the other organsystems fell like a row of dominoes—first circulation, then respiration, and finallythe organs of secretion and excretion.87

Some medical men hoped chemistry would solve the cholera puzzle. Virtually allobservers agreed that the rice-water stools contained a large amount of water, a lit-tle bit of protein and various salts, almost no bile or other recognizable componentsof normal feces, and some cellular components that were probably shed epithelialcells from the inner lining of the gut.88 William Brooke O’Shaughnessy (1809–1902)performed some pioneering experiments on the chemistry of the blood in choleraduring the 1831–32 epidemic. He reported that the blood retained its normal ana-tomical structures but had lost much of its water and neutral salts; and that elementsdeficient in the blood were found in excess in the stools.89 In the 1840s Alfred Bar-ing Garrod, Snow’s Westminster and Aldersgate colleague, confirmed these find-ings.90 The chemical analyses by O’Shaughnessy and Garrod would explain why theblood of cholera victims appeared unusually viscid at autopsy.


Even so, other medical men, including Edmund Parkes and Lauder Lindsay, de-nied that the postmortem appearance of cholera blood differed materially from thefindings in other diseases. Parkes argued that the blood was indeed affected in cholera,secondarily to changes that occurred in the heart and lungs, but that it was the fi-brin in the blood rather than the fluid and salt content that was altered.91 GeorgeJohnson of King’s College Hospital agreed that the blood was altered in appearancebut denied that the amount of fluid lost via the bowels could account for the changesin the blood. Johnson agreed with Parkes that death occurred in cholera because thecholera poison impeded the circulation of the blood through the right side of theheart and the pulmonary vessels. That is, death by cholera resembled death by as-phyxia: The blood was unable to circulate through the lungs and so could carry nooxygen to the rest of the body. Johnson insisted that no matter how the poison mightenter the system, its final point of action was the bloodstream. In this regard, John-son added, the cholera poison acted in a manner analogous to an inorganic poisonlike arsenic.92

When it came to treatment of cholera, traditional bedside remedies remainedlargely unchanged; the new laboratory medicine had yet to eventuate in a therapeuticrevolution.93 The efficacy of every treatment was still judged in terms of whether ithelped restore the body’s internal balance. Sydenham’s theory of “epidemic consti-tutions” might have lost most of its currency in the debate about cause and trans-mission, but it was largely undisputed among clinicians. They selected therapeuticsbased on their assessment of the interaction of external environmental factors (suchas the season), constitutional peculiarities of individual patients, and the natural his-tory and progression of disease. For example, in slower-progressing cases of cholera,the earliest phase of diarrhea resembled the stool in typical mild gastrointestinal ill-nesses, and it should be treated as such. Early implementation of an aggressive reg-imen of therapeutics, such as one should use in later stages, might push a relativelyinnocuous case of premonitory choleraic diarrhea into full-blown cholera.94

The range of contradictory therapeutic approaches was huge and ultimately con-fusing.95 A reporter for the Lancet noted, “The drinking of water ad libitum, the em-ployment of sulphur, of calomel and opium, of sulphuric and tannic acids, of ni-trate of silver, of large quantities of whey, of saline injections, of creosote, of charcoaland lime water, had each its advocates” among members of the Medical Society ofLondon in 1854.96 The contradictory recommendations of calomel and opium areexemplary: If one assumed (as did George Johnson) that vomiting and diarrhea werenatural efforts by the body to rid itself of the cholera poison, then calomel was anideal remedy because it promoted these processes. However, if one considered thediarrhea in cholera an excessive reaction indicative of a severely imbalanced system,opium should be administered to bind the stools.97 Drinking huge quantities of wa-ter containing neutral salts was called the “saline treatment,” an adaptation of a pop-ular hydropathic method to the results of chemical researches on choleraic evacua-tions.98 Also reflective of these results was the recommendation to employ “saline


injections” into the veins to restore the fluid lost via the bowels and to replace themissing elements in the blood. Saline injection, which today is considered the mostrational therapy for cholera, was proposed by O’Shaughnessy in 1832 as a way to re-store the salts his experiments had shown to be depleted in the blood.

Dr. Thomas Latta of Leith, near Edinburgh, decided to try O’Shaugnessy’s pro-posal on patients in the last stage of cholera after finding that fluid replacement byrectum only aggravated their symptoms.99 After initial failures he was able to reportseveral successful outcomes. Perhaps the most remarkable case was that of a fifty-year-old woman in far advanced collapse. He administered two prolonged fluid in-jections, but each time the cholera symptoms returned a few hours later. However,the third injection resulted in complete recovery. More than twenty pints had beeninjected in all.100 Wakley in the Lancet praised Latta and his treatment,101 but oth-ers were very critical. The air fizzled from Latta’s balloon as he spent more time re-butting charges that his method was unsafe than he did in trying to save patients.102

By the 1848–1849 epidemic there was so little interest in this mode of therapy thatthe GBH did not bother to mention it in its official report.103 The results were de-cidedly inconclusive. George Johnson, reviewing the total body of evidence from the1832 experiments, noted that of 156 patients injected, only twenty-five recovered, “aresult which can scarcely be considered satisfactory.”104 Moreover, with the socialprestige of the profession at relatively low ebb during this period, physicians couldnot afford to put their reputations further in jeopardy by therapeutic experimentslikely to be regarded as rash by the laity.105 Practitioners who experimented on pa-tients with newfangled measures risked being labeled “empirics,” viewed as only onestep (if at all) removed from quackery.

Government authorities produced a fairly standard list of recommended treat-ments whenever cholera broke out. When cholera struck Exeter in 1832, the localhealth board posted handbills that repeated information distributed by the GBH inLondon. Therapeutics, whether self-administered or prescribed, were consideredmost effective during the premonitory diarrheal phase and less likely to work in therice-water stool and collapse phases. When the symptoms of cholera first appeared,health officials recommended external warmth and stimulants, including hot blan-kets and frictions, hot poultices, perhaps with oil of turpentine, and hot water bot-tles applied to the stomach. Brandy and laudanum were recommended as internalstimulants. Treatment should be geared from the outset to prevent the extreme cold-ness of the body surface and extremities characteristic of the collapse stage.106 Twoepidemics later, little had changed. Cholera victims in 1854 who were transportedto the Middlesex Hospital received the same stimulant regimen under the nursingcare of Florence Nightingale.107

Because of the prevalent view that cholera was caused by a blood-borne poison,bleeding to remove as much of the poison as possible was frequently recommendedduring the 1831–1832 epidemic. G. H. Bell’s Indian experience had convinced himof the special value of bloodletting. Bell, following his teacher Annesley, argued that


the nervous derangement of cholera led to marked venous congestion, preventinghealthy arterial blood from flowing to the lungs. Drawing off venous blood couldreverse the disease process; by contrast, bleeding from an artery only worsened thepatient’s condition.108 Bell was extremely optimistic that cholera patients could becured if medical men employed the correct treatment.109 By midcentury medicalmen were less sanguine about the benefits of bleeding: “It is sufficiently notoriousthat in severe visitations of the disease in different localities in Scotland in formeryears, when many cases were totally left to themselves in consequence of desertionby friends, or the inability of the medical officers to pay them any attention, theseconstituted the first and most favourable recoveries; and the mortality was seldomor never found greater in cases thus abandoned than in those subjected to the mostactive and careful treatment by the most experienced members of the profession.”110

Lauder Lindsay’s views were representative of the therapeutic nihilism that emergedwhen all the touted remedies failed to bring the promised results.

* * *

Snow’s writings and public comments between 1836 and 1848 suggest that his viewson epidemic diseases and their treatment followed conventional lines, although hegenerally opposed the use of alcohol. The terms Snow used in his teetotal addresssuggest that his general theory of diseases contained key features from Cullen (“de-bility,” “reaction,” “secondary fever,” and “inflammation in the head and elsewhere”)and Brown (“reaction” and “aesthenic”) and shared by all medical men who believedthat cholera was a febrile, infectious disease. His scattered comments suggest he be-lieved typhus, influenza, and smallpox were contagious diseases. The analogy he citedbetween smallpox and cholera in particular environmental circumstances suggestshe was a contingent contagionist with respect to that disease, but something hap-pened in the fall of 1848 that changed his mind.

Notes

1. Clutterbuck’s comments were published in “Cholera at Peckham.—Use of chloroform,”LMG 42 (1848): 767–68; and “Treatment of cholera by chloroform,” LMG 42 (1848): 988. Thesurgeon who devised the treatment was James Hill, and the particulars were described in“Treatment of the cholera by chloroform &c. in Peckham House (Poor) Asylum,” Lancet 2(1848): 514, a reprint of Hill’s letter to the Times, 30 October 1848. Two weeks later he senta brief notice to LMG that was published in the correspondence section as “The cholera—Re-sults of treatment by chloroform,” LMG 42 (1848): 902–03; and a longer report that the Lancetsummarized under “Cholera and its treatment by chloroform,” Lancet 2 (1848): 694–95.

2. See, for example, “Research,” “Suggestions for the treatment of cholera by anæstheticagents” (Letter), Lancet 2 (1848): 82–83; P. Brady, “Asiatic cholera successfully treated by chlo-roform given internally,” MT 18 (1848): 237–38; and James Moffat, “On chloroform incholera,” Lancet 2 (1848): 551–52.


3. See Jones Lamprey, “Chloroform as a remedy for cholera,” MT 19 (1848–49): 286–87,for the view against giving chloroform to cholera victims.

4. Wohl, Endangered Lives, 121, in turn citing Pelling, Cholera, 60. Baldwin notes that someGerman wags diagnosed a new epidemic they called “bibliocholera,” which was clearly con-tagious even if its subject matter was not; Baldwin, Contagion and the State, 38.

5. “Cholera and quarantine,” MT 17 (1847–48): 198.6. Editorial, Lancet 1(1853): 393. Because disagreements about the pathology and trans-

mission of cholera continued throughout Snow’s lifetime, our discussion of this context doesnot discriminate between ideas proposed before or after Snow first published his hypothesisin 1849.

7. Shephard uses the phrase “confusion and controversy” to describe English responses tocholera epidemics; JS, 151.

8. “Medium of contagion,” Lancet 1 (1842—43): 111. At the time, infection meant diseaseacquisition by the inhaled route only.

9. Durey, Return of the Plague, 105–06.10. Southwood Smith, in Examiner (1 March 1832), quoted in Ibid., 107.11. Durey, Return of the Plague, 115.12. Today authorities tend to suspect both a change in the biotype of the cholera organism

around 1817 plus the enhanced prospects for wide transmission provided by increased global com-merce; Colwell, “Global climate and infectious disease,” 2025–26; Crowcroft, “Cholera: Currentepidemiology,” R158–59. A detailed account with statistical tables of the progress of cholera fromIndia to the West until 1844 can be found in William J. Merriman, “Some statistical records of theprogress of the Asiatic cholera over the globe,” M-CT 27 (1844): 404–31.

13. While most authors regarded rice-water diarrhea as the hallmark of cholera, some insistedthat severe muscle spasms and cramps were more distinctive features, as indicated in the choiceof the descriptive term spasmodic cholera. In “Account of the epidemic spasmodic cholera, whichhas lately prevailed in India,” M-CT 11 (1821): 110–56, Frederick Corbyn recounted, “then fol-lowed spasms so violent as sometimes to require six men to hold the patient” (113).

14. Samuel Jackson of Philadelphia said of the typical patient in the collapse stage, “Theappearance he exhibits is frequently that we may conceive of a corpse, inhumed some days, suddenly reanimated”; “Personal observations and experience of epidemic or malig-nant cholera in the city of Philadelphia,” American Journal of Medical Sciences 12 (1833): 88.

15. For a detailed and representative catalog of cholera symptoms, see Greenhow, Cholera,As It Recently Appeared, 11–12. Contemporaries often stressed the peculiar facial expression(described as anxious and as having an “earthy” quality) that might precede the developmentof other symptoms; see Bell, Cholera Asphyxia, 10. A similar description occurs in Shapter,Cholera in Exeter, 211.

16. Cholera was the name given to any enteric disease, reflecting the humoral doctrine thatsuch illnesses were caused by an excess of choler (yellow bile). Cholera morbus was a later re-finement designating a particular diarrheal disease; OED. By the nineteenth century the twoterms were often used synonymously. See also Thomas Laycock, “Summer diarrhœa, cholera,and typhus fever,” LMG 38 (1846): 227–28; and Thomas Watson, “Lectures on the principlesand practice of physic,” LMG 30 (1841–42): 114.

17. Relatively few works on cholera of that era provided mortality statistics. Merriman, inhis extensive statistical analysis of the epidemic of 1831–1832, calculated mortality rates ofthirty percent in England, fifty-three percent in Scotland, thirty-five percent in Wales, andthirty-nine percent in Ireland; M-CT 27 (1844): 404–31. Jacob Bell, editor of the Pharmaceu-tical Journal, declared that the case–mortality rate during the height of the 1848–1849 epi-demic was between twenty-five and sixty percent; “The cholera,” PharJ 9 (1849– 50): 53–54.


A survey of legally qualified practitioners in 1855 produced a mortality rate of 45.6% in 4,271cases; UK GBH, Supplement 1 to Report of CSI, 87.

18. Some believed that the Asiatic cholera reported in India after 1817 was a variant of En-glish cholera, or cholera morbus, and that both were first described by the ancient Greeks; seeW. F. Chambers, “Three lectures on cholera,” Lancet 1 (1849): 37–39. Others argued that Asi-atic cholera was a different disease and was never seen in England before 1831; see ThomasWatson, “Lectures on the principles and practice of physic: Epidemic cholera,” LMG 30(1841–42): 117. The etymology of cholera was in dispute from the outset. G. H. Bell, an earlyBritish authority, dismissed two possible Greek derivations: �� (bile) and �� (intes-tine); Cholera Asphyxia, 8. Robley Dunglison, the American (but British-born and -trained)medical lexicographer, suggested ��ε�� (the rain-gutter of a house), which many contem-poraries accepted; see Dunglison, Dictionary of Medical Science, 199; and Raufman, “Cholera,”386. The evolution of terms from cholera morbus to Asiatic cholera is summarized in Jackson,Spasmodic Cholera, 3–4.

19. W. F. Chambers described Asiatic cholera as “the most formidable epidemic by whichthe human race has ever been scourged”; “Three lectures on cholera,” Lancet 1 (1849): 137.Thomas Watson noted that “the cadaverous aspect that sometimes precedes death in long-standing diseases, would come on in the course of an hour or two in [cholera]”; “Lectures onthe principles and practice of physic: Epidemic cholera,” LMG 30 (1841–42): 116. Dr. ThomasAddis Emmet, attached to the Emigrant Refuge Hospital in New York City (later a pioneergynecological surgeon), included in his memoirs a description of an incident that occurredtwice during the 1854 cholera epidemic. Newly afflicted cholera patients were brought into award to join patients already receiving care. The ward, including night attendants, was lockedeach evening. When physicians and day attendants opened the ward the following morning,everyone in the ward—patients and attendants alike—had died during the night; Walsh, Med-icine in New York, 110, citing Emmet, Incidents of My Life. Emmet’s successor lasted less thana week before dying of cholera, although Emmet, like many English writers, noted that suchdeaths among physicians were unusual.

20. From the 1820 report of assistant surgeon James Johnson for the medical board of Ben-gal, quoted in [Jackson], Spasmodic Cholera, 8.

21. “In Asia, the fiend was contemplated by us with curiosity—in the wilds of Russia, withsuspicion—in Germany, with alarm—but on English soil, with TERROR!” [James Johnson],“Epidemic cholera,” M-CJ 16 (1832): 163.

22. E. O. Spooner,“The contagion of Asiatic cholera,” PMSJ 13 (1849): 34–37, 62–66, 91–97,esp. 65–66.

23. Bell, Cholera Asphyxia, 79–80. W. F. Chambers also argued that the trade route hy-pothesis was based on inaccurate or selective observations; “Three lectures on cholera,” Lancet1 (1849): 222–23.

24. Kay-Shuttleworth, Moral and Physical Condition, 8.25. For professional medical dissatisfaction with the effects of the New Poor Law on the

poor themselves, the medical officers who worked for the unions, and the emergence of theradical British Medical Association in 1836, see Desmond, Politics of Evolution, 31, 124–29.

26. Porter, Greatest Benefit, 409–10. Bentham, in his will, had left his body to be dissectedfor the benefit of medical science and appointed Southwood Smith to carry out the dissec-tion, which he did; Webster, Caring for Health, 45–46.

27. Chadwick, Report into the Sanitary Condition of the Labouring Population. In the Lancet,Wakley argued that medical men should lead efforts at sanitary reform because they under-stood best what was needed to improve health; Lancet 1 (1847): 101; Lancet 2 (1847): 578.Snow echoed this view in his inaugural address when he assumed the presidency of the Med-


ical Society of London in 1855. For a comprehensive study of Chadwick and the sanitarymovement, see Hamlin, Age of Chadwick. See also Halliday, The Great Stink of London, 35–42.

28. LMG endorsed the Health of Towns Bill then before the House of Commons, highlight-ing the statistical analysis of “wasted lives,” that is, the calculated number of lives unnecessarilylost to filth-induced diseases in large cities compared to the death rates in the countryside; “Ed-itorial,” LMG 39 (1847): 634–39. The same editorial quoted Southwood Smith testifying beforethe Health of Towns Commission that filth from sewer gases produced fevers (635).

29. Porter, Greatest Benefit, 411–12; Webster, Caring for Health, 46, 55, 69–71.30. Baldwin, Contagion and the State, 127–29.31. Ibid.32. “Influenza and cholera,” Lancet 2 (1836–37): 115. See also Thomas Laycock, “Atmo-

spheric changes as causes of disease,” LMG 38 (1846): 1043, in which he noted that “changesin temperature have a considerable influence on the health of man, but not always directly.The problem is one of considerable complexity, because the changes in temperature are com-plicated with tidal changes in the atmosphere, and with disturbance of the magnetism of theearth and of the electricity of the air.”

33. “Westminster Medical Society,” Lancet 1 (1841–42): 598.34. See examples in Ackerknecht, “Anti-contagionism,” although his generalizations have

been superseded by Durey, Return of the Plague; Delaporte, Disease and Civilization; and Bald-win, Contagion and the State.

35. Durey, Return of the Plague, 105–06.36. Ibid., 107. Edmund Parkes believed cholera was caused by a “specific morbid agent or

virus” that was presumably one “of the more subtle gases” undetectable by the chemical meansthen available; Parkes, Researches, 156.

37. Southwood Smith, Treatise on Fever, 41–42.38. “Cholera and quarantine,” MT 17 (1847–48): 198–99; see also Southwood Smith, Trea-

tise on Fever, 66. Greenhow accepted Sydenham’s “epidemic constitution” with a local mias-matic twist: “That the atmospheric condition, be it what it may, on which depends the effi-cient cause of Cholera, has been gradually forming itself in the course of the summer, isrendered yet more probable, when we review the character of the diseases which have prin-cipally prevailed, in the neighbourhood, during that period. . . . It has been a general re-mark, amongst medical men, that the ordinary complaints of the season all tended to resolvethemselves into the prevalent febrile affection. Throughout the epidemic, a marked determi-nation has been observed in the mucous membrane of the intestines, showing the irritablecondition of that tissue . . .”; Cholera, As It Recently Appeared, 100.

39. Southwood Smith, Treatise on Fever, 364. However, a few pages earlier he wrote, “With-out doubt, a febrile poison, purely of animal origin, in a high degree of concentration, wouldkill instantaneously” (360).

40. Southwood Smith, Treatise on Fever, 354–55.41. Lindsay, “Clinical notes on cholera,” AMJ 2 (1854): 1116. G. H. Bell, in fact, argued that

one reason physicians who had seen service in India were so strongly anticontagionist was be-cause so few physicians had been struck down, whereas because “fatigue of mind and body isa powerfully predisposing cause” of cholera, “every medical man, who has done his duty toCholera patients, must feel, that had the disease been communicable from one individual toanother, he could scarcely by possibility have escaped”; see Bell, Cholera Asphyxia, 86–87.

42. Lindsay, “Clinical notes on cholera,” AMJ 2 (1854): 840. Farr showed that cholera deathswere more common on Saturdays, as well as Mondays through Wednesdays, which he attrib-uted to the payment of weekly wages on Saturdays and the heavy drinking that typically oc-curred thereafter; Farr, Cholera in England, 1848–49, xlix.


43. Florence Nightingale may have held similar views to the very end of the nineteenthcentury; Rosenberg, Explaining Epidemics, 93–107. Rosenberg believes that Nightingale neveraccepted the germ theory of disease, although this is currently a matter of dispute.

44. Durey states that the only point on which all contagionists could agree was approvalof quarantine, and anticontagionists were in agreement only that quarantine was unworkable;Return of the Plague, 107. Similarly, Baldwin found a division between quarantinist and envi-ronmentalist views; Baldwin, Contagion and the State, 4–5. See also Worboys, Spreading Germs,39–40. However, some contagionists offered only conditional support for quarantine; see“Contagion and quarantine,” LMG 30 (1841–42): 262–64. Ackerknecht argued that anticon-tagionism during this period tended to be associated with political liberalism and contagion-ism with defenders of the status quo and bureaucracy; “Anti-contagionism,” 567. Delaporteconsiders this generalization overly simplistic; Disease and Civilization, 145–49. While Britaingenerally had trading interests that made quarantine an unpopular measure, forces within thecountry did not necessarily line up for or against quarantine solely because of their own pe-cuniary interests; Baldwin, Contagion and the State, 97. Baldwin adds that traditional quar-antine fell out of favor as the century wore on less because of a shift in the basic understandingof disease and more because it proved practically impossible and inordinately expensive; Bald-win, Contagion and the State, 79, 120, 123–89.

45. “Asiatic cholera,” MT 19 (1848–49): 11–12.46. William Budd wrote of the GBH of the era from 1848 to 1855, “To make unceasing

and implacable war against contagion and contagionists seemed with the [GBH], indeed, tobe, for some years, the chief purpose of its existence”; “On intestinal fever: its mode of prop-agation,” Lancet 2 (1856): 694. On the GBH’s reaction to Snow’s theories in 1855, see Panethet al., “A rivalry of foulness.”

47. On why sanitarianism led to practical accomplishments despite its theoretical limita-tions when viewed from today’s perspective, see Winslow, Epidemic Disease, 244–49.

48. Baldwin, Contagion and the State, 101.49. Baldwin, Contagion and the State, 7. M-CR attributed the theory that “contagious or

infectious matters enter the body . . . by . . . the skin” to “Fracastor, and [the theory] hashad but few advocates since his time”; Lancet 1 (1842–43): 111. However, an editor at LMGthought the dispute was long-standing, and a century hence anticontagionists would still re-gard contagionists as “men lagging behind in the march of intellectual improvement, as fol-lowers of an idle fantasy of the brain, incapable of proof; as well-meaning, but weak-mindedand prejudiced”; “Contagion and quarantine,” LMG 30 (1841–42): 262.

50. Porter argues that Fracostorius imagined his “seeds” as spores, not microorganisms;Porter, Greatest Benefit, 174–75.

51. Morton, Medical Bibliography, 447.52. For a detailed discussion of ways to disinfect clothing and bedding as a preventive for

cholera, see LMG 43 (1849): 199–202.53. “Diseases are propagated either by inoculation and contact (contagion) or by inhala-

tion (infection) . . .”; [Farr], Cholera in England, 1848–1849, lxxx. However, infection was of-ten used in contradictory ways; for usage during the 1831–1832 epidemic, see Durey, Returnof the Plague, 112–14; more generally, see Hudson, Disease and Its Control, 142.

54. “[Cholera] does not appear to be in the least degree contagious, and scarcely, if at all,infectious, unless, perhaps, where many sick are congregated together, as in the wards of ahospital; in fact, I should consider it as an almost true epidemic, such as the influenza whichhas prevailed here since the last cholera disappeared”; report of Vice-Consul Bassam of Mossul,quoted in E. O. Spooner, “The contagion of asiatic cholera,” PMSJ 13 (1849): 63. Anticonta-gionists frequently used epidemic as a synonym for miasmatic.


55. “The infectious nature of pestilential cholera,” LMG 38 (1846): 520, excerpted fromCopland, Dictionary of Practical Medicine, part 10.

56. “Westminster Medical Society,” Lancet 1 (1837–38): 868. It is unclear from this exam-ple whether Snow distinguished typhus from typhoid fever.

57. An editor at LMG listed smallpox, measles, scarlet fever, and whooping-cough as un-deniably contagious diseases; “Contagion and quarantine,” LMG 30 (1841–42): 263.

58. Indeed, it seems safe to say that, on balance, there existed more data favoring anticon-tagionism than contagionism in the first half of the nineteenth century. The eventual su-premacy of contagionism depended on an understanding of factors (largely unknown duringthe period we are studying) such as animal vectors and asymptomatic carriers, without whichcontagionist theory could not fully explain data presented by typical epidemic diseases;Winslow, Conquest of Epidemic Disease, 182. Thomas Watson, however, hypothesized that anasymptomatic carrier could explain the (occasional) contagiousness of cholera; “Lectures,”LMG 30 (1841–42): 118. See also Daniel Noble, “On the question of contagion in cholera,”LMG 43 (1847): 141–49, esp. 146.

59. Ackerknecht states that Anglo–Indian surgeons and physicians were “uniformly” anti-contagionist; “Anti-contagionism,” 575, but Durey states that a number of Anglo–Indian physi-cians supported contagionism; The Return of the Plague, 110. The committee of the Massa-chusetts Medical Society, reviewing the extant European literature in 1832, reported thatopinion among the Indian physicians was “divided” but that “a decided majority” embracedanticontagionism; [Jackson], Spasmodic Cholera, 40–41. Thomas Wakley, editor of the Lancet,was strongly contagionist in the 1830s but moderated his stance thereafter as sentiment wentagainst him; see Lancet 1 (1831–32): 669–84, esp. 674–79.

60. The stomach route was “an ancient notion, . . . advocated recently by Lind, Darwin,and Jackson”; “Medium of contagion,” Lancet 1 (1842–43): 111. The reference to James Lind(1716–1794), discoverer of the lemon juice cure for scurvy, is perplexing. He claimed that theseeds of infections like yellow fever, plague, and jail distemper were suspended in the air andinhaled and added simply that the stomach and intestines were often the first organ systemsto be affected by them; Lind, An Essay on Health of Seamen, 236–41, 256–57, 316. The otherreferences are to Erasmus Darwin and Robert Jackson. Autoexperiments with plague and yel-low fever had produced negative results as well; Ackerknecht, “Anticontagionism,” 567–68. Ed-mund A. Parkes, who converted to a contagionist position in the 1860s, mentioned these au-toexperiments as one of the main reasons he had initially rejected contagionism; PracticalHygiene, 74–75. A 1971 study on prisoner volunteers in the United States in which varyingdoses of cholera vibrios were administered orally produced some evidence of cholera in onlytwenty-six percent. When the volunteers were also given sodium bicarbonate to neutralize thestomach acid, the response rate rose to eighty-five percent; Hornick et al., “The Broad Streetpump revisited.” However, it has more recently been discovered that the cholera vibrio un-dergoes changes in gene expression upon passage through the human gut that make the bac-teria acquired in epidemic situations more virulent than bacteria grown under laboratory con-ditions; Merrell et al., “Host-induced epidemic spread of the cholera bacterium.”

61. Worboys suggests that it is anachronistic to imagine that an inability to reach consen-sus about the cause of cholera posed a serious problem for the medical profession of that day:“Traditional physic and modern medical science had not constituted disease in causal terms,where treatment would focus on removing causes. Disease involved structural or functionalperturbations, and hence treatment was in large part about positive interventions to promoterepair, to restore function or to aid in the regeneration of damaged structures”; Worboys,Spreading Germs, 33. He also cautions against overcharacterizing British medical thinking inthe 1830s and 1840s about the cause and spread of cholera, because “one of the few things


doctors did agree on was to avoid ‘theory’ and to try to be empiricists who did not have over-arching principles” (28). At the time the pejorative use of theorist referred to an adherent ofan outmoded medical “system” from the eighteenth century.

62. Baldwin, Contagion and the State, 123.63. He twitted the GBH for making an abrupt shift from a strongly contagionist view of

cholera to contingent contagionism, indicated by a fall in temperature from 120° to 92° inonly three weeks. The highest degrees on this “loimometer,” or “pestgage,” for “measuring thetemperature” of disputants about the causes of cholera indicated ultra-contagionism. The mid-dle range was indicative of contingent contagionism, while the lowest was ultra nonconta-gionism; J. Johnson, “Cholera in England,” M-CR 16 (1832): 267, who credited an “ingeniousfriend” with constructing this cholera thermometer.

64. J. Johnson, M-CR. (1832), cited in Durey, Return of the Plague, 115.65. J. Johnson, “Epidemic cholera,” M-CR 16 (1832): 163. Watson, a contingent conta-

gionist, thought the most common predisposing influences were poverty, poor ventilation,and abuse of alcohol; “Lectures on the principles and practice of physic: Epidemic cholera,”LMG 30 (1841–42): 118–19.

66. “Derobe a typhous patient of filth and foul air . . . and you take away from the feverthe power of propagation. You may then feel his pulse, examine his tongue, analyse his evac-uations, press his abdomen—and, when he dies, dissect his body, with about as much chanceof catching the fever, as of learning from him the secret of alchemy”; J. Johnson, “Cholera inEngland,” M-CR 16 (1832): 268.

67. J. Johnson, “Epidemic cholera,” M-CR 16 (1832): 163. See also Durey, Return of thePlague, 114–17.

68. Edmund Parkes became a contingent contagionist based on observations in India dur-ing two epidemics between 1843 and 1845. He had seen no evidence of contagion from per-son to person, but insisted, “I by no means wish to generalize this observation, and to con-clude that the poison of Cholera is never reproduced by the human body”; Researches, 192.E. O. Spooner had Parkes in mind when he stated, “A disease cannot be contingently conta-gious, though it may spread or not according to certain contingencies. The theory of a diseasebeing sometimes contagious and sometimes not, is self-contradictory and absurd. Similarkinds of matter always possess similar properties, and the specific virus of the choleric pesti-lence forms no exception to the general rule”; E. O. Spooner, “The contagion of Asiaticcholera,” PMSJ 13 (1849): 36.

69. In the previous century Cullen had suggested such a category of “doubtful” fevers, some-times contagious and sometimes not, thereby giving the notion of contingent contagionisma respectable pedigree; Porter, Greatest Benefit, 261. Watson adopted a contingent contagion-ist position because neither the contagionist nor the anticontagionist hypothesis alone could“reconcile the phenomena of the appearance and extension of the malady”; “Lectures,” LMG30 (1841–42): 117.

70. An excerpt from an article in M-CR from October 1842 listed three routes by which“contagious or infectious matters enter the body”—the lungs, the stomach, and the skin. Theauthor endorsed the lung route, “the most ancient conjecture . . . advocated by Lucretius;it has been supported also in recent times by Sir A. Cooper”; “Medium of contagion,” Lancet1 (1842–43): 111.

71. Delaporte found a rural–urban theoretical division in France during the 1831–1832epidemic. Rural physicians were likely to see relatively small epidemics up close and often hadcontact with each person afflicted. They could readily trace any pattern of spread from oneperson to another and could obtain detailed information as to the circumstances and timingof each illness. By contrast, no single urban physician was likely to see every cholera sufferer


within a circumscribed area. By the time urban health authorities and medical men realizeda cholera outbreak had occurred, scores of cases had already occurred, creating the impres-sion that the disease had broken out everywhere at once. After the fact the victims were of-ten unable or unwilling to provide details about their contacts and previous habits. There-fore, a rural practitioner’s experience generally conformed to contagionist doctrine, whereastheir urban counterparts tended to think that cholera was not contagious; Disease and Civi-lization, 171–72.

72. E. O. Spooner, “The contagion of Asiatic cholera,” PMSJ 13 (1849): 35. When J. G.Swayne, Budd’s Bristol colleague, sought confirmation for his fungus cell theory in 1849, hesent samples to E. O. Spooner as well as to Edwin Lankester and Arthur Hassall in London;Pelling, Cholera, 175. Hence, Spooner must have been a respected microscopist.

73. For the reliance of both contagionists and anticontagionists on “model” diseases, seeDelaporte, Disease and Civilization, 163-70.

74. Frederick Corbyn disagreed, citing the instance of three natives in a general hospital inSeroor who had not contracted cholera despite being surrounded by cholera victims and “in-haling by day and night at every inspiration, mouthfuls of the infection.” Thus, cholera couldnot be contagious, even contingently; “Account of the epidemic spasmodic cholera, which haslately prevailed in India,” M-CT 11 (1821): 143. Other contagion theories of cholera very sim-ilar to Spooner’s were J. H. James’s, “Some remarks on the nature and probable causes of thepropagation of cholera maligna,” LMG 42 (1848): 929–34; and Ogier Ward’s, “Contagion ofcholera,” LMG 41 (1848): 559–62.

75. See Dr. Bushnan, “Progress of German medical science,” MT 18 (1848): 120 (where thepathologist’s name is given as “Boehm”).

76. Snow, “Case of malignant hæmorrhagic smallpox,” LMG 35 (1844–45): 586. By “spo-radic cholera” Snow meant summer, or English, cholera—various intestinal complaints withattendant diarrhea. The cases of epidemic Asiatic cholera he refers to were presumably thosehe had treated at Killingworth in 1832.

77. See Eyler, “William Farr on the cholera”; and Desmond, Politics of Evolution, 28, 31.78. “A single word, such as Zymotic, is required to replace in composition the long pe-

riphrasis ‘epidemic, endemic and contagious “diseases,” [sic] with a new name and a defini-tion of the kind of pathological process which the name is intended to indicate”; Farr, 4th An-nual Report of the Registrar-General (1842), in Vital Statistics, 246. Farr’s new term took a whileto catch on. A few years later, “A reader” sent a letter to the editor of the Lancet: “Sir: will you be so good as to give a definition of the word ‘Zymotic,’ which occurs in the Registrar-General’s “Return,” and say from whence the word is derived?” The reply offered several der-ivations, and noted that ferment “may also be employed in English . . . as general designa-tion of the morbid processes and their exciters”; Lancet 1 (1848): 55.

79. Farr was also familiar with the work of Jacob Henle (1809–1885), who assembled andanalyzed a mass of evidence accumulated by other investigators and drew the conclusion thatcontagious diseases were caused by microscopic living organisms, probably of a plant variety.He was influenced by the fact that these diseases displayed an incubation period (evidencethat the causative agent must be capable of multiplying within the body), as well as the pat-tern of specific symptoms and a specific time course whenever the disease appeared. Henlewas known only second-hand by most English authorities, as his works had not been trans-lated from German at this time; Pelling, Cholera, 193–94. Henle’s research was summarizedin M-CR. of October 1842, but the excerpt in Lancet stated (contra Pelling) that Henle be-lieved contagious diseases “depend for their existence and propagation on certain parasiticalorganised beings, or their germs. . .”; Lancet 1 (1842–43): 111. Henle’s Miasma and Conta-gions (1840) was admittedly more the framework for a set of future scientific investigations


than a fully developed scientific theory. Robert Koch, Henle’s pupil, eventually carried outmuch of the envisioned research program; Rosen, “Jacob Henle’s medical thought.” Winslowcredits L.-B. Guyton-Morveau (1737–1816) as perhaps the first nineteenth-century thinker toposit specific living particles capable of reproducing themselves as the causative agents of con-tagious diseases; Guyton-Morveau was also a godfather to the sanitary movement, arguingthat chemicals that eliminated the smell of putrefaction should for that reason be useful agentsin preventing this class of diseases; Winslow, Conquest of Epidemic Disease, 239–42. PerhapsHenle influenced Farr’s postulate that each “zymotic” disease was caused by its own specificand discrete particle.

80. Liebig, Chemistry and its Application, 121–27.81. Farr, Cholera in England, 1848–1849, lxxx–lxxxiii (footnote). See also Eyler, “William

Farr on the cholera,” 84–85.82. Pelling, Cholera, 100–12; Eyler describes how Farr gradually modified his views as new

bacteriological evidence became available and made a smooth transition to a germ theory;“William Farr on the cholera,” 94–95. Around 1850 Farr was unwilling to state exactly whatsort of material or particle cholerine was. By that date the collateral sciences had shown thatfungi could cause plant diseases and at least one human disease (favus, a skin disorder). Thisdiscovery led Charles Cowdell (1815–1871) to argue that the specific causative agent of cholerawas a type of fungus that developed morbid properties under certain atmospheric conditions,was inhaled, and infected the blood; Cowdell, Pestilential Cholera, 198–210. With respect totransmission, however, he seems to have been a contingent contagionist. He believed Cop-land’s notion of infection had merit in some situations, when “germs given off by exhalationsfrom the bodies of the sick” seemed to enter the local atmosphere and infect others (201).

83. Worboys, Spreading Germs, 34–41.84. Farr, Sixteenth Annual Report of the Registrar General, in Vital Statistics, 250–53.85. “The examination of the dead bodies threw no light, that I know of, upon the nature

of this frightful disease”; Watson, “Lectures,” LMG 30 (1841–42): 116. The clinical approachincluded reliance on medical statistics as well as on autopsy findings.

86. David M. Morens read an early draft of this chapter and suggested that French physi-cians, too, could not agree on the pathological lesion that typified cholera. Morens’s view isconfirmed by Delaporte, who categorized the major pathophysiological theories during the1831–1832 epidemic as physiological, with inflammation of the gastrointestinal tract the defin-ing feature (Broussais); experimental, with depleted cardiac function as primary (Magendie);nervous, with the nervous system as the seat (various authors); and humoral, with chemicalchanges in the blood the basic problem (Bonnet); Delaporte, Disease and Civilization, 115–30.Broussais believed cholera was noncontagious, and his recommended treatment was exten-sive bleeding.

87. Southwood Smith, Treatise on Fever, 346–47. Many other authors during the 1830s and1840s adopted the nervous-system explanation of the pathology of cholera. See Annesley (G. H. Bell’s teacher in India), Most Prevalent Diseases of India, 147; and Shapter, Cholera inExeter in 1832, 226. Indirect evidence for a nervous “seat” was deduced from a report of thetherapeutic success of cannabis tincture in eleven cases of cholera in Cairo; “On the employ-ment of cannabis indica in cholera,” LMG 43 (1849): 217.

88. See a report of experiments by Robert Dundas Thomson of Glasgow, “Royal Medicaland Chirurgical Society,” Lancet 2 (1850): 154–55.

89. William B. O’Shaughnessy, “Experiments on the blood in cholera,” Lancet 1 (1831–32):490, a summary of his Report on the Chemical Pathology of the Malignant Cholera. In 1830 aProfessor Hermann of Moscow had reported roughly similar findings. O’Shaughnessy drewtherapeutic conclusions from his experiments, advocating intravenous injection of saline flu-


ids in severe cases but did not conduct clinical trials of this mode of therapy. Later he was amedical officer in India and helped establish the Indian telegraph system; Moon, “Sir WilliamBrooke O’Shaughnessy.” Snow was aware of O’Shaughnessy’s 1832 researches (some of whichwere conducted in Newcastle while Snow was an apprentice there); “Principles on which thetreatment of cholera should be based” (1854).

90. Alfred B. Garrod,“On the pathological condition of the blood in cholera,” LJM 1 (1849):409–37.

91. Parkes, Researches, 103–13. Parkes thought that “fibrin” was deposited in the smallervessels and that this obstructed the flow of blood to various organs. See also Lindsay, “Clini-cal notes on cholera,” AMJ 2 (1854): 412.

92. G. Johnson, Epidemic Diarrhœa and Cholera, 123–24. Thomas Watson agreed that theblood in cholera victims was invariably black and tarry;“Lectures,” LMG 30 (1841–42): 116–17.

93. Rosenberg, “The therapeutic revolution,” in Vogel and Rosenberg, Therapeutic Revolu-tion, 3–25; Warner, Therapeutic Perspective.

94. Shapter’s suspicion of specific remedies reflected a humoral therapeutic perspective: “Isthere no cure for Cholera? I would make this reply: There is no specific cure for Cholera; but,as in fever and other diseases, its various stages require management and treatment accord-ing to the phenomena that are developed, and the individual constitutions in which they arise,and that a wise conduct and judicious management of these are likely, under God’s blessing,to be attended with benefit; while a wild and indiscriminate resort to specifics must inevitablybe injurious”; Cholera in Exeter in 1832, x–xi. The Lancet remained a staunch defender of ho-listic, bedside medicine until well after midcentury: “Physicians who have learned their les-son at the bedside, and who know that the object of the healing art is not to cure a disease,but to treat a patient, will not waste their labour in the vain search for specific methods”;Lancet 1 (1869): 164; quoted in Worboys, Spreading Germs, 31. In this mind-set, the use of“specifics” was equivalent to crude empiricism and quackery.

95. Following the 1853–1854 epidemic the Scientific Committee of the GBH undertook acrude nonrandom statistical analysis of various treatments grouped under four classes: alter-atives (of which calomel was the most commonly employed), astringents (chalk, or chalk andopium, or sulphuric acid), stimulants (ether and brandy), and eliminants (castor oil). Theoverall death rate across Britain based on surveys of local practitioners ranged from twenty-seven percent when astringents were used to seventy-six percent when eliminants were em-ployed. For patients in the collapse stage, the range was fifty-seven percent with alteratives toseventy-eight percent with eliminants; UK GBH, Report on Different Methods of Treatment.

96. “Medical Society of London,” MTG 8 (1854): 98–99. Discussion occurred after Snow de-livered a paper,“Principles on which the treatment of cholera should be based.”“Saline injections,”we should note, do not refer to intravenous saline injections, but rather to the much more com-mon rectal route. For an overview of treatments used in the 1832 epidemic, see P. Smith, Cholera: An Inquiry, 26–29. N. Howard-Jones dismissed most treatments as ineffective;“Cholera therapy in the nineteenth century.” Baldwin adds that the failure of medical opinion toagree on an optimal treatment approach and the associated diminution in the public respect forphysicians created a marvelous opportunity for quackery; Baldwin, Contagion and the State, 38.

97. Parkes considered excessive diarrhea one of the major components of cholera and im-portant to treat. But he did not consider arrest of the diarrhea as synonymous with cure ofcholera; Researches, 202.

98. Many were dismissive of this treatment: “However it might be with pigs or herrings,salting a patient in cholera was not the same as curing him”; Thomas Watson, “Lectures,” LMG30 (1841–42): 119.

99. “Letter from Dr. Latta to the secretary of the Central Board of Health, London, af-


fording a view of the rationale and results of his practice in the treatment of cholera by aque-ous and saline injections,” Lancet 2 (1831–32): 274–77.

100. Ibid., 275.101. Lancet 2 (1831–32): 284–86.102. Thomas Latta, “Reply to some objections offered to the practice of venous injections

in cholera,” Lancet 2 (1831–32): 428–30. Latta died in 1833, after which fluid injections fellout of favor until the 1890s; Dhiman Barua, “History of cholera,” in Barua and Greenough,Cholera, 1–36.

103. UK, GBH, Report on Epidemic Cholera of 1848 & 1849.104. G. Johnson, Epidemic Diarrhœa and Cholera, 112. Johnson was unconvinced that vir-

tually all would have died had the injections not been given, because experimenters generallyselected only the sickest patients. He concluded in 1855, “There are probably few practition-ers who now expect any practical benefit from saline injections in cholera” (114). Cowdell haddrawn similar conclusions in 1848; Pestilential Cholera, 98. Parkes also mentioned in passingthat intravenous saline injections had been tried by some Indian practitioners with notablelack of success; Parkes, Researches, 219–39. Merriman quoted a Canadian report from 1832 inwhich saline transfusion was attempted in twenty “hopeless” cases with no cures, althoughone patient survived for seven days as a result of the treatment; “Some statistical records ofthe progress of the Asiatic cholera over the globe,” M-CT 27 (1844): 429. Samuel Jackson ofPhiladelphia adopted a view similar to O’Shaughnessy’s in 1832 to 1833 regarding the centralrole played by dehydration of the blood and had good success at his cholera hospital by giv-ing patients copious amounts of oral fluids; Samuel Jackson, “Personal observations and ex-perience of epidemic or malignant cholera in the city of Philadelphia,”American Journal ofMedical Sciences 12 (1833): 76–121.

105. Durey, Return of the Plague, 133.106. Shapter, Cholera in Exeter in 1832, 18–20.107. Winterton, “Soho cholera epidemic 1854,” is based on a contemporary report from

the apothecary to the hospital. Florence Nightingale, according to one of her correspondentsof that time, was “ ‘up day and night, undressing them . . . putting on turpentine stupes,etc. herself to as many as she could manage.’ . . . From Friday afternoon until Sunday af-ternoon she was never off her feet”; quoted in Woodham-Smith, Florence Nightingale, 80.Nightingale had at this time in her career not yet traveled to the Crimea, where she achievedfame for her wartime nursing efforts.

108. Bell, Cholera Asphyxia, 25–26, 104. See also Annesley, Most Prevalent Diseases of India,166. Greenhow, who also held miasmatist views and attributed the pathology of cholera tonervous derangement, opposed bleeding in part because freely flowing blood was so hard toobtain in advanced cases; Cholera, As It Recently Appeared, 22–32.

109. Bell, Cholera Asphyxia, 3. George Johnson favored bleeding because he thought cholerawas caused by a specific poison in the bloodstream that produced right-sided heart conges-tion, which venesection could relieve; Epidemic Diarrhoea and Cholera 2: Section 10. For sim-ilar views, see review of G. Calvert Holland, Nature and Treatment of Cholera in Lancet 2(1837–38): 488.

110. Lindsay, “Clinical notes on cholera,” AMJ 2 (1854): 1118. Consider also T. M. Green-how: “When patients rally from collapse, it is often most difficult to ascertain on what causestheir emergence from it has depended. I fear various remedies have often obtained the creditwhich has been due to the spontaneous efforts of nature”; “Treatment of malignant choleraat Newcastle,” Lancet 1 (1832–33): 52.


AFTER NOTING WITH INCREASING ANXIETY that cholerawas spreading across Russia and into western Europe in the sum-

mer of 1848, the Lancet reported several confirmed cases of cholera in the Londonmetropolis early in October.1 However, Dr. John Webster, the incoming president ofthe Westminster Medical Society, stated at the opening meeting of the session on 21October that it had not “made much progress in the metropolis” since then despitethe attention given to its advance, whereas influenza and scarlatina received littlepress but were no less dangerous. The minutes reveal that the society was prosper-ing: “the rooms in Saville-row were completely crowded, reminding us of the soci-ety in its most palmy days. About sixty fellows and visitors were present.”2

After the president concluded his remarks and a fellow presented a case report onremoval of a placenta while the patient was under the influence of chloroform, Mr.Francis Hird read a paper on “The pathology and treatment of cholera.” “After giv-ing an account of the disease, and describing the symptoms in a highly graphic man-ner” (perhaps for the benefit of members who were not in the profession during the1831–1832 epidemic), he reviewed “post-mortem appearances he had observed intwelve cases of the disease.”3 In his mind “no known remedies have any specific powerof counteracting the peculiar agency of the poison,” so it was imperative that med-ical men choose remedies likely to counter the known pathological effects of the disease at each stage. Among others, he recommended chalk powder, opium, calomel,

199

Chapter 8

Snow’s Cholera Theory

cayenne, sugar, spirits of cinnamon, mustard emetic, and an enema of starch. If thesedid not check the symptoms, “a mustard poultice, or a flannel wrung out of hot wa-ter, and saturated in a mixture of equal parts of liquor ammoniæ and turpentine,and frictions to the chest, abdomen, and extremities” should be used to maintaincirculatory function and prevent “internal congestions.”4 In the ensuing discussion,Dr. Thomas Peregrine seconded the use of chalk powder and opium in the earlystages of cholera as well as friction and hot applications to the chest and abdomenin its advanced stages, but “Dr. Snow objected to the application of warmth in casesof cholera and founded his objection to its employment on the fact that in cases ofasphyxia such application was injurious. Cholera was not asphyxia, but in somepoints resembling it, so far as the internal congestion was concerned.”5 His thinkingabout the pathology of cholera appears unchanged from that of 1836—that it is afebrile disease.6

Even so, ten months later, at the end of August 1849, he wrote and paid to havepublished an essay, On the Mode of Communication of Cholera, in which he arguedthat “the disease is communicated by something that acts directly on the alimentarycanal,” analogous to intestinal worms (MCC, 8–9).7 He claimed in this essay that “ithas always appeared, from what the writer could observe, that in cholera the ali-mentary canal is first affected” (MCC, 7). Something had raised doubts in his mindabout the theory of cholera asphyxia, for he had come to believe that “the thickenedstate of the blood, which will scarcely allow it to pass through the capillaries,” char-acteristic of late-stage cholera, was a consequence of the “fluid lost by purging andvomiting” in the early stages (MCC, 8, 7). Moreover, it seemed logical to Snow thatthe mucous membrane of the alimentary canal was irritated by a local rather than“an inhaled poison” (MCC, 6). Based on his understanding of gas laws, the physiol-ogy of respiration, and the action of intestinal parasites, he now dismissed the con-ventional notion that cholera was propagated as an effluvium by the respiratoryroute.8 It is unclear why Snow became so interested in the communication of choleralate in the fall of 1848. Perhaps he was intrigued by claims that chloroform was prov-ing effective in treating symptoms as the number of reported cholera cases rose dra-matically. Dr. Webster was wrong about the mildness of this epidemic. Snow dis-cussed his views with several colleagues, including two researchers on the chemistryof cholera evacuations, mailed written inquiries about sewage and water conditionsin areas that were experiencing unusually high mortality, and began a systematicsearch of medical journals and government reports on the subject. When two out-breaks in metropolitan London seemed to offer sufficient evidence to make his caseplausible, he finished a sketch of his hypothesis (MCC) that the cholera poison wastransmitted in the evacuations of its victims and then inadvertently ingested by oth-ers. Within two months he presented a complete theory of the pathology and modeof communication of cholera (PMCC), with substantiating evidence about the as-sociation of the incidence of cholera mortality, water supply, and sewage disposalthroughout England. Because PMCC was produced within two months of MCC and


yet has so much additional confirmatory evidence, one wonders if PMCC was reallySnow’s intended work all along. If so, MCC was, in effect, forced out of him earlyby a sense of public health urgency in the late summer of 1849, when cholera deathswere still mounting during the second year of the epidemic.

The change in his thinking from infection via the lungs to oral–fecal transmissionrequired only a lateral move among contemporary contagionist perspectives. In theopening paragraph of MCC, Snow stated that “an examination of the history of thatmalady, from its first appearance, or at least recognition, in India in 1817, has convincedhim, in common with a great portion of the medical profession, that it is propagatedby human intercourse” (5). While he could have come to this conclusion in 1848 or1849, his known views on typhus, smallpox, and cholera prior to that date suggest thathe was a modified contagionist (perhaps contingently so in certain circumstances) aboutepidemic diseases. He thought the morbid matter could be produced in the bodies ofthe sick and in an effluvial form be inhaled by others; that is, he accepted infection asa mode of transmission as late as his comments about cholera asphyxia at the West-minster in October 1848. The shift from lungs to stomach as the portal of entry re-quired no conversion to a new doctrine. The ingestion route had already been proposedby some contagionists as an alternative to contact and inhalation, but it would have re-quired him to assume that the negative results of autoexperimental ingestion of choleramatter during the 1831–1832 epidemic were inconclusive and to find an analogous dis-ease in which a known agent was not destroyed by stomach acid.9 Snow brought tocholera his personal biases as well as his knowledge and scientific skill. He had longbeen committed to John F. Newton’s philosophy of vegetarianism, including the valueof pure drinking water. Newton’s theory may have prepared Snow for the idea that epi-demic diseases could be caused by material taken orally into the body at a time whenmost believed that causative agents were inhaled.

Out with the Old

After the opening endorsement of the communication of cholera by humans, Snowused the next three paragraphs of MCC to refute the notion that the disease couldbe transmitted only in the form of effluvial infection. He defined the term precisely:“emanations from the sick person into the surrounding air, which enter the systemof others by being inhaled, and absorbed by the blood passing through the lungs”(MCC, 6). As such, he rejected the modified contagionist perspective he seems tohave held until then, as well as the view of local miasmatists who were willing toconsider contingent contagionism in specific circumstances. Snow found it particu-larly “difficult to imagine that there can be such a difference in the predisposition tobe affected or not by an inhaled poison, as would enable a great number to breatheit without injury in a pretty concentrated form . . . , whilst others should be killedby it when millions of times diluted” (MCC, 6).

Snow’s Cholera Theory 201

While his reasoning about the improbability of effluvial infection was respectful,he was downright dismissive of those who supported “the hypothesis of a cholerapoison generally diffused in the air, and not emanating from the sick” (MCC, 6)—that is, general miasmatists of the “epidemic constitutions” persuasion. Perhaps hisresearch into the nature and mechanisms of anesthesia by inhaled gases made himcertain that gaseous vapors alone, whether general or local, could not cause specificepidemic diseases, as miasmatic theory posited. Moreover, his investigation of ar-senical candles had suggested that when a body inhaled a specific poison, it showedthe specific effects of that poison, not the generalized fevers typically claimed for mi-asmatic and local effluvial poisoning. Contrary to the older generation of medicalmen, who dismissed the law of the diffusion of gases as armchair theorizing, Snow’straining and daily experience administering anesthesia made him believe that care-ful attention to the chemistry and physics of gases could have practical benefits. Itwas precisely that which permitted him to use otherwise dangerous medicinal agentswith safety and with exact application to the peculiar needs of each patient and eachsurgical operation.

Neither miasmatic nor effluvial notions that cholera was primarily a blood-bornedisease squared with the clinical and pathological evidence of which Snow was aware.Diseases in which the blood is poisoned at the earliest stages due to an inhaledcausative agent show general symptoms such as headache, chills, and rapid pulse be-fore any localized symptoms appear (MCC, 6–7). In cholera, however, all the con-stitutional symptoms occur later and can be better accounted for by the amount offluid lost from the gut as the result of the massive vomiting and diarrhea and theconsequent state of dehydration (MCC, 7–8). He reasoned, moreover, that the fluidlosses were most likely due to “some local irritant of the mucous membrane” of thegut, rather than to some generally circulating poison, “no instance suggesting itselfto the writer in which a [blood-borne] poison causes irritation of, and exudationfrom, a single surface” (MCC, 8).

In with the New

The argument in MCC is a complex blend of epidemiological evidence, pathologi-cal observations, and bold analogies (Fig. 8.1). Snow needed to formulate some ba-sic assumptions in order to launch his theory. He had to assume that cholera was aspecific disease attributable to a specific exciting cause. He also had to assume thatthe cause of cholera did not act like a typical mineral poison—it caused the diseasein a statistically significant portion of those exposed to it, but not in all of them.That is, “proof” would be a matter of statistical probability and not certainty.10

First, he emphasized humans were central to the spread of cholera. There was sim-ply too much positive evidence to doubt “its communicability” (MCC, 5). He pointedto the many known incidents “in which cholera dates its commencement in a town or


village previously free from it to the arrival and illness of a person coming from a placein which the disease was prevalent . . .” (MCC, 5). The first two cases of cholera inLondon in 1848 proved his point: “Who can doubt that the case of John Harnold, theseaman from Hamburgh . . . was the true cause of the malady in Blenkinsopp [thesecond victim], who came, and lodged, and slept, in the only room in all London inwhich there had been a case of true Asiatic cholera for a number of years? And if cholerabe communicated in some instances, is there not the strongest probability that it is soin the others—in short, that similar effects depend on similar causes?” (MCC, 29–30).


Snow’s Theory

Causative agent

Rice-waterstools

(+ vomit)

Transmissionwithin a household

Transmission overlarge distances

and areas Orally ingested

Entersintestine

Multiplies

Attaches tomucous

membrane

Local irritation,intense exosmosis

of fluids & salts

Hand-to-mouth spread

Constitutionalsymptoms of cholera

Drinking watercontaminatedwith choleraevacuations

Figure 8.1. Snow’s 1849 theory of cholera.

However, the undeniableness of person-to-person spread still left open the specific mode of communication. Having dispensed with the idea that transmissionmust necessarily be by inhalation, he reasoned “by analogy from what is known ofother diseases . . . that in cholera the alimentary canal is first affected” (MCC, 6–7).The primary intestinal symptoms characteristic of cholera suggested that the mor-bid poison had to be ingested. If one looked for an agent that would cause local ir-ritation of the alimentary mucous membrane, the most likely hypothesis was that“the excretions of the sick . . . [contain] some material which, being accidentallyswallowed, might attach itself to the mucous membrane of the small intestines, andthere multiply itself by the appropriation of surrounding matter, in virtue of mo-lecular changes going on within it, or capable of going on, as soon as it is placed incongenial circumstances” (MCC, 8–9). The capacity to undergo “molecular changes”meant that the morbid “material” causing cholera was “organized,” whether living ornot, and obeyed chemical laws. The German researcher Henle argued that some con-tagious diseases were caused and propagated by “certain parasitical organised beings,or their germs,” and Snow’s analogical argument parallels Henle’s.11 Snow thoughtit possible that the unknown causative material in cholera behaved like the ova ofintestinal worms. Extremely small and undetectable by the unaided senses, they re-produce and multiply in the gut. As in cholera, in many cases one cannot trace acase of worm infestation to a known carrier or discover the exact means by whichthe second victim swallowed the ova, but one would not thereby conclude in the sec-ond case that the disorder arose spontaneously (MCC, 9). There were problematicaspects to this analogy. With respect to differences in disease manifestation, wormsproduce indolent, chronic, seldom fatal diseases, whereas cholera is a severe, acute,and often rapidly fatal condition. In addition, Snow had not identified the micro-scopic morbid matter or particles that caused cholera, but neither had anyone else.Still, because the ova of intestinal parasites possessed some of the same properties,he proposed that such a particle was sufficiently within the realm of possibility forhim to proceed with a discussion of its likely modes of communication.

A fecal–oral transmission explained the most likely means by which choleraspreads within a limited area, such as a household. The copious diarrhea of choleravictims makes it certain that clothes and bedding become saturated, and becauserice-water stools lack the usual feculent color and odor, members of the house mayunknowingly soil their hands with cholera evacuations and transfer the morbid ma-terial to their mouths while eating. If the caregivers also prepared food, others wouldprobably ingest the morbid material as well. In any case, the likelihood of such in-gestion increased in the absence of hand-washing facilities and habits of cleanliness(MCC, 9–10). By contrast, when cholera spread rapidly over wide areas, the mostlikely explanation was contamination of drinking water by sewage containing theevacuations from cholera victims (MCC, 11–12). The potential for spread via a con-taminated drinking water supply suggested, in turn, that cholera particles were ca-pable of being infective despite great dilution (MCC, 27).12 In keeping with Snow’s


general scientific approach, his reasoning on the modes by which cholera couldspread were subject to empirical disproof. He realized that his theory would becomesuspect if one were to find that cholera spread within a household in which verycareful hand washing was practiced or throughout a town with an undoubtedly puresource of drinking water.

Elements of Snow’s Hypothesis

In MCC Snow was a pathologist first, a clinician second, and an epidemiologist third.His reasoning proceeded from pathological hypothesis to clinical effects to mode oftransmission, followed by an epidemiological method by which the transmission hy-pothesis could be empirically tested.13 He reinterpreted a point of general agree-ment—what caused the “exudation of the watery part of the blood” into the intes-tines and subsequent discharge by “purging” (MCC, 7). Recent chemical analyses ofthe blood of cholera victims had shown dramatic increases in the proportion ofblood solids to water: “The valuable analyses of Dr. Garrod have recently confirmedwhat had been stated in the former visitation of Europe by the cholera, viz., that thesolid contents of the blood of patients labouring under this disease are greatly in-creased in proportion to the water—a state of the blood that is not met with in anyother malady” (MCC, 7–8).

However, the thickened consistency of the blood was compatible with either oftwo explanations: A poison in the blood pushed water and salts into the intestines,or a poison in the intestines irritated the mucous lining and pulled serum from theblood. Snow’s hypothesis required the latter explanation, whereas it turns out thatGarrod assumed the cause was blood poisoning: “It would appear that the cholerapoison, when introduced into the blood in sufficient quantities, causes an intenseexosmotic action of the mucous membrane of the alimentary canal, at the same timedestroying its endosmotic power. The blood therefore being deprived of a certainamount of water and salts, by the intestinal evacuations, and not possessing the powerof regaining these by absorption from the stomach, becomes altered in the mannerwe have seen. . . .”14 Garrod’s interpretation of his own analyses did not troubleSnow because the evidence supported his own hypothesis. He conducted no chem-ical analyses of his own. It is unclear why at that time he did not cite evidence fromthe 1831–1832 epidemic, which unequivocally favored his view: that the injection ofsaline into the circulatory system temporarily restored bodily functioning in choleravictims. Instead, he offered only personal observations and his experience as a cli-nician in support of intestinal transmission (MCC, 7–8).15

He postulated the existence of an unknown agent or particle that, upon being in-gested, would irritate the mucous membranes of the intestines and eventuate in thefluid losses detailed by Garrod. For his purposes it was sufficient for the cholera agentto be external, capable of being ingested by humans, and then multiplying within


the gut. The agent’s action, not its structure, was critical to Snow’s hypothesis aboutcholera pathology and transmission. Hence, he “appeal[ed] to that general tendencyto the continuity of molecular changes, by which combustion, putrefaction, fer-mentation, and the various processes in organized beings, are kept up” (MCC, 9). Aslong as the agent behaved as required, Snow could be circumspect about the agent’snature without affecting his argument: “The writer . . . does not wish to be mis-understood as making this comparison [to ova of intestinal worms] so closely as toimply that cholera depends on veritable animals, or even animalcules [microscopicorganisms]” (MCC, 9).16 It did not matter whether the agent was living or nonliv-ing as long as it obeyed universal physical and chemical laws and was capable of theaction and transmission that Snow hypothesized.

Snow’s analogy between an unknown causative agent of cholera and the better-known ova of intestinal worms was critical to establishing ingestion as the mode ofentry. His mode of transmission required that the particle could multiply, for whichthere existed an analogy in the reproduction of animal parasites. Snow was a rarityamong midcentury contagionists in thinking that parasitic worms could illuminatethe problem of contagious diseases generally.17 Many of his contemporaries believedthat parasitic worms were spontaneously generated within the human gut rather thanarising from ingested ova.18 The most extensive work on parasitic worms during theperiod 1780 to 1840 was conducted in Germany by scientists who tended to supporta theory of spontaneous generation. According to Farley, “the more expert one wason parasitic worms, the more likely one was to embrace the doctrine of spontaneousgeneration” (106). V. L. Brera, however, had proposed in 1798 that one could becomeinfested with worms by ingesting their eggs as part of a diet of animal food. His Trea-tise on Verminous Disease was translated into English. Although most English writ-ers on worms opposed spontaneous generation, usually on philosophical grounds,Snow the vegetarian would have found Brera’s argument congenial long before writ-ing MCC.19 Also available to him was an English translation of J. J. S. Steenstrup’sOn the Alternation of Generations (1845). Steenstrup described the life cycle of theliver fluke, showing that the source of the egg might be an animal superficially quitedifferent in appearance from the generation that hatches from it. His research elim-inated a major barrier to a contagionist view of parasitic infections, showed that in-testinal worms issued from the ova of worms, and generally undermined the doc-trine of spontaneous generation shortly before Snow used the worm analogy forcholera.20

Supporting Evidence in MCC

Snow formulated his new hypothesis of cholera pathology and transmission duringthe last few months of 1848. At the time “he hesitated to publish them, thinking theevidence in their favour of so scattered and general a nature as not to be likely to


make a ready and easy impression. Within the last few days [of August 1849], how-ever, some occurrences have come within his knowledge which seem to offer moredirect proof . . .” (MCC, 12). The bulk of his essay is a description and analysis oftwo local outbreaks south of the River Thames, followed by some suggestive remarkson cholera mortality in relation to metropolitan water supply. He intended to pre-sent more evidence but was content with the proviso that, “These opinions respect-ing the cause of cholera are brought forward, not as matters of certainty, but as con-taining a greater amount of probability in their favour than any other, in the presentstate of our knowledge” (MCC, 29).

The “occurrences” that tipped the balance toward premature publication were tworeports by John Grant, an assistant surveyor for the Commission of Sewers. On 9August 1849 Grant had written up the results of his investigation into “The Condi-tion of Surrey Court, Horsleydown,” in which there had “been an excessive mortal-ity from cholera—nine or ten deaths in five days”:

There are thirteen houses in the court, which is built up at both ends, andbadly ventilated; there is an open ditch at the end, and the house-drainage isinto cesspools, with common privies in small back areas. The houses in thiscourt and those in Truscott’s buildings (another court) have a double set ofsmall privies, cesspools, and small areas between the backs of them. Althoughthere has been such mortality in Surrey court, there has been but one case (thatof an infant) of cholera in Truscott’s buildings. The only apparent cause towhich this difference can be attributed is, that in Surrey court the inhabitantsused the water of a well in the court, the mouth of which was on a level withthe paving and a gutter or side channel by which foul water was admitted intothe well. This well the parish authorities have had cleaned out, and the mouthof it raised.

Despite the renovations to the well, however, Grant recommended that the inhabi-tants be temporarily relocated until the open ditch was replaced by sewer pipes. Inhis mind escaping sewer gases during drainage repairs could produce more choleracases.21

Two aspects of this report would have caused Snow to think that the Horsley-down outbreak could provide empirical evidence for his new notion that the mor-bid matter of cholera was ingested rather than inhaled. First, drinking water hadbeen contaminated by sewage. Second, the contamination had occurred only inone of two neighboring courts—that is, the outbreak had a control sample, or, inthe terminology of the time, it constituted a “natural experiment.” Grant’s reportwas insufficient to establish that the well had been contaminated by excrementfrom cholera patients, so Snow spoke with the attending practitioners to deter-mine the chronological order of attacks and details about their disposition (MCC,12–15).


The second local outbreak of cholera that Snow believed offered support for hishypothesis had occurred in late July and early August 1849 in Albion Terrace,Wandsworth Road. Again, a report by Grant on sewage overflow into drinking wa-ter caught his attention (MCC, 16). As with Surrey Court, Snow described the lay-out in great detail for readers of MCC, drawing upon Grant’s investigation.22 Weconstructed diagrams of the drains and water supply at Albion Terrace based onSnow’s description in MCC (Fig. 8.2 and Fig. 8.3). Snow was thinking in spatial andtopographic terms, although he made no diagrams himself.23

Snow’s investigative technique for the two cholera outbreaks described in MCCconformed to that of a “village epidemiologist” who attempts to establish the sourceof an outbreak of infectious disease within an area no greater than several cityblocks.24 He established that the two outbreaks shared a number of defining features.One or two cases of cholera appeared in the neighborhood, probably contracted else-where, which was no greater than the general incidence of cholera in that part ofmetropolitan London. In Snow’s view these cases of cholera could not have produceda sudden epidemic outbreak unless the means existed by which water contaminatedwith the evacuations from resident cholera victims could become mixed with thedrinking water supplied to nearby houses. In Horsleydown the means for contami-


Brick drain (to sewer to Battersea Fields)

Water storage tank(brick & cement)

Brick drain

48"

HOUSE

Lead pipe to pump in kitchen

Cesspool(beneath privy)

6" stonewarepipe (from

spring)

Figure 8.2. Diagram of house drainage at Albion Terrace. Drains, water pipes, and tanks were

found to have leaky joints. Water levels in the cesspools and drains were higher than the lev-

els in the water tanks (adapted from Snow, MCC).

nation were ongoing, whereas in Albion Terrace contamination had occurred onlyonce, during a severe rainstorm. Consequently, after several days many cases brokeout almost simultaneously in other houses using the common water supply. Snowbelieved he detected organic impurities when making visual examinations of thedrinking water supply that he considered suggestive of sewage contamination. Thefact that no similar outbreaks occurred in nearby houses with different sources ofdrinking water but exposed to similar local atmospheric conditions meant that thecause in both locations was communicability of a specific cholera poison via inges-tion, not inhalation of miasmas.

In addition to the two outbreaks traceable to local contamination of drinking wa-ter, Snow hypothesized that river water contaminated by cholera evacuations ex-plained variations in cholera mortality throughout metropolitan London. The de-termining factor was the source of the drinking water supplied by various watercompanies. From the Weekly Returns of Births and Deaths published during the cur-rent cholera epidemic, Snow devised a table that listed the number of deaths by re-gional districts. The west, north, and central districts had the smallest percentage ofdeaths, and many residents there received piped drinking water from commercialcompanies whose sources were upstream of any major contamination by sewage.The greatest percentage of deaths—seven times higher than in north London—oc-curred in south London, where the water companies supplying those districts drewfrom the tidal zone of the River Thames, near the outlets of large municipal sewers.The east district had four times the average mortality, which was surprising to Snowbecause the East London Water Company had shifted its source to a point abovetidal reach of the River Lea. He suspected the company still drew some water from


765

Cesspools full;apparently over-flowinginto drinking water tanks

1 2 3 4 1413128 9 10 11 15 16 17

Drinking water in all housesfound to be impure after 26 July

Spring

Drains

To sewer,Battersea Fields

First cholera case(28 July)

Drain burst duringheavy rain on 26 July;

lower level floodedwith fetid water

Figure 8.3. Diagram of Albion Terrace showing main events suggesting sewage contamination

of drinking water at a time when cholera evacuations were present in the sewage (adapted

from Snow, MCC).

reservoirs at Old Ford that were filled from a portion of the Lea heavily contami-nated by sewage outflows. He had been unable, however, to obtain the “exact infor-mation” he desired on water supply for each part of London (MCC, 25). His tablecould show only a rough association among the rate of cholera deaths in each of fivebroad districts and what he could preliminarily determine about the sources of drink-ing water used by the commercial water companies. That is, his argument that cholerawas transmitted in metropolitan London via contaminated river water was very in-conclusive, but he did note that population concentrations and associated effluviain South London would not favor local miasmatic or contingent contagionist ex-planations of high cholera mortality in that region: Central London is “quite on apar with the worst parts on the south of the Thames as regards overcrowding andbad smells” (MCC, 25).25

Anticipating Criticism

Snow anticipated possible objections to his hypothesis, especially from sanitary au-thorities who reasoned that general impurities either contained the cholera poison orpredisposed individuals to fall victim to it. He was aware that Dr. Gavin Milroy, whowas associated with the GBH, had investigated the outbreak in Albion Terrace and at-tributed the high mortality to a combination of factors: In Snow’s words, “firstly, to anopen sewer in Battersea Fields, which is 400 feet to the north of the terrace, and fromwhich the inhabitants perceived a disagreeable odour when the wind was in certaindirections; secondly, to a disagreeable odour from the sinks in the back kitchens of thehouses, which was worse after the storm of July 26; and lastly, to the accumulation [ofoffensive rubbish] in the [cellar of] house No. 13 . . .” (MCC, 21–22). Snow coun-tered each of Milroy’s explanations with several of his own:

With respect to the open sewer, there are several streets and lines of houses asmuch exposed to any emanations there might be from it, as those in which thecholera prevailed, and yet they were quite free from the malady, as were alsonineteen houses situated between the sewer and Albion Terrace. As regards thebad smells from the sinks in the kitchen, their existence is of such every-day,and almost universal prevalence, that they do not help to explain an irruptionof cholera, like that under consideration; indeed, offensive odours were cre-ated in the thousands of houses, in London, by the same storm of rain on July26th; and the two houses in which the offensive smell was greatest, viz. Nos. 8and 9,—those which were flooded with the contents of the drain,—were lessseverely visited with cholera than the rest; the inhabitants having only had di-arrhœ a or mild attacks of cholera. The accumulation in the house No. 13could not affect the houses at a distance from it.

MCC, 22


Because local spread of effluvial vapors could not explain why some residents in ad-joining houses did not contract cholera or why vapors generally present should sud-denly become poisonous, Snow concluded “that the only special and peculiar causeconnected with the great calamity which befel the inhabitants of these houses, wasthe state of the water, which was followed by the cholera in almost every house towhich it extended, whilst all the surrounding houses were quite free from it” (MCC,22–23).26

Snow also anticipated a possible objection to the contaminated river water por-tion of his hypothesis. To those who assumed that the immense quantity of waterin rivers as large as the Thames would sufficiently dilute the cholera poison to ren-der it harmless, he proposed that “the poison consists probably of organized parti-cles, extremely small no doubt, but not capable of indefinite division, so long as theyretain their properties” (MCC, 26). Although cholera evacuations diluted in theThames lessened the chances that a given glassful of Thames water contained poi-sonous particles, every particle retained the power of reproducing within the gut anddoing its mischief.

He anticipated criticism of his hypothesis on two other counts. Some might ob-ject that stomach acid would destroy the ingested cholera poison, whatever its formor source. Snow admitted the possibility, noting that it might explain why some peo-ple were able to resist “its effects,” whereas those whose “digestive powers have beenweakened by a fit of drunkenness” could not (MCC, 26). In this instance he referredto a common belief that excessive drink increased one’s susceptibility to cholera. Forsome reason he decided not to anticipate a reasonable anticontagionist rebuttal: sev-eral autoexperiments in the 1830s in which those who had swallowed cholera ex-cretions or vomitus generally failed to contract the disease.27 He admitted the pos-sibility of airborne transmissions from victims to healthy persons, but not asunderstood by the theory of infection. In his view airborne cholera particles had tobe ingested to cause the disease: “the organic part of the fæces, when dry, might bewafted as a fine dust, in the same way as the spores of cryptogamic plants, or thegerms of animalcules, and entering the mouth, might be swallowed” (MCC, 27).28

Prevention of Cholera

In the penultimate paragraph of MCC, Snow outlined a few socially practical andcommercially unintrusive measures by which “cholera might be checked and kept atbay” (MCC, 30). He considered it prudent for “all persons attending or waiting onthe patient to wash their hands carefully and frequently, never omitting to do so be-fore touching food, and for everybody to avoid drinking, or using for culinary pur-poses, water into which drains and sewers empty themselves; or, if that cannot beaccomplished, to have the water filtered and well boiled before it is used” (MCC,30).29 These recommendations would deter the ingestion of cholera particles,


whether dissolved in drinking water or invisibly saturated in the victim’s linens. Theyalso reflect his extension of Newton’s distilled water regimen into the public healtharena, as he had advocated years earlier in his teetotal address. Whereas simple clean-liness in the household could prevent incidental transmission of cholera, Snow be-lieved “the sanitary measure most required in the metropolis is a supply of water forthe south and east districts of it from some source quite removed from the sewers”(MCC, 30). That would prove to be a more contentious and expensive proposal.

Snow’s simple measures for preventing cholera were significant at the time forwhat they did not include. He did not advocate quarantine. Much of the anticonta-gionist sentiment, especially in maritime nations, was a reaction to quarantine. Snowmade it clear that the preventative measures his hypothesis called for “would not in-terfere with social or commercial intercourse” (MCC, 30).30 In his view cholera wascommunicable in only very limited circumstances and in very specific ways. If onelinked quarantine with “contagion” theory and equated “contagion” with transmis-sion either by touch or by (inhaled) infection, then cholera was not contagious bythose criteria. His hypothesis suggested that focused reforms in behavior would keepcholera at bay. He supported cleanliness in general, but only certain practical mea-sures would prevent the spread of cholera—hand washing by caregivers and foodhandlers who were likely to encounter cholera patients and assuring that drinkingwater was not contaminated with sewage that might contain cholera evacuations.

Initial Elaborations of MCC

After MCC appeared Snow became preoccupied with additional on-the-spot researchat Albion Terrace. Later published reports had differed from his own account, por-traying events in such a way that a local miasmatic explanation of the outbreakseemed more probable.31 Snow reinterviewed one of the local surgeons and inter-viewed a gardener who had helped clean up debris from a burst drain after a sec-ond thunderstorm in August. The gardener had subsequently fallen ill of cholera butrecovered. Snow recounted for the medical audience the facts that confirmed his ownexplanation of contaminated water as the source of the outbreak and that rendereda miasmatic account unlikely. He concluded the letter with a remark that he hadnearly finished a more extended paper containing “a variety of details, collected fromdifferent parts of the country, which show the connection between tainted water andthe extension of cholera, and also the great freedom from cholera, both now and in1832, enjoyed by certain large towns . . . that have a plentiful supply of water thatis totally unmixed with the contents of sewers.”32

Snow kept his promise, delivering the paper “On the pathology and mode of com-munication of cholera” in mid-October at the Westminster Medical Society, whichwas published shortly thereafter under the same title (hereafter PMCC). Althoughhe reused passages (some verbatim) from MCC and preserved its organizational


structure, PMCC provided the additional substantiation necessary to transform asuggestive hypothesis into a theory that could be falsified by evidence at variancewith its conclusions (PMCC, 746–47).33 Snow slightly expanded the discussion ofthe pathological process found in MCC. He noted that the difficulty in breathing ex-perienced by cholera victims in advanced stages was caused by the thickened stateof the blood obstructing pulmonary circulation. Such capillary congestion also ex-plained reduced urinary output, accumulation of urea in the blood, and the albu-men present in whatever urine was produced (PMCC, 745). The other significantdifference in the pathology section was his replacement of the phrase “general ten-dency to the continuity of molecular changes” with a vaguer reference to “a kind ofgrowth . . . like any other morbid poison” (PMCC, 746). Near the end of the es-say, he stated that “a poison capable of multiplying in the body must, one wouldconclude, be organized, and therefore consist of particles, however minute . . .”(PMCC, 928). He admitted the possibility that the poison might be a chemical com-pound capable of being imbibed by epithelial tissue.34 Even so, he considered its na-ture relatively unimportant because its action, mode of propagation, and the mea-sures necessary to prevent it from spreading were clear if one accepted his theory.

Snow devoted the bulk of the two-part article to substantiating his theory by pre-senting “instances of severe [cholera] visitation, or of exemption from its ravages”(PMCC, 747) (Table 8.1). By what means did Snow accumulate such a rich set of ex-amples to support his theory in October, when in August he had almost withheldpublication because he had so little evidence? His footnotes (much more numerousin PMCC than in MCC) show that he had consulted published literature, includingreports by parliamentary committees and case reports in medical journals. In otherinstances he made use of personal contacts and correspondents. For example, hecited excess fatality in the village of Newburn, near Newcastle. He learned of it bywriting a general letter of inquiry to a friend in Newcastle, Dr. Dennis Embleton,who procured information from a Rev. John Reed and put Snow in touch with a lo-cal surgeon, Mr. Robert Davison. Examples from York and Bath indicate he reliedon personal and family acquaintances. In other cases it appears that fellow membersof the Westminster Medical Society provided information or names of potential in-formants. Perhaps, as Snow’s theory matured in the summer of 1849, he had begunto initiate these inquiries by post but had not received enough complete answers intime to include the data in MCC. After his water-borne theory of cholera transmis-sion was printed in early September, correspondents submitted unsolicited examplesand counterexamples in letters to the editors of the medical journals.

He limited evidence from the London metropolis to “instances of severe visita-tion, or exemption from its ravages”(PMCC, 747), beginning with a summary of hisfindings in Horsleydown and Albion Terrace. He noted similar point-source out-breaks where well or Thames-ditch water, contaminated by evacuations from choleravictims, had caused the epidemic outbreaks regardless of the level of the ground, thestate of the air, the classes of the inhabitants, or the type of housing. He also noted


places where cholera should have occurred, according to a rival theory, but had notbecause the water was uncontaminated by sewage. He noted that districts south ofthe Thames had suffered the greatest mortality in both epidemics, indicated that hewas “endeavouring to compile a full account of the recent epidemic in London, inits relation to the water,” but that he would say no more about it until he had com-pleted his investigations (PMCC, 747).


Table 8.1. Substantiating evidence in PMCC

Provincial towns: Provincial towns:London Affected Exempted

(Study of south Londonwater supply: deferred)

1. Horsleydown: SurreyBldgs. affected; Truscott’sCourt exempt

2. Albion Terrace: affected;nearby houses exempt

3. Silver Street, Rotherhithe

4. Charlotte Place,Rotherhithe

5. Specific examples:(a) Contaminated wells

and ditches(b) Bethlem Hospital,

Queen’s Prison:exempt with unconta-minated wells despitenearby neighbor-hoods affected

c) Millbank Prison: waterdrawn from Thames,affected althoughnearby neighborhoodexempt

6. Westminster districtsovercrowded and low-lying, but little cholerabecause water pure

7. Brixton: open streets,rising ground, middleclass, but high mortalitybecause water sewage-contaminated

1. Bath (one neighborhoodonly): local wellcontaminated bycesspools

2. York: mortality dependedon whether water drawnfrom river above orbelow sewers

3. Exeter: water worksrepositioned upstream,reduced mortality

4. Hull: New water worksbut drew water from tidalriver, mortality increased

5. Dumfries: water fromtidal river, high mortality

6. Newburn (nearNewcastle): well watercontaminated by sewerdrain

7. Bilston: watercontaminated by minepits, high mortality

8–10. Metthyr, Tydvil,Kendal: sewage seepedinto wells

1. Birmingham: riverpolluted by sewers butdrinking water obtainedelsewhere

2. Bath: piped water fromsurrounding hills

3. Cheltenham: drinkingwater free of sewage

4. Leicester: river pollutedwith sewage, low-lying,but drinking water fromsprings

5–7. Preston, Oldham,Paisley: drinking waterfrom surface drainage ofnearby hills

8. Nottingham: filtered riverwater upstream fromsewers

9. Stafford: watercontaminated withsewage, but individualwells with no centralsupply, so any outbreaksconfined to only a fewhouses (i.e. impure wateritself did not causecholera)

Snow discussed several provincial towns visited by cholera in the epidemics of1831–1832 and 1848–1849 where the water could be blamed. Some outbreaks couldbe attributed to water drawn from wells, springs, and mine pits contaminated by fe-ces from cholera initially transmitted interpersonally. In others the attributed causewas a river that served both as a source of water and a receptacle for the town’ssewage. In two towns Snow associated mortality differences in the two epidemicswith the water supply. The water works in Exeter had been repositioned upstreamof sewer outlets after 1832, and mortality was reduced in the current epidemic. InHull, however, the water works built after 1832 drew river water from a tidal zonecontaining intermittent sewage, and the mortality rate increased dramatically dur-ing the second epidemic.

Snow considered negative evidence equally significant for his theory, and he de-scribed nine towns he believed were exempt from cholera because their water wasuncontaminated by sewage. It did not matter whether drinking water came fromwells, rivers, springs, or surface run-off as long as it was pure. He cited Stafford toshow that impure water would not cause cholera unless the impurities includedevacuations from cholera victims. According to a resident physician, water in thetown’s many wells often contained sewage sediments, but each well was used onlyby a small cluster of houses. There were no epidemic outbreaks of cholera inStafford because the water sources were separate from one another, not intercon-nected as in many large cities. Cholera outbreaks were thus limited to one house-hold, or a few at most.

Snow explained how his theory of the pathology of cholera explained the differ-ences in epidemic duration exhibited in villages, towns, and cities. Population sizedetermined when the disease ran out of fresh victims in which to multiply, and con-trary to “the usual theory of contagion or infection . . . all the members of thecommunity are not liable to be reached by a poison which must be swallowed, asthey would be by one in the form of an effluvium” (PMCC, 928). As in MCC, hepresented a list of preventive measures, adding recommendations to avoid “the fruitthat is hawked about the streets” during an epidemic (it was often stored at nightunder beds and was liable to become contaminated) and altering the shifts in minesso workers did not have to eat in the pits (PMCC, 929).

Snow and the Bristol Cholera Fungus Theory

Snow was not the only English investigator to be alert to the intestinal worm anal-ogy and thereby to decide that fecal–oral transmission would explain cholera databetter than any inhalation theory. MCC appeared less than a month before a pam-phlet on the cause and transmission of cholera by William Budd of Bristol. The dis-missal of the Bristol fungus theory by the London medical establishment suggestedthe barriers Snow had to overcome before his theory would be accepted.


William Budd (1811–1880) is best known today for his discovery that typhoidfever is a water-borne contagion. In 1828 he visited Paris to study under François J. V. Broussais and other figures in the development of hospital medicine. Broussaisbelieved that all fevers were caused by local inflammations seated in the gastroin-testinal tract, which may account for Budd’s inclination toward a localized gas-trointestinal pathology in cholera as well as in typhoid.35

In late September 1849 Budd presented a theory of cholera in the form of fivepropositions:

1. That the cause of Malignant Cholera is a living organism of a distinct species.2. That the organism . . . is taken . . . into the intestinal canal, and therebecomes infinitely multiplied by self-propagation. . . .3. That . . . the action that [the organisms exert in the intestine is] the causeof the peculiar flux which is characteristic of malignant cholera. . . .5. That these organisms are disseminated . . . in the air, . . . in contact witharticles of food; and . . . principally, in the drinking water of infected places.36

Budd had timed publication of his theory to coincide with reports from two fellowinvestigators in Bristol, Frederick Brittan and Joseph Swayne, who claimed to havediscovered the fungus particle that was the causative agent of cholera,37 but micro-scopists in London were unconvinced. On 17 October 1849 George Busk demon-strated to the Microscopical Society of London the presence of the same fungus par-ticles in a loaf of bread; the suspected cholera cells were simply spores of the uredosimilar to that that causes smut in grain.38 Three days later Edwin Lankester affirmedBusk’s findings at a meeting of the Westminster Medical Society.39 Other researcherswondered if the particles were even fungoid. Regardless of the precise identificationof the particles, professional opinion expressed in the London medical journals wassoon virtually unanimous that the Bristoleans’ claim to have discovered the causativeagent of cholera was premature.40

Although Budd’s theory could stand independently of his colleagues’ identifica-tion of a specific fungus or causative organism (Fig. 8.4), his later willingness to ac-cept inhalation for the transmission of cholera under certain circumstances raiseddoubts about the consistency of his theory. In 1854 he described a cluster of casesarising in a hospital ward among patients who shared the use of a privy and blamedthe spread on inhalation of “effluvia” arising from cholera evacuations.41 This mod-ification put him in the position of claiming, on the one hand, that cholera wasclosely analogous to intestinal diseases caused by animal parasites, which presum-ably spread only when one ingested the parasitic eggs orally, and on the other, thatcholera could be spread just as readily by inhalation as by fecal–oral transmission.If one postulated the latter, it was easy to see why cholera should be first and fore-most a disease of the alimentary canal, but if the cholera agent could also be takeninto the body via the lungs, it becomes more difficult to understand why only the


gastrointestinal tract should be affected—or why cholera transmitted via the lungsshould show the same signs and symptoms as cholera transmitted by a fecal–oralmode.

Snow agreed with Budd that cholera was a gastrointestinal disease, that its non-gastrointestinal features arose from dehydration, and that water contaminated withcholera evacuations was a major source of spread, but they disagreed on two keypoints: that inhalation was a feasible mode of transmission under some circum-stances and that the actual causative agent of cholera was the “fungus” identified byBrittan and Swayne. Budd’s reasoning on the inhalation issue was similar to that ofthe contingent contagionists, who argued that if two cholera outbreaks seemed to


Budd

cholera fungusevacuated

in stool

Cholerafungus

oralingestion

symptomsof cholera

inhaledin lungs

reproducesin gut

notexplained

spread overdistancesby water

supply

householdspread

bycontact

Figure 8.4. Budd’s contagion theory.

follow two different patterns, it must mean that the cholera poison acts differentlyunder different circumstances (“contingencies”). Snow, by contrast, considered hisview of cholera pathology the foundation of his theoretical edifice and refused to al-ter it in order to explain apparently anomalous outbreaks. Given the mind-set ofmost of his colleagues, Snow’s decision guaranteed that he would be viewed as a rad-ical, inflexible thinker compared to someone like Budd, whose willingness to con-sider multiple routes was mainstream at the time.42

Apparently, Budd considered it premature to suggest that cholera could spread viawater contaminated by the excrement of its victims unless he could point to a spe-cific cholera-causing agent in the water. Hence he joined his Bristol associates inidentifying a fungus as that agent. Snow at first suggested that the Bristol fungus dis-covery lent credence to his own theory, but he soon drew back and then dissociatedhimself completely from the fungus claim.43 In so doing he continued a policy oftheoretical parsimony that played to his strengths as a medical researcher. He hadtwo pathways to follow in building evidence for his hypothesis: the microscopic routeof identifying and investigating the particle, or the epidemiological–statistical routeof tracing the consequences of his theory over large areas and among large popula-tions. He was not a microscopist, but his understanding of the collateral medical sci-ences of statistics and epidemiology was sophisticated. Detailed suggestions aboutthe specific nature of the cholera agent would have been distracting and potentiallycounterproductive to his purpose: to prevent the transmission of cholera withinhouseholds and through contaminated drinking water.

In taking this approach Snow revealed a singular sense of focus. He realized thathe had to ground his theory of cholera transmission in the pathology of cholera inorder to make it plausible. The spread of cholera by oral ingestion and the nature ofcholera as a localized disease of the alimentary canal were two sides of the same coin.The pathological account forced him to propose the existence of a particle with thecapacity to multiply and produce the characteristic symptoms of the disease. Heneeded to say no more about the cholera agent to propose a testable hypothesis,44

but this line of reasoning made Snow vulnerable to criticism from infection conta-gionists and local miasmatists, who assumed the morbid material was transmittedthrough the air and then inhaled. The poisonous agent for their mode of transmis-sion was as mysterious as Snow’s, but why reject clinical wisdom accumulated overtwo millennia on hypothetical grounds alone? Perhaps that was why Budd and hisBristol colleagues believed they could proceed no further with their line of investi-gation unless they could demonstrate the existence of the infectious agent. In fact,Budd’s endorsement of Snow’s 1849 hypothesis was conditional precisely becauseSnow did not specify the nature of the infectious particle: “Of being the first to de-velop and to publish this very important conclusion”—that cholera is transmittedby contaminated water—Snow “must, therefore, have the whole merit. To no part ofthis merit do I lay the slightest claim. . . . The detection of the actual cause of thedisease, and the determination of its nature, were all that was wanting to convert


[Snow’s] views into a real discovery.”45 Presenting a plausible mode of transmissionwithout identifying the “actual” particle fell short of the ideal for some who other-wise agreed with Snow.

The Structure of Snow’s Thought

Snow’s early writing on cholera displayed the patterns of scientific inquiry that he de-veloped during his early research work between 1838 and 1846 and then consolidatedin his work on ether and chloroform. Table 8.2 shows how the multilevel systems-pattern of his thinking came to full fruition in the study of cholera transmission.

Snow considered the human organism a complex system in interactions with othercomplex systems. For him the “person” was a hierarchy of systems that could be stud-ied at many different levels of organization, from molecules at the lowest and small-est end to nations and continents at the highest and largest end. Each level of orga-nization was associated with a collateral scientific discipline that was suited for thestudy of the natural phenomena that tended to occur at that level.46 This hierarchyof systems provided the medical scientist with alternative ways of investigating healthand disease. Sometimes one could observe the phenomenon directly. At other timesthe phenomenon could best be understood by observing its ripple effects at otherorganizational levels. For example, one could understand something about the ovaof parasitic worms by direct microscopic inspection, whereas one could understandthe contagious poison of smallpox only by seeing how it affected the body and itscomponent organs and tissues. He was (in today’s terms) an interdisciplinary thinker.He appreciated not only the horizontal levels of the hierarchy but also the verticalchannels of communication that linked the levels. He saw causal linkages at a singlelevel, where one could understand cause–effect chains within one science, and be-tween levels, when one needed to integrate the methods of different sciences to cap-ture the phenomenon under study. His use of the term “mode of communication”broadly suggests how he envisioned the cycling of matter both within and amonglevels.47

Snow’s systems thinking required a sequence of steps. First, he reviewed the vastscientific literature on cholera and selected the key facts that seemed least open todispute. He laid out in the opening pages of MCC what he took to be the leadingfacts: how cholera followed trade routes across continents; how early symptoms af-fect the gut and how constitutional symptoms arise only after dehydration; and howthe blood is thickened and lacking in water and salts. As such, he was thinking atmultiple levels by collating geographic and epidemiologic data with clinical, patho-logical, and chemical data. In somewhat similar fashion Snow took as his point ofdeparture in ether anesthesia the realization that the inconsistent clinical effects of ether might be explained by the quantity inhaled, which depended largely on concentration of the vapor at different air temperatures. For a coherent theory of


Table 8.2. Snow as a systems thinker on cholera transmission

Hierarchical level Collateral science Reasoning Cholera findings or implications

Nation or continent Geography Induction Appeared to follow trade and travel routes

Large town or city Vital statistics, descriptive Deduction Cases increased in areas where populace used sewage contaminated sociologya water (especially river)

Neighborhood Vital statistics, numerical Deduction Cases increased where point source of drinking water (pump,method (of Louis), cistern, etc.) contaminated with cholera feces, or wheredescriptive person-to-person communication occurred (due to, e.g.,sociology occupational patterns such as in coal mines)

Household Vital statistics, numerical Deduction Cases increased where food preparer or eater had hands soiledmethod (of Louis), descriptive with cholera feces, or where drinking water was contaminatedsociology with feces

Person Clinical medicine Induction Constitutional symptoms arose only after dehydration

Organ systems Physiology, pathology Induction Early symptoms confined to gut

Deduction Other organ systems affected late by thickened blood anddecreased circulation

Tissues Pathology Induction Minimal autopsy findings overall; sometimes bowels filled with fluideven when there had been no cholera evacuations during life

Deduction Causative agent or particle must be local irritant to gut membranecausing massive fluid loss

Microscopic particles Microscopy Deduction Causative agent not yet seen but has functional attributes:swallowed; excreted via feces; capable of multiplication withingut; in process of multiplication causes gut irritation that leadsto diarrhea, partial analogy to ova of intestinal worms

Molecules Chemistry, Physics Assumption Continuous molecular changes: complex particles capable ofmaintaining structure and multiplying by assimilatingsurrounding material; follow laws of chemistry and physics;no clear line between vital and nonvital processes; analogies toputrefaction and combustion

Induction Blood lacks elements (water, salts) that are found in increased quantity in stools

a This term was not in use in Snow’s day. We mean by it a qualitative understanding of the habits and practices of the population in question.

cholera to emerge from the disparate facts he gathered in the fall of 1848 and earlywinter of 1849, he needed the insight that the dominant view, (contingent) conta-gion equals infection, was an unwarranted and unproven assumption. Thereafter, heneeded the analogy between the postulated cholera particle and the ova of intestinalworms to link his pathological hypothesis (cholera as confined to the gut), his chem-ical hypothesis (cholera poison as a sort of organized particle capable of multipli-cation in a suitable environment), and his transmission hypothesis (fecal–oralspread).

Once he had a unified hypothesis, he could deduce expected phenomena at otherlevels of the systems hierarchy.48 At this step he used a hypotheticodeductive modelof science similar to Herschel’s formulation, including the insight that advances of-ten come from collating information among several scientific disciplines rather thanfrom pursuing research solely within a single discipline.49 He then surveyed variousdeductions and asked which occurred at levels of the hierarchy where the relevantcollateral science had developed the most useful tools of observation and inquiry.Snow began with a suspicion that microscopy was the thinnest reed upon which tolean his inquiries. Therefore, he made deductive leaps to adjacent organizational lev-els, the tissue and the molecular levels. From observations at those adjacent levels,he could in turn deduce the functional properties of the purported cholera particle,such as its irritation of the mucous membrane resulting in exudation of fluid. WhenSnow heard about the Bristol fungus, he realized that Budd and colleagues claimedto have discovered a structure without discerning anything useful about its function.Until he had some reason to believe that the fungus particle shared important func-tional characteristics with the cholera agent that he had deduced, Snow felt littletemptation to pursue that line of inquiry.50

Finally, Snow adopted the scientific tools of the relevant collateral sciences to de-termine if cholera behaved as his theory predicted. He found empirical evidence tosupport his theory. The evidence would be stronger to the extent that it could befound at multiple levels of the systems hierarchy and discovered by the techniquesof different collateral sciences. Snow reported the results of his initial inquiries re-garding the household and the neighborhood levels of organization in MCC. InPMCC he was able to add evidence drawn from larger geographic regions thanks tohis correspondence and more extensive review of the literature. Snow believed thata more detailed inquiry into the water supply of the different districts of London—especially south of the Thames, where cholera mortality was highest—would pro-vide even more telling evidence, but he decided to publish PMCC without substan-tiating his theory at the metropolitan level of population density.51 Snow approachedthe highest level of sophistication in systems thinking when he proposed in PMCCthat one could use his theory of the mode of transmission of cholera to explain thedifference among villages, towns, and cities in the duration of epidemic outbreaks.To a modern epidemiologist he was beginning to explore the idea of the “epidemiccurve,” the mathematical laws that epidemics must follow. He appreciated the fact


that if one took the same mode of communication, fecal–oral spread, and applied itto populations of different sizes, the disease should behave in different ways. He was able to reason directly from disease pathology in the individual patient to pop-ulation-level manifestations. That is, he reasoned from micro- to macro-level phenomena.

Snow addressed the cholera problem from this intellectual platform in 1848 and1849 in full confidence. He had, after all, used this same approach to ether anesthe-sia during the first half of 1847, placing both the science and the practice of ether-ization on a firm footing in short order. Snow saw no reason why cholera transmis-sion should not be amenable to the same strategy, but he miscalculated his intendedaudience. When Snow administered ether to a patient, he had a known agent, andthe results of the intervention could be directly observed by any witness. With re-spect to cholera, however, he posed an unknown agent and argued for a mode ofcommunication that was essentially invisible. Although he believed in the late sum-mer and fall of 1849 that the available evidence satisfied his personal threshold forpublishing a new cholera theory, he would soon find that his medical colleagues andthe public health bureaucracy considered it inadequate and unpersuasive.

Notes

1. “Medical news,” Lancet 2 (12 August 1848): 195–96; Lancet 2 (9 September 1848): 303–04;Lancet 2 (16 September 1848): 331–32; and Lancet 2 (14 October 1848): 436. For a progressmap, see Bonderup, “Cholera-Morbro’er” og Danmark, 20.

2. “Westminster Medical Society,” LMG 42 (1848): 768.3. LMG 42 (1848): 769.4. Ibid., 769–70.5. Ibid., 770. Copland classified both “asphyxy” and “cholera” as “nervous diseases”; Dictio-

nary, 1: 128, 318. Cholera asphyxia was a commonly used term at the time; see J. G. French,“Observations on cholera.” LMG 38 (1846): 328, in which he wrote, “Dr. Copland states thatparalysis of the lungs is essentially the disease, and proposes the name of Pestilential Asphyxyfor it.” Copland’s definition of asphyxy was “suspended animation proceeding from a primaryarrest of the respiratory actions, the other functions being thereby abolished”; Dictionary 1:128. Snow may have had this parallel in mind when he compared cholera and asphyxia.

6. “The brandy treatment has been extensively tried in Cholera, but it is now abandonedin all parts of the world. If the debility is not so great that life is not destroyed by [brandy],still it hurries on and makes more violent that reaction, that secondary fever which is mostto be dreaded, and increases the tendency which there is to inflammation in the head andelsewhere”; Snow, “Teetotal address” (1836).

7. Snow, On the Mode of Communication of Cholera (August/September 1849), 8. Hereafter,citations to this pamphlet are made parenthetically using the abbreviation MCC.

8. “At a time when the chemistry of gaseous substances did not exist, and when certain dis-eases were attributed to a putrefaction of the fluids of the living body, these diseases were sup-posed to be occasioned by the effluvia given off during ordinary putrefaction”; Snow, “On thechief cause of the recent sickness and mortality in the Crimea” (1855).

9. P. E. Brown suggests that the idea that cholera was a local affection of the intestines wasan “old-standing foible” of Protheroe Smith; “Another look at John Snow,” 650. While Smith


did state that “the peculiar action of the inciting cause [of cholera] is clearly that of morbidimpression on the follicular apparatus of the intestines,” he thought the pathological processwas triggered by the body’s nervous system to “resist the assailant” by “an abnormal and in-ordinate increase of action . . . in the functions of the alimentary canal”; Cholera: An In-quiry, 14–15. For the contagionist opinion closer to Snow’s thinking, given his interest inLiebig’s work and parasites, see “Medium of contagion,” Lancet 1 (1842–43): 111.

10. We are grateful to Christopher Hamlin for pointing out the need for these assumptions.Snow did not articulate these assumptions in MCC. He did, however, come much closer toboth explicating and justifying these assumptions in his oration CMC (1853).

11. “Medium of contagion,” Lancet 1 (1842–43): 111.12. P. E. Brown claimed, “Snow had hit on an idea which he had not the means nor the

abilities to put to the test,” in part because “his original inspiration was the result of a hap-hazard process of reasoning which no later rationalisation could ever turn into a convincingargument”; “Autumn loiterer,” 527.

13. Margaret Pelling wrote that Snow’s theory rested on twin pillars: “a consideration of thepathology of the disease and from a conviction, based on cholera’s predilection for lines ofhuman intercourse and on consecutive cases in the one household, that the disease was com-municable person to person”; see Cholera, 204. Similarly, Shephard argues that Snow the epi-demiologist should not distract us from his clinical and pathological perceptions; JS, 163.

14. Alfred B. Garrod, “On the pathological condition of the blood in cholera,” LJM 1 (1849):409–37; the quotation is from 436. Garrod’s article was a companion piece to Edmund A.Parkes, “On the intestinal discharges in cholera,” LJM 1 (1849): 134–52, published two monthsearlier. Parkes and Garrod were then assistant physicians to University College Hospital andhad collaborated in their respective chemical analyses of the blood and stool of cholera pa-tients. Both believed the cholera poison entered the bloodstream first, the alimentary canalsecondarily, if it at all. Although Snow did not cite Parkes’s article, he had broached his hy-pothesis with him and Garrod before writing MCC.

15. Snow strengthened his pathology argument after MCC. In 1855, for example, he citedGarrod’s article at length and added other references: “The analyses of Dr. O’Shaughnessy andothers, during the cholera of 1831–32, showed that the amount of water in the blood was verymuch diminished in proportion to the solid constituents, and that the salts of the blood werealso diminished. The analyses of Dr. Garrod and Dr. Parkes, in the spring of 1849, were morenumerous and exact. The amount of water in the blood of healthy persons is on the average785 parts in 1000; whereas, in the average of the analyses performed by Drs. Garrod and Parkes,it was only 733 parts, while the amount of solid constituents of the blood, relatively to thewater, was increased from 215—the healthy standard—to 267. . . . Dr. Garrod is of the opin-ion that a chemical analysis will determine whether or not a specimen of blood has been de-rived from a cholera patient”; MCC2, 11–12. For the 1855 edition of his essay, Snow also cal-culated that one would have to replace 5 pints of water to restore the blood of a cholera victimin the state of collapse to normal health, which showed that the amount of fluid lost was wellwithin the estimates of the total amount of fluid evacuated through the intestinal tract; MCC2,14. Snow added that the dramatic reversal of cholera symptoms by intravenous saline injec-tions was strongly in favor of the dehydration hypothesis and went against the theory that thesymptoms of cholera were caused by a blood-borne poison; MCC2, 13.

16. We have found no evidence that Snow had “proof” before 1853 that cholera was causedby a “microorganism,” as asserted by Shephard, JS, 152–53.

17. As early as 1843 Snow was aware of entozoa from the perspective of comparative anat-omy: “In many species of the lowest tribes of animals, the circulation of the blood which takesplace in capillary tubes is independent of contractions and all mechanical forces, and must


arise from the functions taking place in the vessels: for instance, the trematoda, an order ofintestinal worms, possess two vessels on each side of the body, in which the blood moves inopposite directions; and, according to the observations of Ehrenberg and Von Nordman, thesevessels do not contract in the least”; Snow, “On the circulation of the capillary blood-vessels,and some of its connections with pathology and therapeutics,” (1843), 811. Thereafter, Snowdid not discuss intestinal worms until he decided the analogy was apt in his first essay oncholera. Surely he had read the reference to Henle’s “parasitical organised beings” as “the ex-citing cause” of contagious diseases in “Medium of contagion,” Lancet 1 (1842–43): 111. Per-haps he had also read the article about Henle’s researches in the October 1842 issue of M-CRabstracted under the title, “Medium of Contagion,” by the Lancet, and Henle’s writings as well.

18. Pelling’s interpretation of the pathology in Snow’s theory stresses an analogy betweensmallpox and cholera, although Snow barely alludes to it in MCC. She does not consider theintestinal worm analogy significant; Cholera, 206–08. According to John Farley, “few conta-gionists believed that living organisms caused infections”; “Parasites and the germ theory ofdisease,” 37. See also Farley, “Spontaneous generation controversy”, and Foster, History of Par-asitology, 6–27.

19. Farley, “Spontaneous generation controversy,”106. On Brera, see Ibid., 111, and Foster,History of Parasitology, 8. It is possible that Snow was aware of a series of lectures that T. B.Curling delivered at the London Hospital, which were serialized as “Lectures on the entozoa,or internal parasites of the human body,” LMG 1 (1837–38): 518–23 ff. Curling argued thatworms derived solely from the eggs of worms, citing well-studied species such as the tape-worm. If only a tiny percentage of eggs found environments suitable for hatching and devel-opment, the species could be maintained. He was troubled, however, by several experimentsthat had failed to produce infestations in animals fed large quantities of ova. Also available toSnow was J. L. Drummond’s article in which he argued against spontaneous generation of en-tozoa on the grounds that they were structurally too complicated; “Thoughts on the equivo-cal generation of entozoa,” Annals and Magazine of Natural History, Botany, and Geology 6(1841): 101–08.

20. On Steenstrup’s research around midcentury, see Farley, “Spontaneous generation con-troversy,” 117–19, and Farley, “Parasites and the germ theory,” 36–37. Steenstrup described an“alternation of generations” whereby the larval stage of the liver fluke developed within thebodies of snails before emerging to infect a mammalian host; his analysis did not include adiscussion of intermediate hosts, however.

21. “Report on the condition of Surrey Court, Horsleydown, by Mr. John Grant, assistant-surveyor,” MCS/477/61, London Metropolitan Archives. Surrey Court, Thomas Street, Hors-leydown, is shown on Reynolds’s 1859 map of London, and the 1870–1872 ordnance surveymap of that area specifically shows a row of buildings marked “Surrey Buildings.” For detailedviews of the 1859 map as well as details regarding Surrey Buildings, see www.ph.ucla.edu/epi,organized and maintained by Dr. Ralph R. Frerichs, University of California-Los Angeles,School of Public Health. In a “Report on two cases of cholera in Mount Place, St. George’sRoad,” dated 6 August, Grant implied that cholera was transmitted by morbid effluvia: these“deaths immediately following the emptying of cesspools by hand, without using the hose orany deodorising agent, struck me so forcibly as bearing the relation of cause and effect . . .”that if such cleansing must be done during a cholera epidemic, it should be “done with cau-tion, and the use of the best means at their disposal of preventing smell during and after theoperation . . .”; MCS/477/56, London Metropolitan Archives.

22. We have been unable to locate Grant’s report of his excavations at Albion Terrace. Thelocation of Albion Terrace was tracked down with the assistance of Dr. Ralph R. Frerichs, Uni-versity of California-Los Angeles, School of Public Health; see Dr. Frerichs’s website,


www.ph.ucla.edu/epi

www.ph.ucla.edu/epi, for details and maps. Albion Terrace and several streets in the immedi-ate vicinity were renamed soon after the outbreak. It appears, however, that Albion Terracereferred to a row of houses on the north side of Wandsworth Road, about two blocks to thenortheast of the street now called Albion Avenue (and named Albion Road in the nineteenthcentury). For another contemporary account see “The cholera,” PharJ 9 (1849–50): 113.

23. Snow did not construct a map to illustrate the results of any of his investigations untilDecember 1854, and he never used a disease spot map as an actual tool during an investiga-tion in progress; see Brody et al., “Map-making and myth-making in Broad Street.” Earlier,McLeod had argued that Snow never intended his Broad Street map as an investigative tool;“Our sense of Snow,” 930–31.

24. Pelling used the term village epidemiologist to describe Budd’s penchant for looking atisolated outbreaks; Cholera, 275–79. The term is apt for Snow’s investigative method in thissection of MCC.

25. Jacob Bell found Snow’s evidence inconclusive. Bell quoted from the Registrar-General’sreturns of 5 January 1850, identifying some of the same patterns observed earlier by Snow,but complained that there were too many confusing variables to conclude that the quality ofthe water was causally associated with cholera. Bell thought it likely that elevation above sealevel and density of population were more important; “On the nature and effects of the organic matter in drinking-water,” PharJ 9 (1849–50): 416–17; “Extract from the Registrar-General’s return,” PharJ 9 (1849–50): 481.

26. Excerpts from Milroy’s report appeared in UK GBH, Cholera of 1848 & 1849, 25–28.27. Ackerknecht, “Anticontagionism,” 567–68. Snow was forced to take up this issue again

in MCC2 after the publication of a case report from the Newcastle Infirmary of a dispenserwho “drank (by mistake) some rice-water evacuations, without any injurious effect whatever”;J. S. Pearse and Jeffrey A. Marston, “Statistics of the cases of the cholera epidemic, 1853, treatedat the Newcastle Dispensary,” MTG 8 (1854): 106–08, 129–31, 182–83; quote from 182. Pearseand Marston specifically allude to Snow’s theory and offer the case of the dispenser as a refutation.

28. Later, some critics overlooked this proviso, claiming that Snow’s theory made contam-inated drinking water the only possible mode for the transmission of cholera. He was adamant,however, that cholera must enter the alimentary canal—the only environment favorable forits multiplication—for the pathological process of cholera to become established.

29. Snow later reinforced this theme: “If the view I am explaining be correct, we have, there-fore, the power of avoiding cholera as easily as one may avoid the itch. Every man may be hisown quarantine officer, and go about during an epidemic among the sick almost as safely asif no epidemic were present”; “Further remarks on the mode of communication of cholera”(1855), 84. There is no discussion of the treatment of cholera victims in MCC, perhaps be-cause his emphasis was that the disease was easily prevented. Snow focused on the treatmentof cholera that was naturally suggested by his pathological and transmission theories in onlyone later work, “Principles on which the treatment of cholera should be based” (1854).

30. The anticontagionist rejection of quarantine has been interpreted as indicative of a defacto alliance of interests between general practitioners and merchants; for example, see Ack-erknecht, “Anticontagionism,” 567. Snow may have equated commerce with jobs and so haveseen himself as supporting the laboring classes.

31. Snow complained in his letter to the editor of LMG dated 15 September 1849 that oth-ers had “contradict[ed], in some points, the particulars which I collected with great pains andtrouble. . . .” He was also upset that the journal had published what he considered a “verybrief and scarcely correct abstract” of Grant’s survey report that gave no indication of thecareful investigation that had been undertaken. To top it off, the anecdotal opinion of a res-


www.ph.ucla.edu/epi

ident of Albion Terrace was given equal weight with Grant’s report and his pamphlet; Snow,“The cholera at Albion Terrace” (1849).

32. Snow, “The cholera at Albion Terrace” (1849).33. Shephard noted that in the ordinary course of events, PMCC, being published in two

parts in a major journal, probably reached a far wider audience than MCC, published as aseparate pamphlet. We agree with Shephard that in PMCC the central element of Snow’s the-ory is fecal–oral transmission, with transmission by water being an important but still sec-ondary issue. However, we have found no evidence that Snow’s theory of the nature of choleraunderwent a major revision between the two publications, as Shephard claims; JS, 173–77.

34. The phrase dropped from MCC reappeared once thereafter in the expansive and spec-ulative address entitled On Continuous Molecular Changes (1853). Later, Snow considered itlikely that the cholera agent was “like a cell”; MCC2, 15. He first used the word cell in rela-tion to the cholera particle in a letter dated 5 August 1854 (“Cholera in the Baltic fleet”). Wor-boys warns against the mistake of viewing Snow as a “proto-germ theorist” (Spreading Germs,117), but he provides no clear explanation of why he regards such a view as mistaken or, in-deed, of exactly what he means by “proto-germ theorist.”

35. Dale C. Smith, introduction to Budd, On the Causes of Fevers, 9. See also Budd, TyphoidFever, although his papers on the disease began in the 1850s. Budd was in Paris during thetime that Louis, using a numerical method, conducted the study distinguishing typhus fromtyphoid.

36. Budd, Malignant Cholera, 5–6 (dated 27 September 1849). Budd had been looking intothe nature of intestinal parasites from about 1841 and had argued that aspects of parasiticdiseases could explain some features of cholera; Pelling, Cholera, 253–54. Superficially resem-bling Budd’s (and Snow’s) views of water as the main vehicle for transmission of cholera wasthe theory presented by John Parkin in 1832. Parkin thought that the cholera poison was takeninto the stomach from polluted water, but he also thought that the poison was generated inthe earth and from there infected various springs, so that his theory was not contagionist atall; John Parkin, “Suggestions respecting the cause, nature, and treatment of cholera,” LMSJ 2(1832): 151–53.

37. J. G. Swayne, “An account of certain organic cells peculiar to the evacuations of cholera,”Lancet 2 (1849): 368–71, 398–99.

38. Pelling, Cholera, 170–77. At least one anonymous member of the Bristol MicroscopicalSociety suspected that the London rejection of their findings was based on metropolitan ar-rogance and an assumption that provincial physicians did not know how properly to lookthrough a microscope; “A member of the Bristol Microscopical Society,” “The Bristol Micro-scopical Society, versus the president of the Microscopical Society of London,” Lancet 2 (1849):450.

39. The main agenda item at this meeting of the Westminster was Snow’s long paper on thepathology and mode of communication of cholera, later published as PMCC. Lankester madehis announcement about the fungus particle during the discussion that followed Snow’s paper.Edwin Lankester (1814–1874), like Snow, grew up in a poor provincial household, was appren-ticed to a provincial surgeon, and later tried to make his career as a London physician. He servedmany years an editor of the Quarterly Journal of Microscopical Science, where he focused on nat-ural history and popular science. He was also an active medical and public health reformer; seeEnglish, Victorian Values. One London editor who was immediately skeptical of the fungus claimwas Jacob Bell of the Pharmaceutical Journal. At the first announcement from Swayne and Brit-tain, he trotted out several reasons to regard their theory as preposterous and was happy to re-port confirmation later from the London microscopists; “Hypotheses of the cause of cholera,”PharJ 9 (1849–50): 223–24; “Fungus hypothesis of cholera,” PharJ 9 (1849–50): 266–67.


40. Pelling argues that the 1849 cholera fungus controversy at least temporarily raised thebar for would-be germ theorists by setting stringent standards for “proof,” which for practi-cal purposes could not be met with the technology available at that time; Cholera, 189–201.This is a puzzling interpretation because fungi and some bacteria could be seen easily withcontemporary microscopes, and favus (a skin condition) was generally thought to be fungalin origin. The cholera bacillus was visible with contemporary microscopes. Hassall drew par-ticles that, in retrospect, he recognized as identical to Koch’s Vibrio cholerae. Filippo Pacini,working in Florence in 1854, detected microscopic particles in the evacuations of cholera vic-tims similar to those Koch discovered and named thirty years later. See Paneth et al., “A ri-valry of foulness,” 1547; Hassall, Memoirs, 76; Filippo Pacini, “Osservazioni microscopiche ededuzioni patologiche sul cholera asiatico,” Gazetta Medica Italiana Toscana 6 (1854): 1; Ben-tivoglio and Pacini, “Filippo Pacini.”

41. Pelling, Cholera, 276. Snow was one of those to raise the question of logical consistency:“Dr. Budd entirely agrees with me that the cholera poison is produced only in the alimentarycanal and acts only on that canal, which it reaches by being swallowed. . . . [T]here is nodifference between us respecting the essential mode of communication of the disease, but onlyas to the extent to which it is communicated through the air. . . . In my opinion the cholerapoison only produces its effects through the air when carried by insects or when the evacua-tions become dry, and are wafted as a fine dust”; Snow, “On the mode of communication ofcholera,” Edinburgh Medical Journal (1855–56): 669.

42. Pelling believes that Budd’s willingness to consider multiple causes made his theorypalatable to most medical men at the time. She compares the “inclusive” nature of Budd’s the-ory with the “exclusive” nature of Snow’s, to the latter’s detriment; Pelling, Cholera, 275–81.Pelling’s view of Snow parallels to some extent P. E. Brown, “Autumn loiterer.” Benjamin W.Richardson, despite his idolization of Snow, agreed with Budd on multiple causation, notingthat poisons often produced identical effects whether swallowed, inhaled, or rubbed onto theskin and that the symptoms of malaria (which Snow suggested was a water-borne infection)were not confined to the gastrointestinal tract; Richardson, “Water supply in relation to healthand disease,” JPH&SR 1 (1855): 133–35.

43. The reporter for the LMG quoted Snow as saying before the Westminster on 13 Octo-ber 1849, when presenting part one of the papers later published as PMCC, that the “recentdiscovery of peculiar microscopic cells, believed to be of a vegetable character, in great abun-dance, in the cholera discharges, tends to confirm [his] view of the nature of cholera”; “West-minster Medical Society,” LMG 44 (1849): 731. When, a short time later, Snow wrote up PMCCfor publication, he omitted any mention of the Bristol “discoveries.” P. E. Brown thought Snowshied away from the cholera fungus group in Bristol to avoid granting them priority in thediscovery of a causative agent; “Autumn loiterer,” 522–23. See also Pelling, Cholera, 169–70.

44. S. Snow agrees that Snow accepted the limitations of his day’s medical science regard-ing the identification of the cholera agent, whereas its mode of transmission could be estab-lished with the tools then at hand; JS-EMP, 235. Christopher Hamlin, on the other hand, incommenting on an earlier draft of this chapter, noted that Snow assumed a major logical riskby failing to identify the causal agent. Without an independent measure of whether any indi-vidual had been exposed to the causal agent, Snow could always be accused of reasoning in atautological mode: People who get cholera are people who have been exposed to the causalagent; people who do not get cholera are people who have not been exposed. This, in a sense,would put Snow in precisely the same position as the miasmatists, who invoked “predisposi-tions” whenever their theory failed to predict who fell ill and who did not. We believe thatSnow was aware of this difficulty and that it was precisely for this reason that he spent somuch effort later in showing via statistical “proofs” that people probably exposed to the causal


agent (via drinking water contaminated with cholera ejections) contracted the disease muchmore often than people not so exposed. That is, Snow realized, as do epidemiologists today,that identifying the causal agent was not synonymous with demonstrating the transmissionof a disease.

45. Budd, Malignant Cholera, 19. Several years later, when Budd posed the possibility thatthe cholera poison could spread through the air, Snow remarked: “if [Budd] can establish thispoint, the credit of it will be due to him”; Snow, “On the mode of communication of cholera,”Edinburgh Medical Journal (1856), 669.

46. Snow’s manner of thinking shares many features with the systems-hierarchical per-spective proposed in 1977 by George Engel as the “biopsychosocial model” of medicine; En-gel, “New medical model.” Although Table 8.2 closely resembles Engel’s model of the hierar-chy of natural systems, we have modified it to conform to the levels of organization and thecollateral sciences known in Snow’s time. We claim that Snow’s pattern of thought resemblesthis modern systems-hierarchical model in terms of understanding how biological phenom-ena lead to networks of “ripple effects” at other levels of organization, requiring the methodsof different scientific disciplines. That is, no study at only one level of organization using thetools of only one scientific discipline can ever provide a full and complete picture of humanhealth or disease. We do not claim that Snow had any understanding of twentieth-centurysystems, cybernetic, and information theories, which Engel drew upon in constructing hismodel in the 1970s.

47. An example of Snow’s interdisciplinary systems thinking is provided by his later com-ment on the transmission of influenza: The fact that many people seem to come down withinfluenza almost simultaneously is not an argument against its contagion by inhalation, sincebad news seems to travel every bit as fast as an influenza outbreak; “Chemical researches onthe nature and cause of cholera,” Lancet 1 (1850): 155. The remark illustrates a systems modeof thinking by being figurative and literal at the same time. Figuratively speaking, Snow sawthe possibility of a functional analogy between processes that occurred at widely separatedlevels of organization—disease spread and human speech. Literally, Snow was arguing for ananalogy in the timing of transmission of verbal information and of influenza, assuming thatboth were spread by the physical medium of the human breath.

48. Although Shephard states that “Snow’s view of communicable disease was an ecologi-cal one” (JS, 265), he contrasts Liebig’s focus on chemical processes with Snow’s on patho-logical processes, as if they were somehow mutually exclusive; JS, 187. In our view, Snow rea-soned back and forth between his understanding of underlying chemical mechanisms andtheir pathological manifestations; theories and observations at the chemical and pathologicallevels were complementary, not competing.

49. Although Snow’s approach to science was not unique in his generation of medical sci-entists, an address by Sir Benjamin Brodie suggests the persistence of an older notion. In hisremarks to a group of medical students, Brodie equated scientific medicine with precise ob-servation and with careful use of an inductive method, not the use of a hypotheticodeductivemethod or a multilevel approach coordinating disparate phenomena; “Introductory discourseon the mode of investigating the sciences belonging to the medical profession,” LMG 38 (1846):603–13.

50. Besides making sense from a systems perspective, Snow’s strategic move with regard tothe fungus particle marked him as a pioneering epidemiologist because the essential featureof epidemiology is gathering scientific information about the occurrence and spread of dis-ease through a population when the causal agent is unknown. A modern example is estab-lishing the causal linkage between cigarette smoking and lung cancer, even if one does notknow at a biochemical and cellular level what it is about cigarette smoke that causes cancer


cells to form. The London Epidemiological Society, and the first developments of epidemiol-ogy as a discipline, were founded in the wake of the cholera epidemic of 1848–1849 by Snowand like-minded colleagues.

51. The occupational level, which Snow also addressed, is difficult to display as a separateline on Table 8.2. Snow’s deductions of how cholera might spread in coal mines, as well as hisrecommendation that a quick and cheap preventive might be splitting shifts into four-hourblocks so the miners could wash and eat above ground, shows that he took occupational pat-terns of human behavior into account. He showed a similar sensitivity to occupational con-cerns in his later work on “nuisance” trades, “On the supposed influence of offensive tradeson mortality” (1856).


“THE ROOMS OF THE SOCIETY, this evening, were crowdedto excess,” noted the Lancet’s reporter at the meeting of the West-

minster Medical Society on Saturday, 13 October 1849. “Dr. Swayne, of Bristol, wasamong the visitors” who, along with the regular membership, had gathered to hearSnow read a paper, “On the pathology and mode of communication of cholera.” Atthe end of his presentation, after outlining preventive measures, Snow mentionedthat the visitor from Bristol was a colleague of “Dr. Brittan [who] had found mi-croscopic bodies in the atmosphere, which he considered to be the same as those ex-isting in the alimentary canal.” Snow was skeptical, however. Other investigators hadbeen unable to replicate Brittan’s findings, and “all the evidence he had collected wasopposed to the idea that the cause of cholera existed in the air.”1

Swayne took the cue. Their microscopical examinations of about sixty samples ofcholera evacuations yielded ninety percent evidence of “the bodies in question.” Hehad found none in diarrheal evacuations that resulted from causes other than cholera.In fact, he had brought a “diagram he had made, which exhibited their peculiar struc-ture.” He “felt quite disposed to agree with the remarks which had been made by Dr.Snow in his paper respecting the probability of cholera being primarily a disease ofthe alimentary canal and not of the blood.” Swayne also offered additional evidencethat cholera could be transmitted via soiled linen, noting “the frequency with whichthe disease attacked washerwomen and others who had had much to do with the

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Chapter 9

Professional Success

discharges of cholera patients.” On the other hand, he did not believe one shouldrule out airborne transmission. He had developed a headache and experienced nau-sea while simply emptying bottles of cholera evacuations, followed by fever and vi-olent diarrhea that night and the next morning.2

Subsequent discussion was equally spirited and wide-ranging. In opposition toSnow’s theory, medical men recounted symptoms they had observed that suggestedthat “local affection” of the alimentary canal was secondary rather than primary; ev-idence that impure water “bore a mere contingent relation to the disease, nothingmore,” which could be eliminated by general sanitary improvements; and the “ex-periment performed by some French physicians, at Warsaw, in 1831, of swallowingsome portion of the cholera stools . . . [with] no ill effects, . . . [contrary] to theopinion of Dr. Snow.” Dr. James Copland, author of the Dictionary of Practical Med-icine, which was in common use at the time, was “greatly interested in the discoveryof the microscopic bodies. He had long been of the opinion that the decomposingeffluvia given off in infectious diseases might take on special organized forms pecu-liar to each disease,” a contingent contagionist view that Dr. Snow’s remarks had notdissuaded him from holding. Time ran out, so the debate was adjourned until thenext meeting.3

The discussion was resumed the following Saturday after two papers were pre-sented, one of them on muscular contractions found in some cholera victims afterdeath. Dr. Francis Sibson, one of the senior members of the society, reviewed Snow’sargument as well as Dr. John Webster’s earlier paper on general atmospheric causesof cholera. He thought neither author had sufficiently accounted for contrary evi-dence and that air and water might both be vehicles for propagation. “He did notagree with Dr. Snow, that the primary seat of the disease was in the mucous mem-brane of the intestines” because he had treated cholera patients in whom diarrheafirst occurred in the latter stages, if at all, but he did agree, citing Garrod andO’Shaughnessy, that if the blood was not the first affected, it became so as the dis-ease progressed. Their researches confirmed his own practice of using saline injec-tions to rally patients in the state of collapse, who uniformly recovered if the uri-nary secretions could be restored. Overall, however, Sibson was not ready to rejectWilliam Cullen’s long-standing doctrine of nervous irritability as the primary cause.Other members shared Sibson’s view that water could not have “more than partialeffect in spreading cholera,” argued that “the atmosphere is the principal channel bywhich cholera is disseminated, though the human recipient of the morbific miasmoccasionally becomes, as in yellow fever and influenza, a secondary agent in propa-gating it” under favorable conditions, and amplified Copland’s remarks from the pre-vious meeting by pointing to their medical experience that intestinal affection wassecondary to “the lost vitality of the blood” and capillary congestion. Someone as-serted that even if “the cholera depended, as some supposed, on the presence of or-ganized bodies in a state of putrefaction in the water,” existing filtration capacitieswere sufficient to render the poison innocuous.


Dr. Edwin Lankester reasoned that if the skin could produce a poison in cases ofsmallpox, it was also possible for the mucous membrane of the intestines to do soin cholera. “No such poison had, however, yet been demonstrated to exist. . . .” Afriend of his, Mr. Busk, had not found “the presence of fungi in the evacuations andvomited matters of cholera patients,” as mentioned by Dr. Joseph Griffiths Swayneat the last meeting. Instead, he had found the usual variety of “organic and inorganicmatters,” spores of a fungus often found in bread, husks of wheat, and “bodies [that]resembled starch granules.” Lankester had “examined Mr. Busk’s preparations, andcompared them with those of Dr. [Frederick] Brittan and Dr. Swayne,” and he agreedwith Busk that “we must look in some other direction for the poison of cholera.”“Dr. Webster and Dr. Snow having replied, the society adjourned.”4

Although the essay the LMG published in two installments as PMCC was essen-tially the paper Snow delivered to the Westminster Medical Society, a few differencesare suggestive of a pattern that he followed for several years while awaiting an op-portunity to complete the study of cholera in south London that he believed wouldconvince all his critics. He never wavered on the accuracy of his fundamental con-clusions about pathology and mode of transmission, but he took seriously all ob-jections to his theory, undertaking literature searches and gathering information tocounter them. Snow was also acutely sensitive to any incident that might support his1849 theory. The tone in his publications and commentary at medical society meet-ings was usually respectful of those who disagreed with him.

On the Mode of Communication of Snow

Snow was in rarified circles on an April afternoon in 1850, applying chloroform di-rectly to the stump of the elderly Marquis of Anglesey, an old, distinguished officerfrom the Napoleonic era revered more for his bravery than his tactical skill.5 LordAnglesey’s stump and the right side of his face had been giving him intense pain,and Snow attempted to alleviate it by using chloroform as a topical anesthetic, ap-plying it with “bibulous paper, and on lint, and covered up closely with oilsilk” (CB,122). After two and a half hours this had had no effect, and Snow suggested that thepatient might inhale. At this moment Anglesey, as master of the ordnance, receiveda dispatch from Woolwich “containing” (as Snow noted in his Case Book) “an ac-count of the death of an artillery man (gunner and driver) on board ship in theMauritius in Feb. last from chloroform given on a handkerchief.” Snow and LordAnglesey discussed the particulars of the case. Although Anglesey was hearing of itfor the first time, Snow had actually known of it for two weeks because he had beeninformed by “the Secretary of Sir William Bennet, on whose son Mr. Fergusson op-erated at Camberwell” (CB, 123; OC, 147–48). The courageous and agonized Anglesey inhaled, undeterred by the implied risk in the report, just to the point ofunconsciousness, suspending the waves of pain and the accompanying spasms.

Professional Success 233

After repeated inhalation, the marquis was feeling better, drifting momentarily outof consciousness. Each time he came to he made a speech: “On recovering his con-sciousness, the patient talked for a minute or two as if addressing the Board of Ord-nance.” Snow gave him chloroform on and off for the rest of the night and againseveral weeks later, and each time the marquis gave an imaginary speech (CB,127–28). Chloroform seemed to possess an uncanny power to reveal underlying con-ditions. If a patient (generally female, but in some cases male) suffered from hyste-ria, Snow found that the drug induced hysterical symptoms (OC, 104–05). If a pa-tient were anemic and weak, this tended to appear under chloroform. If a patientwere physically active and robust, this might come out as a struggle or rigors. Pa-tients who could be violent in daily life might become violent under the anesthetic.In the case of Lord Anglesey, it revealed his lifelong propensity to make speeches “asif addressing a meeting or a dinner party” (CB, 127).

In a different but related way, chloroform revealed the increasing momentum ofSnow’s career, his widening circle of acquaintance, and the degree to which his ex-pertise had plugged him into the nerve centers of London as they touched upon hisresearch. If anything happened connected with chloroform, he would know about itbefore almost anyone. While his old Soho general practice, which had never beenvery large, languished, Snow was tending to the illustrious and the wealthy and us-ing these connections to gain more and more information.6 As with his cholera re-search, Snow readily exchanged information about chloroform and had a networkof informants that was intimate and far-flung. By the late 1840s and early 1850s,chloroform allowed Snow to circulate almost as widely as had cholera when it vis-ited the metropolis; it afforded him new modes of communication. He was privy tomilitary dispatches and the phantom speeches of an old marquis. Snow was the firstto assiduously track and analyze case reports of anesthetic fatalities longitudinally.He left an assembled record in On Chloroform of his researches from 1847 until 1858,but it was his ability to gather information—through correspondence, medical so-ciety meetings, and the social nexus of his anesthesia practice—that enabled him tobecome a leading authority.7

This facility led to moderate degrees of financial and social success. In 1851 hewas appointed a physician to the Hospital for Consumption and Diseases of theChest in Brompton, south of London. At the end of 1852 he moved from the apart-ment in Frith Street to a house of his own at 18 Sackville Street (Fig. 9.1). This newlocation, a fifteen-minute walk from his old premises, was just northwest of Pic-cadilly Circus, a fairly posh neighborhood. Snow convinced his former landlady’sservant, Jane Wetherburn, to move with him as his housekeeper.8

In terms of research, Snow was in a confirmatory mode rather than one of freshdiscovery. The long series of articles “On narcotism” in LMG had been something ofa dissertation for Snow in which he had laid out all his basic principles and meth-ods. Toward the end of that study in the early 1850s, delayed as it was by the need“to repeat many experiments and institute fresh ones,” his ideas about the cellular


mechanisms of anesthesia were having an impact on his notions of cholera, and viceversa.9 He was beginning to formulate a full answer to the many questions that chlo-roform raised.

Snow, ever the advocate of chloroform, was continually aware of the controversy,fear, and public outcry that dogged the drug. For the rest of his life he sought to de-bunk and demythologize the chlorophobia that circulated throughout the generalpopulace and, often as not, “informed” medical opinion. This was the impetus be-hind his public letter to Lord Campbell in 1851 arguing against any special legisla-tion punishing those who used chloroform in the commission of a felony. Snow con-sidered the bill unnecessary and misguided and marshaled his clinical knowledge ofchloroform to criticize apparent inconsistencies and fallacies in the reports of crimesinvolving chloroform, even though he was perfectly aware of the usefulness of chlo-roform in subduing violent patients in what he deemed legitimate medical contexts.10

He wished to calm the public about chloroform, and this desire seemed to spring


Figure 9.1. John Snow’s house at 18 Sackville Street.

from his own sober, cool temperament and a deep understanding of the nature ofthe drug and its effects. He always brought a sense of tranquility to the use of chlo-roform. When patients were recovering from its effects, he advised that it was bestnot to speak to them but to leave them to collect themselves and wait until they wereconscious enough to make a remark or initiate a conversation (OC, 99). In this erain which surgery might very well take place in a home surrounded by friends andfamily, when medical practice and procedure was not quite so removed from every-day life, and when operating theaters were commonly visited by the general public,medicine was subject to a kind of interference we seldom see today. By the 1850s inBritain, chloroform anesthesia was becoming a mass phenomenon, available to vir-tually everyone, yet its effects made it nearly impossible for lay people to understandwhat they were observing when it was used in controlled medical situations. If theywere actually coming under its effects, the disorientation and loss of consciousnessequally obscured their understanding of the degrees of narcotism involved. Snow, amedical man arguing for medical control over the use of anesthetics, always had amixture of solicitude and skepticism when it came to the public. He observed,

If not prevented by the medical attendant, the friends of the patient often ad-dress him the moment he opens his eyes; and the words they generally use areof a very equivocal meaning to one who cannot understand their application.They usually say “It’s all over,” which very often has the effect of raising an in-definite feeling of alarm in the patient; for, until he has time to recover hismemory, the operation he was to undergo is generally the farthest thing fromhis mind. When left to himself the patient usually recovers from the insensi-bility in a very tranquil manner . . . and in a great number of instances willcontend . . . very stoutly, even after a protracted operation . . . that thechloroform has not taken effect. It is well to let him remain in this conceit fora while, or even till he finds out the mistake himself; for, if reminded of thepain they have been spared, just on waking after an operation, persons are li-able to be excited by emotions of pleasure and gratitude; but a few minuteslater . . . they are better able to control their emotions.

OC, 99

This passage contains Snow’s ethics for the administration of chloroform: promoteneither dread nor excessive gratitude, and keep the family and friends from med-dling. Excitement and emotion needed to be controlled for good medical reasonsbut also to avoid as much as possible the embarrassment of Victorian propriety thatsurgery and anesthesia necessarily entailed.

The two subjects for which John Snow is remembered, chloroform and cholera,both produced a host of symptoms seemingly calculated to embarrass the Victoriansensibility. Cholera produced uncontrollable diarrhea, and chloroform produced ageneral lack of control, not to mention that its chief drawback was that it frequently


made people vomit. It was Snow’s contribution to see that one could control manyunpleasant manifestations by controlling, in some measure, what people put in theirmouths. With chloroform and ether, nausea and vomiting seemed to be an inevitableside effect, and one reason for Snow’s search for better anesthetics was to find onethat did not make the patient sick. By the 1850s he had seen enough cases to lay outthe basic guidelines to reduce the chances of vomiting during inhalation: avoid mealsbefore surgery; do not move the patient after inhalation; and do not give the patientanything to eat or drink for about an hour after inhalation. These rules still basicallyapply today and have become routine parts of surgical protocol. Snow had little sym-pathy for the naysayers who believed that chloroform could make people perma-nently ill. In 1852 he saw a clergyman who was convinced that he had been unwellever since he inhaled chloroform. After the patient laid out a host of symptoms anda list of eminent physicians who had failed to make him well, Snow dismissed him.“It was my opinion,” he later wrote “that the complaint of this gentleman was com-ing on long before he inhaled the chloroform, and that it depended on a much lesstransient cause. I have not heard from him since” (OC, 107).

Professional Enhancement and Recognition

In the 1850s Snow completed his credentialing as a medical man. He became a Li-centiate of the Royal College of Physicians, the penultimate hierarchical status withinthe medical corporations of the day. This was as far as a working-class lad from York-shire could go. Whether or not he aspired to the higher status of fellow, Snow’s med-ical degree from the University of London prevented him from becoming a candi-date, which was still limited to graduates of Oxford and Cambridge. However, hewas elected to membership in another prestigious medical society and became pres-ident of two societies of which he was a long-standing member. He also helped foundthe Epidemiological Society of London in order to further research into the causesand treatment of epidemic diseases.

The examination to become a Licentiate of the Royal College of Physicians of Lon-don (LRCP) was an oral examination like those he had taken in 1838 to qualify asa surgeon and an apothecary. Until 1830 the examination was a viva voce in Latinof classical medical texts lasting an hour or so. In June 1850 the viva was conductedin English, although Latin could enter the conversation at the examiner’s discretion.There were neither practical dimensions nor written preliminaries. The licenciate-ship augmented Snow’s professional status, but it did not gain him access as a GPto fashionable society in the metropolis. Fellows, not licentiates, dominated thatrealm, and Snow was an outsider. As a student he had not become the protégé of anestablished surgeon or physician. After 1850 his Case Books show that although hebecame the anaesthetist of the upper classes in the London metropolis, he never be-came their physician.11 Even so, this social limitation mattered little, because by the


early 1850s his practice was almost exclusively anesthetic, and he made a comfort-able living from it.12

One benefit from the LRCP was election to the Pathological Society of London inthe fall of 1850. This prestigious group acknowledged Snow’s accomplishments byan offer of membership after he received his license as a London physician.13 Soonthere were further indications of his growing reputation among professional col-leagues. The Medical Society of London (which had amalgamated with the West-minster Medical Society in 1850) elected Snow to the coveted role of orator for the1852–1853 session, vice-president for the following session, and president in 1855.In 1854–1855 he was also president of the Physiological Society, a specialty groupwithin the Medical Society of London that met once or twice a month on Mondayevenings. In addition, he maintained his membership in the Royal Medical andChirurgical Society and the Provincial Medical and Surgical Association (forerun-ner of the British Medical Association), as well as attending meetings of other soci-eties (including the Royal Medico-Botanical) as a visitor when the topic interestedhim.14

As president of the Medical Society of London, Snow was responsible for chair-ing weekly meetings on Saturday evenings, conferring with members of the councilwho set the agenda, controlling the society’s finances, and supervising a small staffat the building in George Street, Hanover Square, where the society met from itsamalgamation with the Westminster in the fall of 1850. The society had dispositionover an assembly room and a large room that had been outfitted as a library. At thehead of the assembly room was a seat for the president behind which hung a largepainting of “the members of the Society at the close of the last century,” includingEdward Jenner. On one side of the room was a large portrait of Dr. Henry Clutter-buck, considered “the Father of the Society” (its oldest member) but a rare visitorin recent years,15 but one Saturday evening when Snow was presiding Dr. Clutter-buck did enter the room. Before he could seat himself Snow “rose, and in a way thatwas irresistible in its simple courtesy resigned his chair to the veteran Esculapian”for the duration of the meeting. In this manner Snow recognized the senior physi-cian’s preeminence in the society, as well as acknowledged an indebtedness for hir-ing him years before as a lecturer at the Aldersgate School of Medicine.16

In addition to achieving a leading position in several of the London medical so-cieties, Snow helped J. H. Tucker, a surgeon, found a society “to one special end—the investigation of epidemic or spreading diseases.”17 Tucker had first proposed asociety with a much narrower mandate: surveying medical men about treatmentsfor epidemic diseases, particularly cholera, in advance of developing “some system-atic plan” of the most successful methods to date.18 The organizing meeting of theEpidemiological Society of London occurred at the end of July 1850. It was held inthe meeting room of the Medical Society of London and presided over by a non-medical man, Lord Ashley, who indicated his sanitarian leanings when he stated thatthe “object of the Society is to exalt the poor, to raise them out of the mire. . . . A


very large proportion of the pauperism of these realms tended to result from defi-cient sanitary arrangements. Bad drainage, bad ventilation, bad water, over-crowd-ing, and filth, tended to propagate disease. . . .” Several resolutions then carriedunanimously, including the formal creation of a society “for the investigation of epi-demic diseases” to which “all gentlemen interested in its objects shall be eligible asmembers” and the selection of Benjamin Babington as president.19

The inaugural public meeting was held the following December, at which Dr.Babington set forth the society’s specific objectives. The Epidemiological Societyshould “endeavor, by the light of modern science, to review all those causes whichresult in the manifestation and spread of epidemic diseases, . . . to collect togetherfacts, on which scientific researches may be securely based, to remove errors whichimpede their progress, . . . to suggest those means by which their invasion may ei-ther be prevented, or . . . combated and expelled.”20 Thereafter, the Society met onthe first Monday of each month except in the summer; papers, letters from corre-sponding members, and subcommittee reports were read and commented upon.

The Epidemiological Society began publishing the Journal of Public Health andSanitary Review in 1855, which included Transactions of selected papers delivered atits meetings or sent by corresponding members. In the opening volume of its newjournal, the Society justified its existence by referring to a recent “philosophical yearn-ing after fixed principles as to the nature of disease. . . . If the elements of diseasedaction are few and simple, the principles of prevention or cure are, it is thought, fewand simple also. The materia medica is thus undergoing a thorough revision andcurtailment. . . . Its principles are preventive, its objects wide, and its elements—some seven only, and the world’s general property—are no more than—Pure air—Proper nourishment—A regulated temperature—Bodily exercise—Cleanliness—Men-tal education—Good morals.” The editors wanted a journal “of free opinion and liberalsentiments; but encumbered by nothing approaching to personality, venality, unfaircriticism, or angry disputations with other journals and publications.” They wereopen to contributions of “all men of science . . . [and] public writers” who wishedto promote “hygiene as a branch of medical education,” elucidate “those great laws,under the influence of which diseases are produced and fostered,” and bring the at-tention of the wider public to “the principles of preventive medicine.”21

Although few of the founding members appear to have supported his cholera the-ory, Snow found the goals of the new society appealing on many counts. He was ac-tive from the outset. In January 1851 he commented on Alexander Bryson’s paperon cholera; at the May and June meetings in 1851 Snow read a paper of his own,“On the mode of propagation of cholera.” In 1852 and 1853 he participated in dis-cussions of several papers on vaccination to prevent the spread of smallpox, em-phasizing its utility because the disease was “invariably communicated by contagion.”In May 1853 he delivered another paper, comparing mortality in large towns withrural districts.22 Over the years the Epidemiological Society became a forum in whichSnow refined his cholera theory in response to objections from opponents. For


example, in December 1853 his comments on a paper comparing “the Indian plague[Asiatic cholera] with the black death of the fourteenth century” included a reminder“that, in a paper read some time ago [May and June 1851], he had come to the con-clusion, from the similarity between the course and localities of the two diseases,that they were propagated in the same manner, probably by the swallowing of in-fectious matter with the food; and he mentioned that the natives of India believethat the infection may be conveyed from place to place in provisions, as in a pot ofghee.” Balderdash, replied Dr. Gavin Milroy (whose views Snow had first criticizedin MCC): “the true plague of the Levant had appeared in India, and that sponta-neously. . . . Probably, at certain times, a malarious influence spreads over the wholeglobe, and causes different forms of disease in different parts of the world.” The nextspeaker agreed with Milroy, noting that plague disappeared in Egypt “when theweather became dryer; but he was not aware that any similar law was known to holdin India.” Snow replied that plague cases appeared in all kinds of weather, and so therepartee proceeded until the meeting was adjourned, after which members and vis-itors chatted amiably.23

Snow met Benjamin Ward Richardson (1828–1896) at meetings of the Epi-demiological Society and the Medical Society of London in 1850. They soon foundthat they had other interests in common, including medical research and anes-thesia. Richardson considered Snow a model GP and medical scientist: “When Iwas living at Mortlake, he would run down, on request, after his day’s duties wereover, to a post-mortem, to see a poor patient, or to take part in an experiment, re-turning as cheerily as if he had been to receive the heaviest fee.”24 In their anes-thesia researches they functioned more as friendly critics than as collaborators.At a meeting of the Medical Society of London in 1853, Richardson read a paperon “The anæsthetic properties of the lycoperdon proteus—Common puff ball,”after which “the President asked, if Dr. Snow had any remarks to make. Dr. Snowcorroborated Mr. Richardson’s observations, having witnessed several of his experiments.”25

Midwifery

When James Young Simpson introduced the use of chloroform in labor in 1847, theoutcry of the clergy could be heard far and wide that this went against biblical pre-cepts that women should endure pain in childbirth. This concern never botheredJohn Snow. His medical interests in childbirth were long-standing, and he adopteda liberal attitude to the use of chloroform in midwifery: “With regard to the casesof labour in which chloroform may be employed, it will be readily conceded that, incases where the pain is not greater than the patient is willing to bear cheerfully, thereis no occasion to use chloroform; but when the patient is anxious to be spared pain,I can see no valid objection to the use of this agent, even in the most favourable cases


. . . and the patient may be fairly allowed to have a voice in this, as in other mat-ters of detail which do not involve the chief results of the case” (OC, 319).

The issue that concerned him was how chloroform should be given in labor, notwhether to give it. Simpson’s application of chloroform in midwifery took place ayear after the introduction of ether anesthesia, at a point when the norms of ether-ization consisted of a light state for dental procedures and a heavy one for surgery.Simpson, who was always heavy on the handkerchief when it came to chloroform,opted for keeping the mother completely unconscious through the labor and deliv-ery, but Snow, taking a cue from some of his London colleagues, found that it wasunnecessary in many cases to put the mother completely under in order to removethe pain of labor.26 A debate arose between some doctors who asserted that paincould always be removed without the mother losing consciousness and others whobelieved (equally mistakenly, according to Snow) that “no relief can be afforded un-less unconsciousness be induced” (OC, 318–19). In his experience labor was highlyvariable from stage to stage and patient to patient, and all of them may or may nothave called for chloroform. Therefore, he believed that the object of chloroform inlabor should be to “relieve the patient without diminishing the strength of the uter-ine contractions and the auxiliary action of the respiratory muscles” (OC, 321). Com-plete anesthesia was never used unless “in cases of operative delivery.” His techniquewas to give the chloroform at the beginning of a labor pain and leave off “when theuterine contraction subsides, or sooner, if the patient is relieved of her suffering”(OC, 320). Snow would, if necessary, use a handkerchief in parturition but preferredto use his inhaler in these cases; it saved on chloroform, especially over the courseof a protracted labor. It also gave him more precise control of the small doses used.He was of the opinion that chloroform seemed to speed up some labors and retardothers. He found that it tended to diminish the strength and duration of uterinecontractions but promoted dilation. It was, of course, of great use in forceps deliv-eries and when it was necessary to turn the child. Snow attended nine forceps de-liveries, and in six it was necessary to turn the child. The use of chloroform in mid-wifery fell somewhere in between that of operations and dentistry. It frequentlyrequired small doses to maintain light anesthesia for long periods of time, with theanesthetist responding to and adjusting to the rhythm of the contractions.

Although in his publications on such matters Snow tended to present himself ex-clusively as an anesthetist, his casenotes reveal that he frequently helped with de-liveries and other problems. The day after Christmas 1850 he was called “by Mr.Cooper of Moor Street, Soho, to assist him in a case of retention of the placenta”(OC, 326). In his published account of the case, Snow explained that the mother hadgiven birth two hours before he arrived: “Mr. Cooper had introduced his hand, buthad been unable to bring away the placenta, on account of firm contraction of theuterus in a sort of hour-glass form. On the chloroform being administered, the handwas easily introduced, and the placenta detached, and extracted. There was very lit-tle hæmorrhage” (OC, 326). Snow’s casenotes clarify that the introduced hand was


his, not Cooper’s (CB, 157–58). By obscuring the active role he played in many casesand representing himself as the anesthetist, Snow reinforced the role that chloroformplayed rather than his own.

As with all other aspects of chloroform, Snow felt embattled because people con-stantly mistook its effects. In the late 1840s Snow was requested to give chloroformto the wife of a medical man during her labor. “I was sent for late one evening, butas there were no pains at the time when I arrived, I was requested to go to bed inthe house. After a time, I was called by a servant, who told me the baby was born”and the doctor had been sent for (OC, 329). The birth had happened so quickly thatthe husband, who had been in the room, could not get to the bedside before thebaby was born. After the birth the patient seemed well enough and Snow went home,but when the doctor arrived shortly thereafter, the patient passed out and the doc-tor thought she might die. This went on for hours, and although she ultimately re-covered, it was quite puzzling because there had been no hemorrhage or any otherobvious cause of her syncope. Snow understood the doctor to say “that if the patienthad inhaled chloroform, he should have blamed it for the condition into which shelapsed” (OC, 329). In Snow’s view chloroform remained suspect, even among doc-tors and especially in labor, when the lives of loved ones, mothers, and children wereat stake.

Queen Victoria

For much of the English-speaking world in the early 1850s, the question was whetherchloroform should be given at all in childbirth. When Queen Victoria neared thecompletion of her eighth pregnancy in March 1853, the possibility of her receivingpain relief was quietly being floated, and Snow was advised that he might be calledin.27 Asked to administer chloroform for a patient in labor residing at 18 James Street,Buckingham Gate, on 24 March, Snow mistakenly wrote the address as “Bucking-ham Palace” in his Case Book, suggesting that he had royal affairs on his mind at thetime (CB, xxx). Two weeks later Snow was, in fact, called to the palace and the queentook chloroform during the delivery of Prince Leopold. Snow recorded the event:

Thursday 7 April: Administered Chloroform to the Queen in her confinement.Slight pains had been experienced since Sunday. Dr. Locock was sent for aboutnine o’clock this morning, stronger pains having commenced, and he foundthe os uteri had commenced to dilate a very little. I received a note from SirJames Clark a little after ten asking me to go to the Palace. I remained in anapartment near that of the Queen, along with Sir J. Clark, Dr. Ferguson and(for the most part of the time) Dr. Locock till a little a [sic] twelve. At a twentyminutes past twelve by a clock in the Queen’s apartment I commenced to givea little chloroform with each pain, by pouring about 15 minims [0.9 ml] by


measure on a folded handkerchief. The first stage of labour was nearly overwhen the chloroform was commenced. Her Majesty expressed great relief fromthe application, the pains being very trifling during the uterine contractions,and whilst between the periods of contraction there was complete ease. Theeffect of the chloroform was not at any time carried to the extent of quite re-moving consciousness. Dr. Locock thought that the chloroform prolonged theintervals between the pains, and retarded the labour somewhat. The infant wasborn at 13 minutes past one by the clock in the room (which was 3 minutesbefore the right time); consequently the chloroform was inhaled for 53 min-utes. The placenta was expelled in a very few minutes, and the Queen appearedvery cheerful and well, expressing herself much gratified with the effect of thechloroform.

CB, 27128

For this event Snow used the hanky instead of the trusty inhaler.29 It was no doubtmore decorous than placing a face mask over the royal nose, and because it was ashort labor he used very little chloroform. He likely considered the amount neces-sary to induce analgesia negligible and more in keeping with the periodic nature oflabor pain.30 The inhaler might have appeared too controlling to the royal physiciansand perhaps overly invasive to the general public.31 His attendance on the Queenwas momentous for Snow’s reputation, and the fact that he was increasingly calledon to administer anesthetics during childbirth reflected a change in attitude aboutbiblical injunctions that women should bear children in sorrow. Giving the queen“that blessed chloroform” set a positive precedent for some: An editorial in the AMJnoted that the excellent reports on the queen’s health after her delivery indicated the“responsible position, and the acknowledged skill” of all the physicians involved.These “circumstances . . . will probably remove much of the lingering professionaland popular prejudices against the use of anesthesia in midwifery.”32 The physiciansattending the daughter of the archbishop of Canterbury during her delivery had nohesitation in calling Snow to Lambeth Palace to administer chloroform in October1853.33

Whereas the main point of public controversy was whether obstetric analgesia wasconsistent with biblical teaching, the issue for some medical men was the wisdomof administering to the queen a medicinal agent that had been held responsible fora number of anesthetic-related deaths.34 In May 1853 a Lancet editorial expressed“astonishment” at the “rumour” that the Queen had received chloroform. Becausechloroform in surgical anesthesia “unquestionably caused instantaneous death in aconsiderable number of cases,” the editorialist (presumably Thomas Wakley) expressed his confidence that “the obstetric physicians to whose ability the safety of our illustrious Queen is confided do not sanction the use of chloroform in natural labour.”35 The AMJ leapt to the defense of Snow and the Queen’s obstetri-cians, pointing out that sufficient chloroform to produce unconsciousness was


neither contemplated nor used and that experience had shown that cautious in-halation of small amounts of chloroform during labor was safe.36 The example ofthe queen would compel the medical world to catch up with the arguments Snowhad been making for several years.

Elaborations of Cholera Theory from 1849

During the early 1850s Snow made little progress in substantiating his cholera the-ory. In his mind the theory still lacked a compelling correlation at the metropolitanlevel between high mortality and a water supply contaminated by cholera evacua-tions. London seemed a promising test case because Southwark had nearly threetimes more deaths than the average in London and was supplied by the SouthwarkWater Works with unsettled, unfiltered, sewage-contaminated Thames water. Be-tween 1832 and 1848 the water company had moved its source of supply upstreamto Battersea, which was still within the tidal zone. Snow had published his 1849 the-ory without “a full account of the recent epidemic in London, in its relation to thewater,” hoping that vital statistics prepared thereafter by the GBH and the Registrar-General’s office would contain the information he needed to determine if the South-wark water company’s move away from the major sewer outlets had reduced mor-tality from cholera in the borough it supplied (PMCC, 747). Neither report musthave entirely suited Snow’s purposes, for his promised comprehensive study of the1848–1849 epidemic in south London did not appear.

While awaiting the next major visitation of cholera in London, Snow used med-ical society meetings and the medical journals to restate his 1849 thesis, with an oc-casional elaboration on a portion of it. An early opportunity occurred at a January1850 meeting of the Royal Medical and Chirurgical Society. Sir Benjamin Brodie reada paper sent by Dr. Robert D. Thomson from Glasgow detailing his “chemical re-searches on the nature and cause of cholera.” The author’s conclusion was that “thecause of cholera is not a specific, tangible poison, introduced into the body fromwithout, but rather a vicarious transference of the cutaneous excretion to the intes-tinal mucous membrane, dependent partly on an atmospheric influence, and partlyon a predisposing state of the system, in those who are affected with the disease.”37

Dr. Thomas Addison, the president, acknowledged Snow as first respondent. Snowbegan by noting that Thomson’s analyses of the state of the blood “confirmed thosepreviously made by Drs. Garrod and Parkes in almost every particular,” thereby sup-porting his own theory of the pathology of cholera that was based in part on Gar-rod’s and Parkes’ papers. Nevertheless, Snow found it curious that while Thomson’scarefully conducted experiments proved “cholera did not depend on a poison dif-fused in the atmosphere . . . [and had] given an account of the fanciful reasonswhich had led medical men to attribute cholera to the presence of a poison diffusedin the atmosphere . . . he did not seem to have emancipated his own mind from


the atmosphere as a cause of the disease.” Snow dismissed both general and local mi-asmatic explanations with an off-hand remark that cholera appeared in “cold andfoggy” Glasgow as easily as it did in warmer London. He returned to the patholog-ical element in his theory by noting that congestion in capillary circulation wasbrought about by a prior withdrawal of water from the system and was thereforesecondary to the intestinal affection. He supported Thomson’s “parallel betweencholera and influenza” and posited that “both these epidemics were propagated bya poison generated in the human body”—that is, carried in the evacuations or ex-halations, respectively, of the sick to the healthy—and “the poison was in each caseapplied to that mucous membrane which was the chief seat of the disease.” Thosewho dismissed the contagiousness of influenza on the grounds that it spread toorapidly were laboring under an outmoded notion of contagion, whereby transmis-sion must occur by direct contact or infection by inhaling morbid matter volatilizedfrom the skin of the sick. “But if it was communicated by the breath, from one per-son to others, this difficulty disappeared, for influenza did not spread so swiftly as apiece of bad news, also communicated by the breath.” Because the cholera poisonhad to be swallowed, according to his theory, cholera spread more slowly than didinfluenza but usually “most extensively where there were the greatest facilities for theswallowing of excretions” such as “want of personal cleanliness” and contaminateddrinking water. Statistical tables recently published by the Registrar-General clearlyshowed that “the epidemic [of 1848–1849] had been most fatal in those districts ofLondon supplied with water obtained from the Thames in the neighbourhood ofthe chief sewers, and which must, when cholera is prevalent, contain the evacuationsof the patients.” He also pointed to a contamination of local water that paralleledthe incidents he had recounted in MCC and PMCC: The cholera had been particu-larly fatal in the Bridge Street neighborhood of Blackfriars, London, “around whichspot the inhabitants used to send to St. Bride’s pump for their drinking water; andthis pump had since been closed, at the instance of Mr. Hutchinson, surgeon, it hav-ing been ascertained that the well was contaminated, by a sewer running into theFleet ditch”—not, in a final jab, by the atmosphere.38

Snow must have talked for many minutes, because the reporter’s account of hiscomments exceeds the space allotted to Thomson’s paper. Snow’s enthusiasm for histheory that the cholera poison must be ingested may explain why he proposed a par-allel with the pathology and transmission of influenza. His dismissal of miasmaticexplanations as “fanciful” shows that there were limits to his patience with oppo-nents from this camp. His disagreement with contagionists and contingent conta-gionists was temperate and respectful. He essentially asked them to substitute“method of communication” for contagion and local affection of the alimentarycanal for systemic blood infection. The reference to the Registrar-General’s tables in-dicates that Snow found enough information in them to support his theory of lo-cal, neighborhood differences in cholera mortality in London, but insufficient in-formation for a full-scale confirmation. The story of the surgeon who identified the


St. Bride’s pump as the source of a neighborhood outbreak was tucked away in Snow’smemory for a later occasion.

We do not know what Snow said a year later at a January meeting of the Epidemi-ology Society when commenting on a paper “On the infectious origin and propaga-tion of cholera.” The reporter noted only that Snow and a few other members made“some remarks,”39 but it seems likely that he would have supported Dr. AlexanderBryson’s dismissal of “a general aërial cause—an epidemic constitution of the atmo-sphere,” and Bryson’s conclusion that “we have no reasonable proof that there ever didexist a specific condition of the atmosphere capable of producing cholera, or that thereever was evolved from the earth, or engendered in the air, a cause capable of produc-ing it.”Bryson saw no merit in anticontagionist reasoning, whether of the general atmo-spheric and seasonal variety (epidemic constitutions) or the production of local mi-asmas view. With respect to Snow’s cholera agenda at the time—refining his 1849theory and seeking more confirmatory evidence—Bryson listed many instances of “thepropagation of cholera from one or more cases transported from an infected localityinto a healthy ship, which can only be explained by the reproduction of an infectiousvirus through a series of consecutive cases.”40 Snow had already pointed out such aprogress of cholera in PMCC, and it would become increasingly prominent in futurewritings. However, he no longer shared Bryson’s view that “an infectious virus” devel-oped in the bodies of cholera victims could be inhaled by others in overcrowded, poorlyventilated spaces and then produce a systemic fever.

Snow did focus on points of agreement with Bryson in the opening paragraph ofa paper he read at meetings of the Epidemiological Society in May and June of 1851,the first formal elaboration of his 1849 essays on cholera. This time he chose a slightlydifferent title, “On the mode of propagation of cholera,” and returned to the open-ing used in MCC on the communicability of the disease from person to person, “be-ing probably the real feature of distinction between epidemic and other diseases.”41

He cited the table in PMCC in which he had used Merriman’s figures on “the directrelation which exists between the number of the population and the duration of thedisease” in the 1832 epidemic to make the case that personal intercommunicabilitycharacterized cholera. He thought it likely that “the same rule has obtained duringthe recent epidemic, but I have no precise information on this point”(559). The ex-pected statistical information was not forthcoming from governmental reports, soSnow had continued his literature searches and extensive correspondence in hope ofbuilding a support for his theory by an enumeration of instances. He had recentlyreceived a letter recounting the spread of cholera from a “want of personal cleanli-ness” (560), another detailing cases produced by eating contaminated cow heels(560), and personal observations by himself and Mr. Peter Marshall, his friend andmedical colleague, of cholera spread through furnishings contaminated by choleraevacuations (560). The paragraph on cholera pathology was essentially a reprise ofwhat he had written in MCC and PMCC, with the exception of a statement that “itappears, indeed, that the cholera poison never enters the circulation . . .” (559).


Then Snow shifted to “another very important medium for transmitting thecholera poison from the sick to the healthy” not covered by traditional concepts ofcontagion—“the water which people drink” (560). Dr. Lloyd had articulated the sameprinciple when he presented his findings on Rotherhite (described in PMCC) at amedical society meeting at the same time MCC appeared. Snow rounded out thefirst part of his paper by quoting extensively from MCC on the outbreaks in AlbionTerrace and Horsleydown, as well as repeating the gist of Lloyd’s study and sum-marizing remarks sent him by a physician from Essex. He concluded part one witha critique of the GBH’s notification that “vitiated water acts as a poison on the stom-ach and the bowels . . .” (562). Not so, said Snow: “However repulsive to the feel-ings the swallowing of human excrement may be, it does not appear to be very in-jurious so long as it comes from healthy persons, but when it proceeds from cholerapatients, and probably patients with some other maladies, it is a means of commu-nicating disease” (562).

He finished reading this paper at the June meeting of the Epidemiological Soci-ety. Whereas part one had enumerated local outbreaks of cholera, part two detailedthe current state of his research on cholera outbreaks “on a more extensive scale,[communicated] by means of the sewers which empty themselves into various rivers,from which the population of many towns derive their supply of water” (610). Firstsummarizing the findings outlined in PMCC, he then turned to his still incompletestudy of mortality in relation to the water supply in London during the 1848–1849epidemic. He confirmed the results listed in the table in MCC showing that mortal-ity was lower in districts supplied by some water companies than others. There werefew deaths from cholera where Chelsea Company water was distributed, except forone location, where it turned out that “many of the people obtained water by dip-ping a pail into the Thames” (610). Dr. Arthur Hill Hassall’s report on London wa-ter confirmed that filtered water from this company was “free from the hairs of thedown of wheat, yellow ochreous substance, (believed to be partially-digested mus-cular fibre,) and other substances which had passed through the alimentary canal,and were found in the Vauxhall and Lambeth Companies’ water” supplied to dis-tricts south of the Thames (610). Snow also mentioned another report by John Grant,the surveyor who had brought the outbreak in Horsleydown to his attention, of a“house to house visitation” that connected unusually high mortality to the con-sumption of water from ditches connected to the Thames. Snow presented a tablecopied from a Weekly Return that showed “the mortality from cholera in the differ-ent districts of London supplied by the various Water Companies” (611). This tablefurther confirmed what he had suggested about London in MCC: “the mortality willbe found to bear a very close relation to the absence or presence of connexion be-tween the sewers and the water supplied. It also appears from the same table thatthe average mortality from all causes in a series of years bears a relation to the qual-ity of the drinking water. There is great reason to believe that typhoid fever and someother epidemic diseases are communicated occasionally through the drinking water;


and . . . [that plague] is communicated exactly the same way as cholera,” and per-haps ague in some situations as well (611). He had sympathetic words for the dis-mal fate of the Bristol fungi researchers. The “supposed fungus” had not withstoodmicroscopic scrutiny, but “it was, perhaps, too much to expect that we should ob-tain a knowledge of cholera more exact than that which we possess of syphilis, small-pox, and other better known diseases” (612). Nevertheless, “the labours of these gen-tlemen” were not in vain, at least from Snow’s perspective, for they “confirm the factof the water in various places being a medium of communication between the ali-mentary canals of cholera patients and those of other people” (612).

In addition to collecting new evidence in support of his theory, Snow elaboratedon the preventive measures he had outlined in 1849. In the paper read at the Epi-demiological Society he listed five: avoid water that might be contaminated by sew-ers, drains, cesspools, and “persons living in boats”; extend availability of wash basinsamong the poor; urge everyone who came in contact with cholera patients, espe-cially food preparers, to be especially attentive to cleanliness; immerse linen soiledby cholera evacuations in water until it can be boiled; and separate cholera patientsfrom the healthy, even placing them in “another abode” if necessary (612). Althoughmost sanitation conscious medical men would have agreed with the first four mea-sures, the fifth was at odds with the views of those who thought cholera was notcontagious. Separation of the sick from the healthy would also be expensive to carryout, which did not incline public authorities toward Snow’s views. In a separate ar-ticle published in MTG two years later, he reiterated the five measures he believedshould be taken when cholera was present, and added a sixth—washing “all the pro-visions which are brought into the house” with clean or boiled water. In addition,he suggested that improvements in drainage, water supply, and lodging houses, aswell as the cultivation of “habits of personal and domestic cleanliness among thepeople everywhere,” should be undertaken to avoid future epidemics of cholera.41a

Snow’s article on prevention, written late in September 1853, when the thirdcholera epidemic had just begun, contained two additional elaborations of the 1849theory. First, he strengthened his argument about the person-to-person transmis-sion of the disease in coal mines by quoting from a letter sent by his brother, RobertSnow, a colliery agent near Leeds.” The pit is one huge privy, and of course the menalways take their victuals with unwashed hands” (368). Second, “a medical friend inNewcastle” had sent him a report on how that town and Gateshead, immediatelyacross from it on the River Tyne, had fared in the last three epidemics. The 1832 epi-demic had been severe, as Snow knew well enough from his own experience thereas an apprentice: “There were no waterworks in Newcastle” at the time, but the springwater used for drinking—stored in cisterns and public fountains—was probably con-taminated. In 1849 the new waterworks drew its supply from distant springs, andthere was little cholera. In the most recent visitation the water company supple-mented its regular supply with water from the Tyne a mile upstream. “The tide, how-ever, flows for several miles further, and, consequently, carries the sewage past the


place where the water is obtained. When the cholera became established in Newcas-tle” early in September, the sewers carried evacuations into the river, which weresucked into the water pipes. As had happened earlier in Bermondsey, the cholerasoon “became generally diffused among all classes of the community” until com-plaints about water quality caused the company to discontinue drawing river water(368). In Snow’s mind this incident was “a fresh illustration” of how “whole townswere, more or less, affected by drinking the water of rivers into which the sewers dis-charged their contents” (368). The problem was that he needed precise figures anda controlled experiment, not more illustrations, to convince the skeptics.42

Treatment of Cholera

Until the third epidemic reached England in 1853, Snow seems to have focused onprevention rather than treatment of cholera, but government authorities had not,generally, adopted the simple sanitary measures he advocated to keep the inevitablecases of cholera that reached port cities from spreading. In January 1854 he turnedto the subject of treatment in a paper read at the Medical Society of London.43 Hereasoned directly from pathology to therapy, noting that one should only employremedies that would coat the intestines and perhaps reduce the loss of fluid and saltsfrom the blood or replace lost fluids. The therapeutic regimen he proposed, there-fore, was considerably more restrained than the heroic measures advocated by manyof his colleagues.

Snow’s therapeutic frame of reference was conventionally humoral. He believedthat the premonitory phase of cholera, resembling an ordinary case of diarrhea inmost features, was part of the overall choleraic disease process, so that successfultreatment of that phase might abort the entire attack. Accordingly, he recommendeda mild antidiarrheal treatment then in common use (such as pulvis cretae composi-tus cum opio, powder of chalk combined with opium), adding that its efficacy pro-vided indirect proof of his hypothesis, because antidiarrheals could act only withinthe gut and could not possibly affect any blood-borne poison (181).

His therapeutic practice was based on the view that the cholera material was in-gested and reproduced in the gut; in this respect, Snow was anything but conven-tional. He assumed (drawing on the researches of Liebig) that a process of continu-ous molecular change analogous to fermentation or putrefaction was going on alongthe mucous membrane of the alimentary tract, so that the best medicine to admin-ister early in the course of cholera would be a substance that would (a) “come incontact, if possible, with every part of the mucous membrane of the whole alimen-tary canal” and (b) “have the property of destroying low forms of organized beings,and of arresting fermentation [and] putrefaction” (181). Because the cholera parti-cle had not been identified, he reasoned by analogy. He did not claim that the cholera particle multiplied or did its damage specifically by means of the processes


of fermentation or putrefaction. Instead, he proposed that as some sort of “low formof organized being” with a cellular structure, the cholera particle was susceptible tobeing killed or inactivated by the same chemical substances that were known to beeffective against processes caused by other low forms of life. Such chemical sub-stances included olive oil, animal charcoal, sulphur, oil of cajeput, camphor, and cre-osote, all of which had been reported by other physicians to have some efficacy incholera treatment. Chloroform taken orally exhibited similar “antiseptic and med-ical properties; and it has gained some reputation as a remedy for cholera, when in-troduced into the stomach. Administered in the way of inhalation, it is merely use-ful in relieving the cramps, and has no effect on the progress of the malady; while,if cholera were a blood disease, it would be by inhalation that this and every othervolatile medicine ought to be exhibited” (181)—a succinct defense of his new choleratheory, based on his expertise as an anesthetist.

For victims who entered the collapse stage Snow recommended saline injectionsinto the veins. He noted that “the results obtained, by injecting the blood-vessels in1832, were so far encouraging, that it is somewhat surprising that this practice washardly resorted to in 1849” (182). Despite mortality data that others interpreted ashighly unfavorable to this procedure, Snow refused to abandon a treatment optionthat fit so well with his theory of cholera pathology. Snow even mentioned that Mr.Henry Lee had suggested injecting a weak saline solution into the arteries instead ofthe veins. Snow calculated the fluid loss necessary to produce the amount of hemo-concentration noted in the 1849 experiments of Garrod and Parkes as approximately100 ounces in a healthy adult. “This calculation may be useful as indicating theamount of fluid, which ought not to be exceeded in the injection of the blood-vessels” (181). He also attributed to Garrod a suggestion that phosphate of soda beused rather than carbonate of soda as a component of the saline solution, so as bet-ter to replace the electrolytes that had been lost from the bowels. On the other hand,Snow thought there were other effective ways to replace lost fluid volume: “To allowthe drinking of cold water, for which there is a great desire, is in accordance bothwith reason and experience” (182), but “reason and experience are just as much op-posed to hot air-baths and other attempts to raise the heat of the surface, which canonly have the effect of increasing the symptoms of asphyxia, so long as the blood re-mains so thick and tenacious.” On this point we find Snow reaffirming one of hisearliest statements about cholera, but on a very different theoretical basis. Whereasin the fall of 1848 he assumed (like most of his colleagues) that cholera “in someways resembled” asphyxia, when new cholera cases appeared five years later he couldoffer a coherent account of precisely how the pathology of cholera could eventuallyproduce secondary, asphyxialike symptoms.

The year 1853 was a banner year for Snow. He continued to advance his under-standing of inhalation anesthesia, and his recognized skill in that field had taken himdirectly to Buckingham Palace. He became even more convinced that his theory ofcholera transmission was correct, and he had continued to accumulate examples of


person-to-person and water-borne transmission. When it became clear late in thefall that a third cholera epidemic was underway in London, Snow began collectingdata from the Weekly Returns to use for the oft-postponed study of cholera mortal-ity in relation to metropolitan water supply.

Notes

1. “Westminster Medical Society,” Lancet 2 (1849): 431–32. Snow had presented a “Lectureon the causes and prevention of cholera” at the Western Literary Institution on Thursday, 4October, which may have been an excerpt of the paper he delivered nine days later; Lancet 2(1849): 413.

2. “Westminster Medical Society,” Lancet 2 (1849): 432.3. “Westminster Medical Society,” Lancet 2 (1849): 431–32. The society’s procedure required

that Snow wait until everyone who wished to comment had done so before he could reply toany comments, so the proceedings of this meeting do not include any of Snow’s reactions tocriticisms. Dr. Stewart’s comment about the autoingestion experiment suggests that Snowadded the reference to a similar Berlin experiment in PMCC subsequent to delivering the pa-per because the Lancet report did not mention it. Stewart also thought “that Dr. Snow’s hy-pothesis did not explain certain great and sudden outbreaks of cholera that had happened inIndia”; PMCC contains a paragraph on that, as well.

4. “Westminster Medical Society,” Lancet 2 (1849): 459–60, meeting of 20 October.5. “Death of the Marquis of Anglesey,” Times (1 May 1854), 8. The implicit point of Snow’s

lengthy first entry in his casebooks also reinforces his sense of the old soldier’s bravery (CB, 122–23).6. Snow continued to provide anesthesia services gratis in three workhouse infirmaries, in

addition to continuing to attend to some of his old general practice patients; S. Snow, JS-EMP,296. John French, the surgeon that Snow assisted at the Poland Street Workhouse, later ac-knowledged his colleague’s commitment to aiding the poor; Lancet 2 (1858): 103.

7. Sykes, “Anaesthetic deaths,” 26–43.8. The enumerator for the 1851 census listed two households at 54 Frith Street: John Snow,

born in the city of York, unmarried, aged 38, physician, MD, University of London, LRCP. Theother consisted of Mrs. Sarah Williamson, widow, aged 70, on an annuity; her daughterEleanor, aged 48, fancy needle and bead worker; Marion Watkin, aged 19, crochet worker; andJane Wetherburn, aged 39, general servant; UK Home Office, 1851 Census, H.O. 107/1510/82.According to Richardson, Snow rented his flat from Mrs. Williamson; L, ix.

9. Snow, “On narcotism” LMG 45 (1850): 622.10. Snow, Letter to the Right Honourable Lord Campbell (1851). The casebooks reveal many

examples of situations in which chloroform was forced on an unwilling patient.11. David Zuck constructed a map of all the general practice (i.e., nonanesthesia) domicil-

iary visits recorded by Snow in CB from 1848 to 1858. The map shows Snow’s failure, by andlarge, to expand his general practice beyond its initial base in Soho. A notable exception aretwo visits paid by Snow to 40 Ampthill Square and 37 Gloucester Road in 1849 and 1851, re-spectively. Both visits were to the home of the same person—Thomas Jones Barker(1815–1882), a historical painter and member of the Royal Academy. Charles Empson knewthe painter’s father, Thomas Barker, in Bath, so it may have been via his uncle that Snow madethe family’s acquaintance. Barker, best known for his battle scenes of the Napoleonic andCrimean Wars, exhibited his portrait of “Dr. Snow” (see Fig. 4.1) at the Royal Academy in1847; see Zuck, “Snow, Empson, and the Barkers of Bath.”


12. Newman, Medical Education, 8–9; G. Clark, Royal College of Physicians, 2: 518, 686–87;Peterson, Medical Profession, 6–7; Shephard, JS, 63–64; and Ellis, CB, xviii. Zuck supplied thedata on Snow’s practice in the 1850s. Snow was probably not disappointed that he would neverbe able to join the elite “club” of fellows among physicians. He was eligible to become a fel-low of the Royal College of Surgeons when that honorific title was established in the 1840s,but had not done so. His view of professional involvement seems to have been egalitarian, nothierarchical. Snow continued to serve as GP to predominantly poorer patients in the Sohoarea until 1849; Shephard, JS, 59.

13. Snow’s name first appears for the 1850–1851 session; Pathological Society of London,Transactions 3 (1850–52): 14.

14. Shephard, JS, 62–64.15.“Medical Society of London,” Lancet 2 (1850): 456–57. See also Storey,“Henry Clutterbuck.”16. Richardson, L, xxiii.17. Richardson, L, xxiv; quotation from JPH&SR 1 (1855): 3.18. “Proposed new society for the investigation of cholera and other epidemic diseases,”

Lancet 2 (1849): 301, issue of 15 September; “Further remarks on the proposed new societyfor the investigation of cholera and other epidemic diseases,” Lancet 2 (1849): 592, issue of 17November.

19. “Epidemiological Society,” MT 22 (1850): 132–33. Benjamin Guy Babington(1794–1866), a physician at Guy’s Hospital, was interested in organic chemistry and is cred-ited with the invention of the laryngoscope in 1830. He shared with Snow an interest in abroad array of sciences and a willingness to draw useful analogies from nonmedical scientificfields; A. Evans, “Let’s not forget B G Babington”; Wilson, “Benjamin Guy Babington.”

20. “Epidemiological Society,” Lancet 2 (1850): 640.21. JPH&SR 1 (1855): 2, 3, 5–6.22. “Epidemiological Society,” MT 2 (1851): 54; “On the mode of propagation of cholera,”

MT 3 (1851): 559–62, 610–12; “Epidemiological Society,” MT 3 (1851): 522–24; “Epidemio-logical Society,” MTG 5 (1852): 177 (papers on “Failure of vaccination in Bengal” and the“Success of vaccination in Bombay”);“On the relations of vaccination and inoculation to Small-Pox,” MTG 6 (1853): 74–76 (from which the quote is taken); Snow, “On the comparative mor-tality of large towns and rural districts, and the causes by which it is influenced,” reported inMTG 6 (1853): 561, and AMJ 1 (1853): 404, published in full in Transactions, JPH&SR 1 (1855).

23. “He used often to meet with opponents to his peculiar opinions at the meetings of thisSociety, but he always retained friendships”; Richardson, L, xxiv. For Snow’s comments on theostensible similarity in mode of propagation of cholera and black death, see “Epidemiologi-cal Society,” MTG 7 (1853): 615.

24. Richardson, L, xxxii–xxxiii.25. “Medical Society of London,” MTG 6 (1853): 610. The president at the time was Forbes

Winslow.26. Snow, “On the use of chloroform in surgical operations and midwifery,” LJM 1 (1849): 54.27. Before being asked to treat the queen in 1853, Snow had worked with two of the royal

physicians, Drs. Clark and Locock, on other cases since 1849 and had administered anesthe-sia to two palace servants and a lady-in-waiting; S. Snow, JS-EMP, 306.

28. About two weeks after administering chloroform to the queen, Snow altered the way heentered notes in his Case Books. Previously, he had entered all his cases, whether general prac-tice or anesthesia, in chronological order. Shortly after the Buckingham Palace experience heseparated the two, placing anesthesia case notes at the front of his book and general practicenotes at the back. S. Snow believes that this change in note taking marks Snow’s sense of him-self as a specialist anesthetist; JS-EMP, 303.


29. For example, within a month of the queen’s delivery, on 23 April 1853, Snow reportedthat he used the inhaler for the last forty-five minutes while Dr. Reid delivered the HonorableMrs. Proctor Beauchamp’s first child; Ellis, CB, xxx.

30. Shephard, JS, 117.31. The general public came only belatedly to know about the use of chloroform and Snow’s

role in administering it. The initial court statements to the press mentioned neither Snow norchloroform. It was not until 23 May that the Times gave an account of Snow’s administrationof the chloroform, after the medical press had already “broken” the story.

32. “Her Majesty’s accouchement: Chloroform,” AMJ 1 (1853): 318.33. Ellis, CB, 300–01.34. Caton, What a Blessing; Pernick, Calculus of Suffering.35. Lancet 1 (1853): 453. The Lancet was careful not to impugn the value of chloroform in

surgical anesthesia and noted with satisfaction that reportedly the queen had never lost con-sciousness. By the time the editorial appeared the fact that chloroform had been administeredto the queen had been authoritatively reported in several places, so Wakley was presumablybeing coy by referring to the fact as a “rumour.”As we have seen (Introduction and Chapter4), this was neither Snow’s first nor last run-in with Wakley’s journal. Snow published ap-proximately 89 separate papers (depending on how one counts multipart articles) in medicaljournals, of which fifteen appeared in Lancet. Eight of the fifteen papers were published after 1853, so the flap over giving chloroform to the queen did not discourage Snow fromsubmitting.

36. “Her Majesty’s accouchement: Chloroform,” AMJ 1 (1853): 450. The AMJ editors notedin passing a similarly approving statement that had appeared in MTG.

37. “Royal Medical and Chirurgical Society,” Lancet 1 (1850): 154–55. Thomson was thechief chemical consultant to the Committee on Scientific Inquiries of the GBH in 1854 and1855. Subsequent citations to the report of Snow’s comments at this meeting are not indi-vidually cited.

38. Lancet 1 (1850): 155.39. “Epidemiological Society,” MT 2 (1851): 54.40. “On the infectious origin and propagation of cholera,” MT 2 (1851): 669, 666. The en-

tire paper was published in three installments; MT 2 (1851): 506–10, 648–51, and 666–71.41. Snow, “On the mode of propagation of cholera” (1851), 559.41a. Snow, “On the prevention of cholera” (1853), 369.42. See also Snow, “The water supply at Newcastle,” Times, 11 November 1853.43. Snow, “Principles on which the treatment of cholera should be based” (1854).


254

OF ALL THE CONVENIENCES that the modern industrializedworld takes for granted, the availability of free-flowing water in

every kitchen and bathroom is surely one of the foremost. During Snow’s lifetimefew in London were so fortunate. Many continued to haul water from a neighbor-hood pump, and those who had water piped to their residence frequently receivedit, albeit with intermittent flow, in cisterns or butts in a courtyard rather than in-side. Nevertheless, a water supply directly to one’s house was a much desired com-modity in London, and private companies had competed for the opportunity to pro-vide it since the previous century.1 In 1817, however, this open market was replacedby a regional patchwork of monopolies within which a single company laid pipes.When water rates under this cartel system rose considerably, limited competition wasreintroduced in the mid-1830s. In north London the Hampstead and New River wa-ter companies were permitted to lay pipes in the same streets and solicit customers.In south London the Lambeth and Kent water companies were given similar accessto neighborhoods previously reserved for the South London Water Works. Elsewhere,the monopoly system remained in force.

Piped drinking water was often foul and became increasingly more so in the firsthalf of the nineteenth century, particularly when the source of supply was the Thamesor the Lea, which flowed into the Thames opposite Greenwich. These rivers servedas the final destination of many sewers constructed as part of the sanitary reform

Chapter 10

Cholera andMetropolitan Water

Supply

campaign to reduce urban effluvial vapors from human wastes, husbandry barns,slaughterhouses, and other so-called nuisance trades. Public clamor at the growingfilth of river water led to the appointment in 1828 of a royal commission to inves-tigate London water quality and supply. Although several medical men testified thatdrinking water contaminated with raw sewage was a likely cause of ill health, thecommission did not recommend significant parliamentary intervention. On theirown volition, however, some water companies established filtration mechanisms andsettling reservoirs, and a few shifted their supply to purer sources after the choleraepidemic of 1831–1832. For example, the East London Water Company added anintake pipe on the Lea River above the tidal reach of the Thames, and the GrandJunction Company (supplying west London) shifted its supply source from Chelseato Brentford, several miles above London on the Thames (Fig. 10.1).2

However, sanitary reformers, led by Edwin Chadwick, were less concerned aboutwater for human consumption than about its potential for flushing dirt and sewagefrom homes and streets. Every town and city, they thought, should have a high-volume water supply and a well-engineered sewage disposal system that, together,would carry the contamination of urban life back into rivers and eventually to thesea. In London the general increase in the volume and pressure of water supplies inthe first half of the nineteenth century did, indeed, lead to more efficient flushing

Cholera and Metropolitan Water Supply 255

Figure 10.1. Map of metropolitan London showing Rivers Thames and Lea, as well as the met-

ropolitan districts served by various water companies.

of sewage into the Thames, but because the Thames also served as London’s princi-pal water source, improvement in sanitation actually increased the admixture ofsewage in drinking water, especially as the sanitary reformers were successful in con-vincing people to replace cesspools with water closets. When objections were raised,sanitary reformers assured the public that all contaminants were harmlessly diffusedin the large volumes of river water.3 After the second cholera epidemic of 1848–1849,public pressure to improve the quality of London water rose steadily. In 1852 Par-liament approved a bill that required private water companies in London to filter allwater, cover all reservoirs, and move their sources of supply above the tidal flow ofthe Thames and the Lea. They were given until the end of August 1855 to comply.4

Snow, who distilled his own drinking water, agreed that London water should beimproved, but he considered the abolition of cesspools and the increasing preferencefor water closets a sanitary disaster. Cesspools were odoriferous, but they did con-tain and prevent the transmission of the morbid agents of cholera until they couldbe disposed of safely. By contrast, water closets connected to sewer lines that emp-tied into rivers also used for metropolitan drinking water were, in his mind, prima-rily an efficient means of recycling the cholera agent through the intestines of vic-tims as rapidly as possible. Sanitary reforms were needed, but flushing the waste ofa town into the same river by which one quenched one’s thirst seemed sheer stu-pidity. The agent that made cholera lethal to humans had not been isolated, but Snowwas convinced that it retained its constituent form regardless of how much waterwas added to it. If he was right, any change in water supply, whether local or mu-nicipal, that lessened the chances of people ingesting sewage from cholera victimsshould be reflected in reduced cholera mortality.

Linking Water Supply to Cholera

Snow’s thinking about cholera and the water supply reflected the extension of a phys-iological hypothesis across a hierarchy of levels of organization (see Table 8.2). Hetook a disease hypothesis, formulated fundamentally from clinical observations insick patients and built on a foundation of insight into likely mechanisms and ob-servations about pathophysiology and clinical symptomatology, and used it to ex-plain the geographic and temporal patterns created by tens of thousands of cases ofdisease occurring in populations of millions. His first principles were physiologicaland clinical; the observations that he predicted (and confirmed) at the populationlevel were experimental evidence for the correctness of the underlying hypothesisabout the way in which cholera is transmitted. He sought evidence for his trans-mission hypothesis at a variety of ecological levels, each of which received differentprominence in his writings. His cholera transmission hypothesis, and its extensionsto different ecological levels, is expressed formally in Table 10.1.


The escalation of Snow’s hypothesis from individual to city is a distinctive featureof his thought. Until that time no hypothesis of disease etiology had successfully ex-plained any pattern of disease occurrence simultaneously at several individual andecological levels. During the fall of 1848, his clinical experience with cholera victimsand his reading in medical journals substantiated the corollary at level A, person-to-person transmission in mines and households, but he had hesitated to publish hishypothesis until he could cite examples of transmission at the next two ecologicallevels. The initial breakthrough came the following August, when Snow learned ofJohn Grant’s engineering reports describing the drainage and water supply in Sur-rey Court, Horsleydown, and Albion Terrace. Snow devoted most of MCC to a minutereconstruction of events that could have produced sewage contamination of a localwater source, followed by water-borne transmission of cholera from the initial vic-tims to their neighbors—exactly as predicted by his corollary at level B. In MCC healso presented evidence that indicated an association between degrees of choleramortality in towns and the nature of their water supplies (level C). The Rivers Nithand Clyde, like the Thames, functioned simultaneously as recipients of human wasteand as sources of municipal water. The information available to him was incomplete,particularly about mortality in the current epidemic, but it appeared that the threemajor cities served by these rivers—Dumfries, Glasgow, and London—suffered moreseverely in 1832–1832 and 1848–1849 than did towns with purer sources of drink-ing water.


Table 10.1. Ecological levels in Snow’s theory about cholera transmission

Hypothesis The morbid agent of cholera is found in the evacuationsof cholera patients and must be ingested to causedisease.

Corollary at level A— Circumstances that promote contact with the evacuationsindividuals of cholera patients (lack of light, lack of washing

facilities, mines, overcrowding, food at wakes) promoteperson-to-person transmission and the clustering ofcholera in families, households, lodging houses, mines,ships, and similar circumscribed areas.

Corollary at level B— Brief localized epidemics of cholera in which manyneighborhoods individuals are simultaneously affected are likely

due to a local water supply contaminated with theevacuations of one or more cholera patients.

Corollary at level C— The general pattern of epidemic cholera in largelarge populations populations such as cities and towns over the

entire duration of an epidemic is strongly related to the extent to which its municipal water supplies are fecally contaminated.

The principal difference between MCC and PMCC (published two months later)was an increase in the number of instances of urban water-borne transmission thatSnow could document, particularly outside of London. He had carefully searchedthe literature, had investigated water supply patterns in some localities, and had en-listed the help of physicians, ministers, and friends in assembling such evidence fromtowns throughout England. The most persuasive new evidence supporting his hy-pothesis of level C transmission came from Exeter and Hull, each of which hadchanged its water supply between the 1832 and 1849 epidemics. Exeter had reposi-tioned its waterworks upstream of the main sewer outlets after the first epidemic,and cholera mortality was less in 1849. In Hull new waterworks were also constructedbetween epidemics, but they were positioned within the tidal reach of the Humberestuary. The result was the opposite of that in Exeter: Whereas cholera mortality inHull was low during the 1832 epidemic, when the drinking water came from springsoutside of town, it increased in 1849, when the water was drawn from a pollutedtidal river.5 The situation in Snow’s hometown offered confirming evidence withinthe same epidemic: “When the cholera made its appearance at York, about the mid-dle of July last [1848], it was at first chiefly prevalent in some narrow streets nearthe river, called the Water Lanes. The inhabitants of this spot had been in the habitfrom time immemorial of fetching their water from the river at a place near whichone of the chief sewers of the town empties itself; and recently a public necessity hadbeen built, the contents of which were washed every morning into the river just abovethe spot at which they got the water” (PMCC, 750). Local authorities eliminated ac-cess to the River Ouse and opened the taps to drinking water supplied from puresources outside the city; cholera mortality soon decreased in the area. The taps wereclosed, and the people drew water from the river and began to die again. When thetaps were reopened and remained so,“the cholera again ceased, and has not recurred”(PMCC, 750). Nevertheless, these examples from Exeter, Hull, and York were onlysuggestive. London was the major metropolis in Great Britain, yet the “want of ex-act information” about its water supply noted in MCC (25) continued to stymieSnow’s effort in PMCC to prove his hypothesis about level C transmission.

Equally troublesome were skeptical reviews of MCC, particularly one in LMG thatchallenged his analysis of Albion Terrace as an example of local level B transmis-sion.6 In essence, that reviewer did not consider Snow’s reasoning more persuasivethan Milroy’s. Gavin Milroy, the physician associated with the sanitarian orientedGBH, had investigated the outbreak in Albion Terrace and turned in a report beforeSnow finished writing MCC. Snow believed he had effectively countered Milroy’s lo-cal miasmatic interpretation that effluvia wafting from nearby sewers and ditchescould have swept across the row of houses in Albion Terrace and caused the out-break. If he did not realize it before, there was no denying after the reviews of MCCthat the editors of two major London medical journals thought he had not answeredthe “Milroy objection” to his theory. In each instance in which cholera was associ-ated with impure water, it was possible for a miasmatist to argue that dirty water


was not the determining factor. Snow had not excluded the possibility that the qual-ity or nature of the local atmosphere could account for the patterns of the disease.The papers he published on cholera in 1851 and 1853 continued to adduce the im-portance of water supplies, but he found no examples at the metropolitan level thatunambiguously answered the Milroy objection to his hypothesis.7

The opportunity he sought occurred in London when epidemic cholera returnedbefore all the private water companies had shifted their sources of supply in com-pliance with the new law. He documented his findings in a book published early inJanuary 1855 as the second edition of MCC. At 137 pages MCC2 was “much en-larged” from the thirty-one-page pamphlet published five and a half years earlier.8

While MCC2 replicated much of the evidence first presented in MCC, it containedeven more from PMCC; in fact, MCC2 is better described as a second edition ofPMCC. The critical evidence presented in MCC2 was the association between dif-ferential water supplies and cholera mortality in south London that Snow discov-ered in the fall of 1853, began investigating the following summer, and finished an-alyzing in 1856.

The Weekly Returns of November 1853

Absent since 1849, cholera returned in the summer of 1853. As autumn came andtemperatures dropped, Londoners hoped that the cholera epidemic would abate, butit was still in the grip of the epidemic in the middle of November. At the main Gen-eral Register Office (GRO) in Somerset House, William Farr’s staff published eachSaturday a new edition of the Weekly Return of Births and Deaths in London.9 Theissues of 19 and 26 November contained new information that Snow found verycompelling. For the previous thirteen weeks Farr’s staff had been retabulating choleradeaths by district in relation to the nine different metropolitan water companies thatprovided piped water to each district. The issue of 19 November included a specialsupplement on “Cholera and the London water supply.” In it Farr reminded the pub-lic (and the water companies) of the 1852 act, which required that by the end of Au-gust 1855 no company could supply water obtained from the lower, tidal portionsof the Thames.10

Farr was as sympathetic to Snow’s 1849 theory as any medical man in London,but he believed it remained unsubstantiated. In his analysis of the GRO data for the1848–1849 epidemic, Farr thought the association between cholera mortality andthe elevation at which people resided was greater than the relationship of cholera tothe purity of their drinking water. His zymotic theory could explain this association:In the London metropolis evaporation rising from certain stretches of the Thamescontained cholera “matter” that, when combined with smog (“London fog”), settledin higher concentrations at lower elevations.11 In his mind impure drinking waterprobably predisposed susceptible individuals living at lower elevations to cholera


(and other diseases), but it was not the cause of them. Farr was, therefore, less con-cerned with the water Londoners ingested than with the water vapors they inhaled.As such, his thinking was closer to that of sanitarians who shared Milroy’s local mi-asmatic concerns about effluvia than to Snow’s. Farr acknowledged that Snow mightbe correct, but he thought the requisite threshold of proof was very high and ulti-mately unattainable: “To measure the effects of good or bad water supply, it is req-uisite to find two classes of inhabitants living at the same level [elevation], movingin equal space, enjoying an equal share of the means of subsistence, engaged in thesame pursuits, but differing in this respect,—that one drinks water from Battersea,the other from Kew. . . . But of such experimenta crucis the circumstances of Lon-don do not admit. . . .”12 Farr’s usage of the same Baconian term that Snow hademployed in his first publication indicates the importance of the hypotheticode-ductive method to some medical men of this generation. In the laboratory one canconduct a “crucial experiment” in which two samples are treated in identical fash-ion except for the factor in dispute. The results of the experiment then tell one withcertainty whether the underlying theory is correct, but London was not a laboratory,so Snow could never satisfactorily disprove Farr’s elevation theory or counter thesanitarians’s argument that other factors—overcrowding, poor ventilation, localsources of effluvia—made the real difference in epidemic cholera, whereas impurewater played only contributing or “predisposing” roles.

While Farr in his comments on 19 November underlined the difficulty of sortingout the contribution of water supply to cholera, Snow drew quite opposite conclu-sions when he read the Weekly Return published the following week (Fig. 10.2).13

The issue of 26 November contained a table describing water supplies and choleramortality that appeared identical to a table in the 19 November issue except for thenumber of deaths, but Snow noticed a critical difference. The new table containeda footnote that “in three cases (marked with an asterisk), the same districts are sup-plied by two companies.” A week after Farr had set the bar at a seemingly impossi-ble height, he had given Snow hope that London could be the setting for a crucialexperiment that would substantiate his cholera hypothesis at the metropolitan level.

The makings of this “natural experiment” took place in 1852, when one of the wa-ter companies supplying south London moved its supply above the tidal reach of theThames, whereas its competitor, serving customers in the same districts, had decidedto defer its transfer closer to the August 1855 deadline.14 There seemed no need tohurry matters; sixteen years had elapsed between the first two cholera epidemics inEngland, but by returning well ahead of schedule, so to speak, in 1853, the thirdcholera epidemic slipped through an open window when the Lambeth Companyprovided pure water, while the Southwark and Vauxhall Company (S&V) still sup-plied sewage-contaminated water. This window for a natural experiment had not ex-isted in 1848–1849 because both companies drew water from polluted points on theThames. It would disappear as soon as the S&V moved its intake source to complywith the law. It existed only because these districts had been opened to competition


Figure 10.2. Weekly Return of Births and Deaths ( 26 November 1853).

261

in the 1830s, and different water companies had laid pipes and solicited customersin the same streets.

The Crucial Experiment

The third cholera epidemic in London began in September 1853, died down the fol-lowing winter, and resumed its deadly work in the first week of July 1854.15 It raged forfourteen weeks in 1854, but a few cases were still appearing when MCC2 went to pressin December of that year. Snow focused most of his attention on the second phase ofthe epidemic in London that began in July of 1854, when he had more time to under-take house-to-house investigations than in the waning weeks of the 1853 epidemic.16

Of course, he did not know in November 1853 that the epidemic would resume thefollowing year, so he began what has since been termed the South London study by an-alyzing the data on the 1853 epidemic compiled by Farr and his staff at the GRO. Forthe thirteen weeks from 21 August through 19 November 1853, mortality in all districtssupplied by S&V alone was 94 per 10,000, whereas for the districts supplied by bothLambeth and S&V, mortality was 61 per 10,000. Snow dug deeper into the Weekly Re-turns, examining cholera rates by district in south London for the first seventeen weeksof the epidemic (through 17 December). He noted that the registration district of Lam-beth, mainly supplied by the Lambeth Company, had improved with respect to choleramortality in London, from the seventh-worst in 1849 to thirteenth-worst in 1853. Snowthen undertook what Farr had not—to compare cholera mortality by water supply atthe subdistrict level. He reorganized all cholera deaths reported in the Weekly Returnsthrough the end of December 1853 by addresses and placed them in three groups: twelvesubdistricts exclusively supplied by S&V, three subdistricts supplied only by Lambeth,and sixteen supplied by both companies (Fig. 10.3).16a Not a single person had died ofcholera among the 14,632 residents of Norwood, Streatham, and Dulwich, whose wa-ter came from the Lambeth Water Company. The mortality rate in the subdistricts servedonly by S&V was 114 per 10,000; in the subdistricts with overlapping supply the ratewas 60 per 10,000 (MCC2, 72–74).

While suggestive, the absence of cholera in the three subdistricts served only byLambeth compared to the high mortality in subdistricts served only by S&V did notgreatly advance Snow’s argument. Other factors could be cited by his opponents.Norwood, Streatham, and Dulwich were pleasant residential suburbs. The areasserved only by S&V were tainted by poverty, overcrowding, and the noxious fumescharacteristic of inner London,17 but environmental conditions in the sixteen sub-districts served by both companies were similar and therefore met the criteria Farrhad set for a crucial experiment:

The intermixing of the water supply of the Southwark and Vauxhall Companywith that of the Lambeth company, over an extensive part of London,


Figure 10.3. Cholera deaths in 1853 in south London organized by subdistricts (Snow, MCC2,

73, Table 6).

263

admitted of the subject being sifted in such a way as to yield the most incon-trovertible proof on one side or the other. In the sub-districts . . . suppliedby both Companies, the mixing of the supply is of the most intimate kind. Thepipes of each Company go down all the streets, and into nearly all the courtsand alleys. A few houses are supplied by one Company and a few by the other,according to the decision of the owner or occupier at that time when the Wa-ter Companies were in active competition. In many cases a single house has asupply different from that on either side. Each Company supplies both richand poor, both large houses and small; there is no difference either in the con-dition or occupation of the persons receiving the water of the different Com-panies. Now it must be evident that, if the diminution of cholera, in the dis-tricts partly supplied with the improved water, depended on this supply, thehouses receiving it would be the houses enjoying the whole benefit of thediminution of the malady, whilst the houses supplied with the [S&V] waterfrom Battersea Fields would suffer the same mortality as they would if the im-proved supply did not exist at all. As there is no difference whatever, either inthe houses or the people receiving the supply of the two Water Companies, orin any part of the physical conditions with which they are surrounded, it isobvious that no experiment could have been devised which would more thor-oughly test the effect of the water supply on the progress of cholera than this,which circumstances placed ready made before the observer.

The experiment, too, was on the grandest scale. No fewer than three hun-dred thousand people of both sexes, of every age and occupation, and of everyrank and station, from gentlefolks down to the very poor, were divided intotwo groups without their choice, and, in most cases, without their knowledge;one group being supplied with water containing the sewage of London, and,amongst it, whatever might have come from the cholera patients, the othergroup having water quite free from such impurity.

To turn this grand experiment to account, all that was required was tolearn the supply of water to each individual house where a fatal attack of choleramight occur.

MCC2, 74–7518

Snow positioned these paragraphs between discussion of the Weekly Returns thatgave him the idea for such a “grand experiment” and his description of the subse-quent investigations of the 1854 epidemic. A possible interpretation is that Snow ac-tually envisioned in November 1853 the procedure he used when conducting thisexperiment the following late summer and fall: attempting to visit every house wherea person had died of cholera in the sixteen subdistricts with intermingled water sup-ply and determining in each instance which water company supplied that house.However, important facts remain unexplained by such a reading of MCC2. Why didhe not begin the investigation in December 1853? He says the days were too short


and he could not spare the time, but neither should have stopped him from solvinga problem that had eluded him for nearly five years (MCC2, 75–76). There was noassurance that cholera would return to London before S&V changed its supply, sowould he let this opportunity slip away in December had he already decided to un-dertake the extensive investigations detailed in MCC2? Moreover, why did he not be-gin house-to-house surveys as soon as cholera reappeared the first week of July ratherthan wait until mid-August if he knew from the outset that he would have to inves-tigate all sixteen subdistricts where there was overlapping supply?

Snow’s conception of the “grand experiment” likely evolved as he carried it out.19

In our view the experiment he anticipated in the fall of 1853 may have been “grand”in the number of people living in the affected portions of London, but not “grand”in the demands he thought it would place on his own time and labor. His reformu-lation of Farr’s data in the winter of 1853–1854 and again in July and early Augustof 1854 suggests that he initially believed he could do most of the required work bycareful sifting of information published in the Weekly Returns, supplemented byhouse-to-house inquiries in selected subdistricts.

Snow’s decision to focus exclusively on deaths from cholera was itself a simplifi-cation with important pragmatic consequences. In a disease with a mortality of fiftypercent, counting only deaths excluded half the cases. Moreover, if, as Snow sus-pected, some asymptomatic or mildly symptomatic individuals failed to receive“cholera” as a clinical diagnosis, the undercount would have been even more severe;many such cases were diagnosed as “diarrhœa.” On the other hand, attribution of adeath to cholera was relatively easy to establish because cholera symptoms are verydistinctive, and death is rapid. Snow made use of a case definition that, while in-complete, was reasonably accurate. In so doing he anticipated modern epidemic in-vestigations in recognizing that the scientific ideal of a perfect all-inclusive case def-inition must be abandoned if progress in identifying the cause of a disease is to takeplace. Lists of cholera deaths were readily available from Farr or district offices ofthe GRO, so Snow took advantage of a system for reporting deaths that had been inplace in England and Wales since 1837.20 At the time, however, there was no way toobtain a list of cholera cases for an area as large as south London.

August 1854: The Investigation Begins

When cholera returned to south London early in July 1854, Snow responded at firstin leisurely fashion, consistent with his activities of the previous winter. He waitedfor several weeks to see if the Weekly Returns would show the same pattern Farr hadnoted for the 1853 epidemic. They did: The intermingled subdistricts had notablyless mortality than did areas supplied only by S&V. Apparently, this was the in-formation Snow wanted before choosing an area in which to check on the water supply at every house where cholera deaths had occurred.21 He elected to begin


on-the-spot inquiries in two subdistricts of Kennington, probably because they hadbeen in the middle range of cholera mortality in 1853 and were so again in 1854.

He learned two things of significance when he began shoe-leather inquiries inKennington. First, his theory appeared to hold up very well. Of the forty-four deathsthat had occurred in the two subdistricts by 12 August (the first five weeks of theepidemic), no fewer than thirty-eight were in houses supplied by S&V water (Table10.2). Snow’s second discovery altered the strategy of his entire investigation. He be-came aware that the intermingling of the water supply was much greater than hehad imagined: “After commencing the inquiry I found that the circumstances werecalculated for affording even more conclusive evidence than I had anticipated. The


Table 10.2. Preliminary results from Snow’s investigation of four subdistricts

Kennington, first partSupply No. of houses

Southwark and Vauxhall 27Lambeth 2Pump wells on premises 2Total 31

Kennington, second partSouthwark and Vauxhall 11Lambeth 2Total 13

Waterloo, first partSouthwark and Vauxhall 7Lambeth 1Not yet ascertained 1Total 9

In Waterloo, second part, 27 deaths have occurred in 24 houses, which are supplied as follow

No. of housesSouthwark and Vauxhall 17Lambeth 3Pump well close to the Thames; water dirty 1Wells at the Lion brewery 1Not yet ascertained 2Total 24

If the cases are enumerated instead of the houses in this last subdistrict, the return is as follows

Supply CasesSouthwark and Vauxhall 19Lambeth 3Pump wells 3Not yet ascertained 2Total 27

Source: Snow, “Communication of cholera by Thames water” (2 September 1854), 247.

pipes of the two water companies not only passed down all the streets, but into nearlyall the courts and alleys. A single house often had a different supply from that on ei-ther side.”22 If it was not clear to him in November 1853 that this “grand experi-ment” was also a “crucial experiment,” it was now. If every other house received S&Vwater and the intervening houses had Lambeth water, ardent local miasmatists andcontingent contagionists could hardly claim that noxious effluvia skipped over everyother house to afflict the nearest neighbor. Snow was energized, and it seems morelikely it was in mid-August, and not a month earlier, that he “resolved to spare noexertion” to complete the necessary inquiries in all sixteen of the intermingled sub-districts (MCC2, 76). Although Snow wrote, “I was desirous of making the investi-gation myself, in order that I might have the most satisfactory proof of the truth orfallacy of the doctrine which I had been advocating for five years,” he soon realizedthat would be impossible (Ibid.). The weekly death toll was rising, and the epidemichad yet to peak. At this point he showed Farr the preliminary data he had gatheredfrom the two Kennington subdistricts. Farr agreed that the ratio of deaths betweenthe two companies was worth pursuing. Farr therefore ordered his registrars to gatherinformation on the water supply of houses each time they recorded a death fromcholera in every subdistrict supplied by either S&V or Lambeth. The employees ofthe Registrar-General could not begin this task until 26 August, however.23 Thatmeant Snow himself would have to investigate all deaths that had occurred in theoverlapping subdistricts through the Weekly Return of 25 August—that is, the firstseven weeks of the current epidemic.

More Problems, Some Solutions

Snow understated matters when he wrote that the “inquiry was necessarily attendedwith a good deal of trouble”(MCC2, 77). He soon discovered that finding out whetherthe water to a given house was supplied by Lambeth or S&V was not as simple ashe had anticipated, for “there were very few instances in which I could at once getthe information I required. Even when the water-rates are paid by the residents, theycan seldom remember the name of the Water Company till they have looked for thereceipt. In the case of working people who pay the weekly rents, the rates are in-variably paid by the landlord or his agent, who often lives at a distance, and the res-idents know nothing about the matter” (MCC2, 77). But Snow’s ingenuity as achemist, combined with a hefty dose of good luck, provided a solution: the waterprovided by Lambeth and S&V during his inquiry contained consistently differentamounts of salt.

On adding solution of nitrate of silver to a gallon of the water of the Lambethcompany, obtained at Thames Ditton, beyond the reach of the sewage ofLondon, only 2.28 grains of chloride of silver were obtained, indicating the


presence of .95 grains of chloride of sodium in the water. On treating the wa-ter of the Southwark and Vauxhall Company in the same manner, 91 grains ofchloride of silver were obtained, showing the presence of 37.9 grains of com-mon salt per gallon. Indeed, the difference in appearance on adding nitrate ofsilver to the two kinds of water was so great, that they could be at once dis-tinguished without any further trouble. Therefore when the resident could notgive clear and conclusive evidence about the Water Company, I obtained someof the water in a small phial, and wrote the address on the cover, when I couldexamine it after coming home.

MCC2, 7824

Finding a way to track the source of the water, however, turned out to be simplerthan calculating death rates from cholera in the intermingled subdistricts. The num-ber of deaths per water company in each subdistrict served as the numerator in thisfraction. This information was readily available from the Weekly Returns during theheight of the epidemic, which listed each death from cholera by residence in the me-tropolis. The ideal denominator for Snow’s natural experiment would be the totalnumber of people living in houses supplied by each water company. Such informa-tion was unavailable, but Snow reasoned that the total number of houses suppliedby each company in each subdistrict would yield a satisfactory approximation, andhe knew that such records had been submitted to parliament.25 Without such de-nominator figures for each subdistrict, cholera death rates by subdistrict could notbe calculated. Five times as many deaths in S&V-supplied houses than in Lambeth-supplied houses would not indicate a higher risk if S&V supplied water to five timesas many houses. But neither Farr nor anyone at the GBH would or could providehim the data he needed. The best information he could locate in the public domainwas a return to the GBH from 1850, which gave “the entire number of houses” thateach water company supplied: 34,217 for S&V, 23,396 for Lambeth.26 In short, hehad denominator data only for each company’s total supply.

Snow faced a major dilemma: either abandon this highly promising crucial ex-periment or extend the inquiry to include all the subdistricts supplied by both wa-ter companies.26a Because his denominator data extended across the entire area sup-plied by each of the water companies, he could calculate death rates only if heobtained numerator data over the same area. That meant that instead of just study-ing sixteen co-mingled subdistricts, he would have to investigate cholera deaths inthirty-two subdistricts.26b Such a task would require personal inquiries from Putneyin the west to Rotherhithe in the east, from the banks of the Thames as far south asStreatham Common—an area of nearly fifteen square miles. Farr’s stable of regis-trars were prepared to cover this area for all deaths that occurred after 26 August,but if Snow was to have a meaningful analysis of the first seven weeks of the cur-rent epidemic, someone would have to help him cover the additional territory. Heenlisted the assistance of “a medical man, John Joseph Whiting, L.A.C.”27


The two investigated 334 cholera deaths, with Snow covering the entire Lambethterritory and Whiting primarily the S&V area. They found that twenty times as manydeaths occurred in S&V-supplied homes. Where S&V supplied the water 286 deathstook place, but only fourteen where they could trace the supply to the Lambeth Com-pany. Twenty-two deaths were associated with dipping pails into the Thames for wa-ter, four with pump wells, and four with ditches. The final four deaths were in in-dividuals away traveling at the times of their deaths. During the first four weeks ofthe epidemic, the 286 cholera deaths they could connect to S&V-supplied houses ac-counted for more than half of the metropolitan total of 563. Snow thought the one-by-one investigation of these 334 cholera deaths sufficiently important to list themeach individually in an appendix to MCC2 “as a guarantee that the water supply waslooked into, and to afford any person who wishes it an opportunity of verifying theresult” (80). In the meantime he had discovered another return to Parliament, ac-cording to which the “Southwark and Vauxhall Company supplied 40,046 housesfrom January 1st to December 31st, 1853, and the Lambeth Company supplied 26,107houses during the same period” (MCC2, 80). Consequently, the death rate from cholera in S&V-supplied houses was 71 per 10,000 houses, while in Lambeth-supplied houses it was 5 per 10,000, a fourteen-fold in risk when S&V supplied the water.

Modern epidemiologists distinguish between a point source (also known as a com-mon source) and a propagated epidemic. When many people drink from a contam-inated water source such as a pump well, a sharp increase in cholera mortality fol-lows, but only in those who drank from the pump well (level B transmission). Thesuddenness of the increase is due to the simultaneous exposure to the cholera agentof a large number of people. Propagated epidemics, on the other hand, build upgradually, because they are composed not just of individuals exposed to a pointsource, if there is one, but of secondary cases resulting from contact with those ini-tially infected—person-to-person (level A) transmission. Snow understood that inthe initial stages of a large urban epidemic transmitted by the water supply, caseswould first appear almost exclusively in populations directly exposed to contami-nated water. Inevitably, however, individuals not directly exposed to contaminatedwater would also contract the disease by virtue of person-to-person contact, therebydiluting the difference in risk between those exposed and unexposed to contami-nated water. That is, level A and B transmission would gradually augment level Ctransmission. Snow predicted that the huge difference in initial risks between recip-ients of the two water supplies would diminish as the epidemic progressed, and soit did. Snow continued to investigate household water sources of cholera victims whohad died during the fifth through seventh weeks of the epidemic in the Lambeth andcomingled subdistricts, but Whiting for unknown reasons was unable to do likewisefor subdistricts where S&V was the sole supplier of water. Snow overcame this ob-stacle by estimating the distribution of cholera cases in relation to water sources for the last three weeks in these S&V subdistricts. He based this estimation on the


distribution of deaths by water supply in the first four weeks, although he admittedthat the dynamics in the transition to a propagated epidemic might lead to an over-estimate by this method.28 After seven weeks the resulting S&V-to-Lambeth choleradeath ratio, although not as high as during the first four weeks of the epidemic, wasstill between eight and nine to one.

For the seven weeks of the epidemic through 25 August, Snow’s personal inquiryinvolved the investigation of 658 deaths. In addition to all subdistricts served exclu-sively by the Lambeth company, Snow covered two subdistricts (Wandsworth andPutney) in the S&V area. Whiting worked only S&V subdistricts, with the exceptionof Clapham, where both companies had water customers. It must have been an ar-duous undertaking, even allowing for the clustering of deaths within families, houses,and streets in a London in which, as Snow tells us, “in many streets there are severalhouses having the same number,” while other house numbers were painted over ormissing altogether (MCC2, 80).29 In fact, many residents did not know their ownaddresses. Consequently, Snow often visited two or three houses before finding theone in which a cholera death had actually occurred. It is unclear if he walked fromstreet to street or hired a hansom cab and asked the driver to wait as he made hisinquiries, but we do know that he reduced his anesthesia practice substantially fromthe middle of August through September to accomplish this time-consuming in-quiry. According to his Case Books, he averaged 1.58 cases per day between 1 Julyand 10 August, whereas the case load drops to an average of 0.57 cases a day between11 August and 30 September.30

Snow and Whiting had together tracked down the water supply to the housesof 860 cholera victims (Whiting’s 202, plus Snow’s 658), but investigating the wa-ter supply where cholera deaths occurred after 26 August became the responsibil-ity of Farr’s registrars. Snow was indeed fortunate he had secured Farr’s assistance,for he would have had to investigate at least 3,000 deaths reported in the area sup-plied by the two water companies through 14 October. The information procuredby Farr’s registrars was less reliable than that collected by Snow and Whiting, but,as Snow put it, they “could not be expected to seek out the landlord or his agent,or to apply chemical tests to the water as I had done” (MCC2, 86). In fully twentypercent of reported deaths, the registrars could not ascertain the precise water sup-ply, but for the remainder Snow’s hypothesis held: 2,353 deaths took place in the40,046 S&V houses, 302 in the 26,107 Lambeth houses, a risk ratio that Snow de-scribed as “nearly five” but which in fact is 5.1 (MCC2, 88). By combining the re-sults of his own investigations with those of Whiting and Farr’s registrars, Snowcould tabulate the rate of cholera deaths by water supply over the entire fourteen-week period of the epidemic. He apportioned the deaths where water sources wereunknown between the two companies in proportion to those whose supply hadbeen ascertained, yielding 4,093 deaths in S&V-supplied houses and just 461 inLambeth houses. The overall risk ratio for cholera deaths over the fourteen weeksof the epidemic was 5.8 to one.31


More Evidence

Although the natural experiment in south London takes up only twenty-one pagesin the middle of MCC2 (Table 10.3), Snow included evidence in the rest of the es-say that complemented the centerpiece in substantiating of his cholera theory. Heset up a discussion of the crucial experiment with a comparative analysis of choleramortality in London during the 1831 to 1832 and 1848 to 1849 epidemics. In hismind the conclusion was inescapable: Sanitary reforms had contributed to an in-crease in deaths, not reduced them. In 1832 London’s population of almost 1.4 mil-lion people experienced 4,736 cholera deaths, a mortality rate of 34.1 per 10,000.32

Metropolitan London of 1849 was larger in area (it had incorporated nine new dis-tricts), and the population had increased by more than sixty percent, to almost 2.3


Table 10.3. Contents of MCC2 (1855), by topic

Topic Number of pages

Pathology and mode of communication (review of materialpresented in 1849, with minor revisions; includes Albion 32Terrace and Horsleydown)

Other water-borne outbreaks over relatively small areas 6(level B)

Broad Street outbreak 16

Transmission by sewage-contaminated river water(level C)—introduction 2

Effect of water supply on mortality in London, 1831–1832 12and 1848–1839

Crucial experiment—Lambeth Company’s intake sitemoved; opportunity to test hypothesis conclusively; 21data obtained

Comparison of Lambeth and Southwark and Vauxhall 2death rates, 1849 vs. 1854

Other examples of water-borne transmission in London, 61853–1854

Reply to Farr’s elevation hypothesis 2

Level C examples: other cities in Britain 11

Replies to objections and alternative theories 16

Other diseases possibly spread by water 8

Preventive measures suggested 5

Appendix: list of all cases in first four weeks of epidemic 24of 1854 personally investigated by Snow

million. Even so, there were more than three times the number of deaths (14,137),and the mortality rate doubled to 62.0 per 10,000 (MCC2, 62–63). Despite the con-struction of new drains to empty ever more water closets and reduce the presenceof ostensibly pestilential effluvia in the metropolis, Londoners had fared worse thesecond time cholera came to town.

Comparative data from south London confirmed Snow’s assessment that waterquality had deteriorated despite the changes in the sources of supply. The three dis-tricts supplied by the Southwark Water Works lost more than one percent of theirpopulation to cholera in 1832. In 1849, however, eight districts supplied by its suc-cessor, S&V, and the Lambeth Water Company suffered just as high a mortality rate.One of the districts, Rotherhithe, lost more than two percent of its population tocholera. By contrast, districts north of the Thames had lower cholera mortality thanin 1832, which Snow attributed to improvements in water quality such as shifting toupriver sources well above the major sewer outlets and the wider use of settling reser-voirs and effective filtering. The conclusion was inescapable: In the 1849 epidemic,“in every district to which the supply of the Southwark and Vauxhall, or the Lam-beth Water Company extends, the cholera was more fatal than in any other districtwhatever . . . [because they were] deriving a supply from the Thames, in a situa-tion where it is much contaminated with the contents of the sewers . . .” (MCC2,64).33

Snow’s argument was especially forceful when he compared mortality in districtssupplied by S&V and Lambeth in the two epidemics preceding and following theLambeth change of water source. Cholera deaths in districts supplied by S&V in-creased by nine percent between 1849 and 1854, while in Lambeth-supplied districtsthey declined by seventy-five percent (MCC2, 90). Similar parishes with differentwater supplies, such as the adjoining Southwark parishes of St. Saviour’s andChristchurch, illustrated Snow’s thesis particularly well. In 1849 their cholera mor-talities, like most of the parishes in Southwark, were exceptionally high. However, in1853, S&V-supplied St. Saviour’s lost 2.3 percent of its population to cholera—al-most one in forty, while Christchurch mortality, with Lambeth as its water source,lost just 0.43 percent. Waterloo Road (part one), the parish immediately east ofChristchurch, was a region of high mortality in 1849, but it experienced just a sin-gle cholera death in 1853. It, too, took Lambeth water (MCC2, 72–74).

Snow reasoned that if the S&V mortality was the same or had actually increasedfrom 1849 to 1854 while Lambeth mortality dropped significantly between 1849 and1854, the most plausible explanation would be that the change in the Lambeth wa-ter intake accounted for the whole of the difference. If Lambeth deaths were less in1854 because of some improvement in the atmosphere, one would assume the samewould be true in contiguous areas served by S&V (MCC2, 89–91). The comparisonacross time was not as definitive a reply to the Milroy objection as was the crucialexperiment of 1854, but it nevertheless showed that all the evidence was lining upin Snow’s favor, no matter how one parsed the data.


The roles of settling and filtering in purifying sewage-contaminated water alsocame under Snow’s scrutiny. He suggested that “detention of the water in the[Chelsea] company’s reservoirs permitted the decomposition of the cholera poison”(MCC2, 94). Again, a comparison lay at the heart of his reasoning. He had observedthat carefully filtered Thames water, such as that supplied to Millbank prison, didnot prevent cholera from killing 4.3 percent of the inmates in 1849, whereas theChelsea Company, although drawing water from virtually the same spot as did theS&V Company, allowed to it to settle in reservoirs before distributing it. While res-idents in the districts supplied by Chelsea water experienced mortality higher thanwas the average in the whole metropolis in the 1853–1854 epidemic—there was alimit to the benefits of settling reservoirs if the water was very polluted—it was stillhalf the rate of that among S&V customers (MCC2, 93–94).

In MCC2 Snow gave examples of provincial towns where the water supply affectedcholera mortality rates. He summarized evidence already presented in PMCC as wellas in the papers and articles prepared since 1849. Most of this evidence came fromthe northern towns with which he was most familiar. The essence of Snow’s argu-ment was that the experience of urban northern England showed that water fromtidal rivers was generally bad, while surface water, especially from hills, was usuallygood. Like the Thames, the Humber, and the Tyne, the Nith, the Trent, and the Clydeall served as vehicles of cholera dissemination during the epidemic of 1854. Someimprovement was possible if the river water was permitted to settle and was then fil-tered. Only towns that depended on surface water from rural hills or rural springswere spared water-borne epidemic outbreaks (MCC2, 98–104). Snow recycled hisdiscussion of the Newcastle experience in July 1853, which documented both the re-liability of rural water and the dangers of using tidal rivers simultaneously for sewagedisposal and drinking water (MCC2, 104–07).34

Completing South London—A Predictive Model

By the beginning of October 1854, Snow had completed his personal investigation(aided by Whiting) of all deaths attributed to cholera through 25 August for all sub-districts served by the S&V and Lambeth water companies. Farr’s registrars were col-lecting similar data for deaths that occurred thereafter, until the cholera epidemicended after a run of fourteen weeks. Snow prepared an interim communication toMTG and then set out to write the manuscript that would be published as MCC2.35

He had now seen his inquiry through several stages, each designed to take advan-tage of an opportunity or to respond to a problem that he had not anticipated ear-lier, but Snow was not satisfied that he had fully completed his analysis of the “grandexperiment” in south London. He still lacked the denominator data on the numberof houses supplied by both water companies at the subdistrict level, which was necessary to calculate comparative death rates. In early October he had thought the


information was forthcoming: “I hope shortly to learn the number of houses in eachsub-district supplied by each of the water companies respectively. . . .”36 He did notreceive it in time, however, to include the promised analysis in MCC2. In what waydid he imagine that a detailed subdistrict analysis would add to the conclusivenessof an already extensive presentation of differential mortality associated with the twocompanies?

First, he believed in October that a comparison of the comingled subdistrictswould constitute the clearest, most unambiguous support for his theory and falsifyboth the Milroy objection (local effluvia) and Farr’s elevation theory. The entire sen-tence quoted in the previous paragraph shows why he thought it was so importantto have subdistrict data: “I hope shortly to learn the number of houses in each sub-district supplied by each of the water companies respectively, when the effect of theimpure water in propagating cholera will be shown in a very striking manner, andwith great detail.”37 It would provide the long-sought parallel to Horsleydown at themetropolitan level of ecological analysis: indisputable evidence that atmospheric ef-fluvia did not explain what was known about the communication of cholera. It wouldalso refute the elevation hypothesis. In August he had written that based on the datacollected “in the [four] sub-districts to which the inquiry has extended, the peoplehaving the improved water supply enjoy as much immunity from cholera as if theywere living at a higher level, on the north side of the Thames.”38

The expansion of the investigation he undertook as an expedient in the absenceof the desired data about water supply turned out to have an unexpected benefit. Hehad already taken into account the relative effects on the mortality rate of the threeecological levels over time. He hypothesized that level C (metropolitan area) mor-tality would dominate early in the epidemic but eventually would be diluted by spreadat levels A (person-to-person and households) and B (neighborhoods), and so it had,as the difference in the ratio of deaths in S&V-supplied houses compared to housesreceiving Lambeth water dropped from fourteen in the early weeks to five duringthe last half of the epidemic.

Statistically speaking, however, Snow came to believe that if one considered theepidemic as a whole, it was likely that level C spread would still dominate level Aand B transmission. To confirm this belief, he devised a statistical model in whichcholera was presumed to have spread over south London only by means of pipedwater. The closer his model came to predicting the actual number of cholera deathsin south London, the stronger would be his evidence that the metropolitan watersupply was the major means by which cholera was transmitted.

However, constructing a model of this sort was impossible with the numbers Snowhad available when he wrote MCC2. He lacked the number of houses supplied byeach company in every subdistrict needed to calculate, by subdistrict, the choleramortality rate that should have occurred on the assumption that the numbers ofdeaths precisely paralleled the numbers of houses supplied with impure water. Withthese data he intended to compare for every subdistrict his calculated number to the


actual number, a total of thirty-two paired data comparisons. A reasonable matchbetween predicted and actual deaths in only a handful of subdistricts could be ex-plained by chance, but a reasonable match across all thirty-two subdistricts wouldstrongly support the soundness of the underlying theory that gave rise to the pre-diction.

Snow finally obtained the desired subdistrict data in 1856 from an unexpectedand disturbing source: the “Report on the last two cholera-epidemics of London asaffected by the consumption of impure water” by John Simon, medical officer of theBoard of Health. Simon essentially duplicated Snow’s south London water analysis,making the same observations about the high cholera mortality in those districtsand also noting the significance of the movement of Lambeth’s water supply toThames Ditton during the interepidemic interval while the S&V supply remainedunchanged. Like Snow had done in MCC2, Simon showed a double contrast betweencholera mortality rates in the areas supplied by the Lambeth Company in 1848 andin 1854, and between Lambeth and S&V consumers in 1854. Not a mention of Snow’swork can be found in this report, even though Simon used words similar to Snow’sin stating that the differences in the purity of water of the two companies had cre-ated a massive human experiment.38a While Simon had access to the data that pro-vided the number of houses supplied by each company within each subdistrict, heused it only to calculate cholera mortality rates by water supply in each subdistrict;he did not propose the kind of predictive model that Snow envisioned. Neverthe-less, now Snow had the numbers he needed to do that himself.

Snow immediately prepared a paper for the JPH&SR that served as a rebuttal towhat he took to be errors in Simon’s report and as an expansion of his MCC2 in-quiry. The centerpiece of this paper was his analysis of the predictive model. Afterrecapitulating for the reader how he came to design the methods for his inquiry andthe data he had previously presented in MCC2, he presented a table for cholera mor-tality over the entire epidemic in thirty-one subdistricts in relation to water supply.39

He found it to be 160 deaths per 10,000 in S&V supplied houses and 27 per 10,000in Lambeth houses.39a Snow then applied these overall death rates to the number ofhouses supplied by each company in each subdistrict and compared these “expectedrates” to the deaths actually enumerated.40 For example, Lambeth Church, part two,had 7,868 houses supplied by S&V and 16,023 by Lambeth. Snow calculated that thisratio would yield a death rate of 71 per 10,000 inhabitants. The actual death rate inthat subdistrict was 73 per 10,000. Snow was similarly on target in the Leather Mar-ket and Rotherhithe subdistricts, predicting death rates of 150 and 160, respectively,while the actual rates were 155 and 159.

As expected in light of the problems encountered by himself, Whiting, and theregistrars in gathering water supply information to houses in which a cholera deathsoccurred, Snow’s predictions were less exact in many subdistricts. A more typical ex-ample was Christchurch, with an expected rate of 57 and an actual rate of 71. In fivesubdistricts he was off the mark. For example, he estimated the death rate in


Putney should have been 160, whereas the actual number was 17. But while Putneylay in the S&V area, only thirteen of its 918 houses were actually served by that com-pany. On the other hand, he underestimated the rate in Borough Road as 104, whenthe actual number was 171 (Fig. 10.4). Taking the entire series of thirty-one subdis-tricts, Snow was content with what he called “a very close relation to the real mor-tality” that “proves the overwhelming influence which the nature of the water sup-ply exerted over the mortality, overbearing every other circumstance which could beexpected to affect the progress of the epidemic.”41

Snow demonstrated in his analysis of the London water supply in relation tocholera that the entire phenomenon of a huge cholera epidemic could be explained.


Figure 10.4. Deaths from cholera in 1854 compared with calculated mortality (Snow, “Cholera

and the water supply in the south districts of London,” Table 6).

Every facet of the epidemic—its origin in water-borne traffic from infected regions,its distribution through the pipes of London, its transmission within households, itsexacerbation in subsidiary outbreaks resulting from a contaminated point sourcesuch as a well pump—were unified by a common theory that found its proof not in any laboratory experiment, but in the record of cholera deaths collected by civilauthorities.

Snow had now pushed his cholera thesis as far as any predictive hypothesis abouthuman disease can be pushed. Not only was the water supply a major determinantof the differences in mortality among subdistricts, it was the dominant determinant,in effect a proxy for cholera mortality. He anticipated modern epidemiological meth-ods by using indirect standardization and modern scientific practice by creating aquantitative predictive model. Snow now finally proclaimed that he had finished hissouth London study and immodestly but accurately noted that his overall analysisof cholera mortality in London “probably supplies a greater amount of statistical ev-idence than was ever brought to bear on a medical subject.”42

This chapter has focused on Snow’s assessment of the relationship of Londoncholera to municipal water supplies, but MCC2 also contains an extended descrip-tion of a level B incident that has become much more celebrated than the south Lon-don study: an outbreak of cholera in Golden Square that killed 500 people livingwithin 250 yards of a single pump, doubling the number of deaths in the entire me-tropolis during the first days of September 1854.

Notes

1. Halliday, The Great Stink of London, 18–24.2. Trench and Hillman, London under London, 83–90.3. Halliday, The Great Stink of London, 34–38; Luckin, Pollution and Control, 11–20.4. “After 31st August 1855, it shall not be lawful for any company to supply London with

water from any part of the Thames below Teddington Lock, or from any part of its tributarystreams below the highest tidal point”; Act, 15 & 16 Vict. cap 84, quoted in UK GRO, WeeklyReturn (19 November 1853). A special one-year extension was granted to one water company,the Chelsea Company; UK GRO, Weekly Return (3 December 1853).

5. Snow, “Cholera and the water supply” (1856), 240.6. Anonymous review of MCC, in LMG 44 (1849): 466–70; anonymous review in Lancet 2

(1849): 318.7. Snow, “Mode of propagation of cholera” (1851); “Prevention of cholera” (1853). Only

the Newcastle experience in 1853 offered support for his hypothesis at the metropolitan level.When, during that epidemic, the local authorities began to use water directly from the sewage-contaminated River Tyne, mortality rose; when that practice ceased, mortality fell as had hap-pened in York during the 1848 epidemic.

8. Snow, On the Mode of Communication of Cholera, 2nd ed., cited parenthetically in thetext as MCC2. In addition Snow added a twenty-four page appendix containing informationabout cholera deaths and water supply to the houses where the deaths occurred during thefirst four weeks of the epidemic.


9. UK GRO, Weekly Return. The data reflected death certificates compiled by registrarsthrough the week ending the Saturday prior to the date of publication; thus the Weekly Re-turn of 19 November contained information gathered through the week ending 12 Novem-ber.

10. UK GRO, Weekly Return 14 (26 November 1853).11. Farr, Report on the Mortality from Cholera in England, 1848–1849, lix, lxi–lxvi.12. UK GRO, Weekly Return 14 (19 November 1853), supplement.13. UK GRO, Weekly Return 14 (26 November 1853), cited by Snow, MCC2, 68.14. It is traditional in epidemiology to refer to opportunities to study the influence on dis-

ease of large changes in the environment as “natural” experiments, but Snow does not use thisterm, although he does speak of the study of contrast in water supplies as a “grand experi-ment” (MCC2, 75). Simon was later to refer to such phenomena as “popular experiments”;“Experiments as a basis of preventive medicine,” Public Health Reports 2: 589–614.

15. On 5 August 1854 Snow submitted a letter to the editor of MTG which suggested asource for the 1854 London epidemic. Responding to a notice about cholera on British shipsin the Baltic fleet, he deduced, with Sherlock Holmes-like finesse, that the outbreak must havebeen communicated from drinking water in the Baltic, which, he claimed, was fresh in earlysummer and preferred by sailors to water stored on shipboard in casks. Because the Britishships had no communication with the shore, the only other source of cholera would havebeen from captured vessels from the cholera-infected towns of Cronstadt or St. Petersburg.Because the Lancet had reported that cholera was restricted to the larger vessels that proceededup to Cronstadt, whereas the capture of prizes was engaged in only by the smaller steamers,Snow identified Baltic water as the most likely source. He also thought that cholera was im-ported to London in July 1854 by mariners returning from the Baltic. As in 1849, Snow re-minds his readers, cases early in the epidemic were noted in individuals living on the Thamesor linked to shipping, a sure sign that water was a key mode of transmission; Snow, “Cholerain the Baltic fleet,” (12 August 1854).

16. A paired set of letters from Snow, published in MTG in September and October 1854,offer preliminary analyses of the epidemic, but virtually the entire content of these letters isreproduced in MCC2; See “Communication of cholera by Thames water”; and “On the com-munication of cholera by impure Thames water.”

16a. Snow soon included another subdistrict, Sydenham, in the Lambeth Company water-shed for a total of thirty-two.

17. Snow admitted that the absence of cholera from these rather favored suburban loca-tions was not a very strong test of his hypothesis, as their “freedom from the epidemic mightbe attributed to other causes than the mere absence of the polluted water”; “Communicationof cholera by Thames water,” 247. Snow anticipated at least one of his critics. In a review ofMCC2, E. A. Parkes pointed to what could be considered favorable social and geographicalfactors in parts of the Lambeth area compared to that of S&V in general; British and ForeignMedico-Chirurgical Review 15 (1855): 449–63.

18. In the late months of 1853, Farr continued to come close to Snow’s theory without everaccepting it fully. Farr concluded that after adjusting for his favorite influence, elevation, “alarge residual mortality remains, which is fairly referable to the impurity of the water.” ForFarr, water remained just one influence. “Its fatality bears a certain relationship to the impu-rity of the soil, the water, and the air”; UK GRO, Weekly Return 14 (3 December 1853).

19. According to Christopher Hamlin, no textbook of clinical epidemiology existed at thetime; private communication.

20. “Just as Snow’s ability to posit an appropriate etiological agent was a product of changesboth scientific and technological, so equally was his epidemiological reasoning a product of


the multiple aspects of change which had taken place in the first half of the nineteenth cen-tury . . . [including the creation of the Registrar-General’s Office]. It would be hard to imag-ine a mid-eighteenth-century student of epidemic disease determining individual cases andthen plotting them on street maps. By the mid-nineteenth century, Snow was only one amonga number of physicians who carefully mapped individual cholera cases in recording and an-alyzing the history of local epidemics”; Rosenberg, Explaining Epidemics, 119. However, Snowwas particularly interested in statistical analyses of deaths rather than cases.

21. “Observing, therefore when the cholera returned in 1854, that there was the same ad-vantage in favor of the districts partly supplied with water from Thames Ditton, I determinedto make an inquiry, the idea of which I had previously entertained”; Snow, “Cholera and thewater supply,” (1856), 241. His pause in July and early August is not explained in MCC2:“When cholera returned to London in July of the present year, however, I resolved to spareno exertion which might be necessary to ascertain the exact effect of the water supply” (76).Only a few lines later he noted, “I commenced my inquiry about the middle of August” (76).This date is confirmed by Snow’s first report of his investigation, in which he stated that hehad been undertaking house-to-house inquiries for ten days. The report was a letter to theeditor without a precise date. Because it was published in the issue of 2 September, he prob-ably penned it on 26 or 27 August; see Snow, “Communication of cholera by Thames water.”His “exertions” from mid-July to mid-August appear to have been solely of a statistical na-ture. Perhaps Snow was not yet aware of the great dangers of delaying such an inquiry, asmany prospective informants often fled soon after an area was afflicted.

22. Snow, “Cholera and the water supply” (1856), 241. The first published report of Snow’sawareness of the intimate intermingling of the pipes and supply was in September; Snow,“Communication of cholera by Thames water” (1854). See also MCC2, 76.

23. According to our reconstruction of the chronology, Snow could hardly have compiledhis data and spoken with Farr until approximately 19 August 1854.

24. At the time Snow was unaware that this large and easily demonstrable difference in salin-ity between the two water sources depended on weather conditions. He originally supposed thatthe high salt content of S&V water came from sewage but later learned from Mr. Quick, an en-gineer at S&V, of the tidal backflow from the North Sea into the Thames, which was exaggeratedunder the hot and dry conditions that characterized the first months of the epidemic; MCC2,95–96. Snow himself tested water from the Thames at Hungerford on three dates in November1854, two months after his investigations, and found that the sodium chloride concentration var-ied from 5.8 grains to 63.3 grains per gallon. He also noted that S&V water tested in 1851 hadbeen found to have only 1.99 grains per gallon. Had that salt concentration been obtained dur-ing the epidemic, Snow’s chemical test might not have reliably distinguished the two water sources.In short, Snow was lucky and acknowledged as much: “for throughout all the dry weather, whichlasted whilst my inquiries were being made, a mixture of the sea water extended farther up theThames than usual”; “Cholera and the water supply” (1856), 242.

25. Snow, “Communication of cholera by Thames water” (1854), 247. He noted in this pre-liminary statement (written at the end of August) of his findings in four subdistricts that thecompanies had sent returns to Parliament and the Board of Health that included the totalnumber of houses they supplied by district, at a minimum. Early in October he thought hewould soon have data on houses supplied for each subdistrict; Snow, “On the communica-tion of cholera by impure Thames water” (1854), 365.

26. Snow, “On the communication of cholera by impure Thames water” (1854), 366.26a. “But as the number of houses which they supplied in particular districts was not stated,

I found that it would be necessary to carry my inquiry into all the districts to which the sup-ply of either Company extends . . .” (MCC2, 78–79).


26b. Davey Smith reminds us that E. A. Parkes noted in 1855 that Snow diluted the signif-icance of the “grand experiment” when he expanded the inquiry beyond the sixteen subdis-tricts in which both companies supplied water: “on first reading . . . we thought that thedeaths referred to took place only in the district with the intermingled supply. . . . But onreperusing the passage, we found that these deaths had taken place in all districts supplied bythe two companies, separately or conjointly”; British and Foreign Medical Review 15 (1855):461, and Davey Smith, “Behind the Broad Street pump,” 925. But neither Parkes nor DaveySmith comment on Snow’s reason for expanding his south London study to thirty-two sub-districts—he lacked the required denominator data (the precise numbers of houses suppliedin each subdistrict by each company) to analyze the co-mingled subdistricts alone.

27. John Joseph Whiting was born in 1827, the son of an apothecary–surgeon, in King’sLynn, Norfolk. After apprenticing with his father, he took the required lecture courses in Lon-don and completed eighteen months of hospital experience at St. Bart’s. He failed in his firstattempt at the LSA in 1850, passed the following year, but his license did not permit him topractice within ten miles of London; Dee Cook, e-mail to David Zuck, 12 April 2002. Zuckhas discovered that Whiting lived in Cambridge in 1856 and in King’s Lynn in 1860. How-ever, he apparently never registered with the General Medical Council set up under the Med-ical Act of 1858, although he may have practiced anyway; Medical Directories for 1856, 1860,1861. LAC, or Licentiate of the Apothecaries’ Company, was a variant of LAS.

28. Snow made minor errors that assigned S&V five more cases in those three weeks thana more precise calculation would have produced. In Table 8 of MCC2, he applied the samepercentage of cholera deaths in each S&V neighborhood associated with S&V water as hefound during the first four weeks of the epidemic (given in Table 7 of MCC2). His calcula-tion was exact for eight of the ten neighborhoods for which data were unavailable during thefollowing three weeks, but using this algorithm, our computation yields one case less to S&Vwater in St. Olave and four fewer cases in St. James.

29. We use the figure, 658 deaths, given by Snow in 1856; “Cholera and the water supply inthe south districts of London, in 1854” (1856), 251 (Table 1). This is twelve fewer than sug-gested by Table 8 in MCC2, 85. The slight variation is explained if in the latter table one sub-tracts Clapham from Snow’s count (it has an asterisk indicating that Whiting investigatedthere) and adds Wandsworth and Putney (both in the S&V-only watershed, and lacking as-terisks) to Snow’s workload. The resulting figures match the number of deaths that Snow at-tributes to each of them in Tables 1 and 2 in 1856.

30. Ellis, CB, 335–44. During what was likely his busiest period of house-to-house investi-gations, Snow traveled to Manchester on Sunday, 17 September, to administer chloroform tothe sister of a physician. However, he did not administer anesthesia at all from 22 Septemberto 1 October. Snow does not tell us precisely when he conducted his investigation, but the re-port of the forty-four deaths to 12 August that he investigated in Kennington and thirty-sixadditional deaths to 19 August in Waterloo were reported on 2 September in MTG, while allof his personal investigations along with those of Whiting and Farr’s registrar’s of deaths to26 August were reported in a letter sent on 2 October to MTG. It seems safe to conclude thatSnow’s investigations took place from the middle of August until the end of September 1854.

31. Table 11 in MCC2 introduces as a denominator the population estimated to live in thosehouses instead of the number of houses supplied by the two companies, but the cholera deathratio is not altered by this change, as the GRO (the source of these population estimates ac-cording to Snow) appears to have multiplied the number of houses in both groups by 6.655to obtain the population.

32. Snow states that he obtained these data from the First Report of the Metropolitan Sani-tary Commission, 1847; MCC2, 57.

33. Only one other company, the Chelsea, drew water from that part of the Thames. “But


this company, which supplies some of the most fashionable parts of London, took great painsto filter the water before its distribution, and in so doing no doubt separated, among othermatters, the greater portion of that which causes cholera” (MCC2, 64). The S&V and Lam-beth companies “professed to filter the water,” but Arthur Hill Hassall examined samples andidentified “hairs of animals and numerous substances which had passed through the alimen-tary canal” in S&V water; Hassall, Food and Its Adulterations, 90. There was no reason to thinkit had been any better during the epidemic.

34. This episode was also detailed in Snow’s two cholera publications in the autumn of1853. See “On the prevention of cholera” (1853) and “The water supply at Newcastle,” Times,11 November 1853. See Luckin, Pollution and Control, 69–86, on additional context for Snow’sinvestigations.

35. Snow, “On the communication of cholera by impure Thames water” (1854). Advertise-ments that MCC2 was available for purchase from the publisher, Churchill, were printed earlyin January, 1855. A note in which George Budd thanks Snow for sending him a free copy isdated 3 January 1855; Clover/Snow Collection, VIII.4.i.

36. Snow, “On the communication of cholera by impure Thames water,” (1854), 365.37. Ibid.38. Snow, “Communication of cholera by Thames water” (1854), 247.38a. In Simon’s formulation, “An experiment . . . has been conducted during two epi-

demics of cholera on 500,000 human beings. One half of this multitude was doomed in bothepidemics to drink the same fecalized water, and on both occasions to illustrate its fatal re-sults. While another section . . . was happily enabled to evince by a double contrast the com-parative immunity which a cleanlier beverage could give”; Report of the Last Two Cholera Epi-demics, 9.

39. Snow, “Cholera and the water supply in the south districts of London in 1854” (1856),255. The first five tables in this paper show data for the thirty-two subdistricts included inMCC2. But he dropped Sydenham from his analysis in the sixth table, presumably because hefound virtually no reliable data there.

39a. In Snow’s 1856 article, Table 1 includes the subdistricts personally investigated by Snow; he figured that the mortality rates were 47.2 per 10,000 for S&V subdistricts and 6.6for Lambeth—a ratio of 6.94. Davey Smith argues that Snow reported a lower death ratio(6.9) for the sixteen co-mingled subdistricts than he had earlier reported in MCC2 for allthirty-two subdistricts during the same period (8.5), a difference that would confirm Parkes’criticism that Snow confounded matters by enlarging the area to include all subdistricts servedby the two companies; “Behind the Broad Street pump,” 925. But Davey Smith’s reasoning issuspect if he derived the 6.9 ratio from Table 1 of the 1856 article, since it does not includeClapham (a subdistrict with co-mingled pipes) and does include Wandsworth and Putney(both in the S&V watershed). Water-supply specific cholera death rates for the sixteen co-mingled districts during the first seven weeks of the epidemic, as calculated from Tables 1 and2 of the 1856 article, are 49.4 and 6.7 respectively, yielding a mortality ratio of 7.3. In short,it appears that Snow did overestimate the difference in risk when he expanded his inquiry,but not as much as Davey Smith suggests.

40. The calculation of expected death rates based on a simple predictive model is a stapleof analytic epidemiology, particularly for studies relying on population death rates from vi-tal data. In this instance Snow is, in effect, performing an indirect standardization of choleradeath rates by water supply. His thesis was that if one took account of water supply, little vari-ance in death rates within subdistricts would remain. That variance was the difference be-tween the expected rates calculated from Snow’s model and the actual rates. This may be thefirst use of indirect standardization in epidemiological research.

41. Snow, “Cholera and the water supply in the south districts of London in 1854” (1856),


248. Snow compared actual rates of cholera in 1854 with rates predicted by assuming that thefraction of the population in each subdistrict exposed to Lambeth water will be 27 per 10,000(the overall Lambeth rate) and the fraction exposed to S&V water will be 160 per 10,000 (theoverall S&V rate). We calculate that the correlation between the predicted and actual rates inthe thirty-one subdistricts is 0.745. Two subdistricts, Putney and Wandsworth, had death ratesmuch lower than predicted, apparently because relatively few residents depended upon thepiped water for drinking. If we remove these two outliers the correlation coefficient for theremaining twenty-nine subdistricts is 0.878, indicating that Snow’s water-supply based modelexplains 77% of the variance in cholera mortality.

Snow was not unique in his statistical approach. In 1852 Farr used subdistrict analysis oncholera mortality during the 1848–49 epidemic and concluded that altitude was the singlemost critical variable in cholera mortality. Our analysis of thirty of the subdistricts analyzedby Snow in 1854 resulted in a correlation of 0.53 between altitude and cholera mortality, com-pared to 0.745 for water supply. In South London water supply and altitude were strongly cor-related during this period, with S&V water supplying almost entirely low lying areas, whileLambeth water also went to relatively higher subdistricts.

42. Ibid.


Monday, 28 August 1854

SARAH LEWIS’S FIVE-MONTH-OLD DAUGHTER had neverbeen very healthy, nor had Mrs. Lewis herself, for that matter. Un-

able to suckle the child, she had to feed her from the bottle on boiled ground riceand milk. She had fed her son that way several years before, and he had been ex-tremely sickly and had died at ten months. For a while it looked as if the little girlwas going to do better, but then she had a bout of diarrhea in June. Dr. William R.Rogers of Berners Street treated her, and she was better after about five days. Thismorning Mrs. Lewis had to send for Dr. Rogers again. The same diarrhea was back,he said—pale or green, slimy, watery, offensive-smelling stools. Now the baby wasalso vomiting, unable to keep down food or medicine.1

The Lewis family lived in the back parlor at 40 Broad Street, an attached multi-storied house of eleven rooms. They were relatively fortunate; nineteen or twentypeople lived in the house, while elsewhere in the district four or five to a room wasnot uncommon. Even so, the back of the house was near the yard of the public houseat 7 Cambridge Street, and the bad smells from the water closet there had been both-ersome for a long time.2

A century earlier the streets around Golden Square, St. James’s, Westminster, werepart of fashionable London, and the houses had originally been erected as single-

283

Chapter 11

Broad Street

family town dwellings.3 As people of fashion moved to the west and the north, GoldenSquare became the abode of the working poor; the houses were subdivided andrented out by the room (Fig. 11.1). “The families of labourers, mechanics, and jour-neymen” was how the majority of the residents of the area were later described (CIC,51). Mrs. Lewis’s husband was a policeman. Other families in the remaining roomsat 40 Broad Street were headed by a carpenter and a tailor, among others.4 Poverty,hunger, and filth were everywhere in evidence, although the area was far from be-ing the most squalid in London. There were also a number of cow yards, slaughter-houses, and similar animal enclosures in the neighborhood, adding to the offensiveodors.5

Since the baby’s diarrhea had commenced at 6:00 that morning, Mrs. Lewis hadbeen soaking the infant’s soiled diapers (napkins, or “nappies”) in buckets of coldwater. Before washing the diapers she poured the water into the cesspool in the frontarea of the house (CIC, 159, 164). Above her, at street level and a few feet to the east,people gathered around the water pump or the pub next door. Strangely, Mr. ThomasLewis absolutely refused to drink the pump water and would not have it in the house(CIC, 126). In general, the cold water from the pump near the corner of Broad and


Figure 11.1. 16-21 Broad Street, 1888; currently 48-58 Broadwick Street (adapted from Fred-

erick Calvert’s watercolor, City of Westminster Archives, new house numbers from Sheppard,

St. James Westminster, 2: 216).

Cambridge Streets was held in high esteem by the residents of Golden Square. Somewho lived a number of streets away, much nearer to another pump, still came toBroad Street for their water.

No one, including Dr. Rogers, suspected that the infant’s diarrhea might be a pre-monition of cholera (CIC, 164). In London’s two earlier epidemics, Westminster andGolden Square had been largely spared. Now, as on those earlier occasions, the worstof the epidemic was raging south of the Thames, where John Snow was at work ona house-to-house study of cholera deaths. He had set aside an entire week for thesurvey. Since 24 August, when he had administered chloroform for Mr. Hewett at St.George’s Hospital while he removed a tumor from a woman’s breast, Snow had hadno calls upon his anesthesia services (CB, 342). The date 26 August 1854 marked animportant turning point in Snow’s south London study. Before that date Snow andhis assistant, Mr. Whiting, had investigated all deaths. After that date the district reg-istrars were instructed by William Farr to inquire into the water supply of each housewhere a cholera death was reported. Nevertheless, Snow still had a backlog of on-site inspections from deaths that had occurred before August 26, and he needed timeto compile and analyze his data.6

Tuesday, 29 August 1854

Mrs. Lewis’s little girl continued to vomit and to pass copious stools (CIC, 164). TheEley brothers owned and managed the percussion cap factory two doors away at 38Broad Street. Their father, who had founded the business, had long lived in BroadStreet nearby. After his death their mother, Susannah, now aged fifty-nine, movedsome miles north to rural Hampstead, but she remained partial to the water fromthe Broad Street pump. As a cart had to go every day from the factory up to Hamp-stead, the Eley brothers made sure that a bottle of water from the pump was care-fully packed for delivery to their mother’s home. Out of respect for their parents’preferences, the brothers also made sure that two tubs of the pump water were keptfresh inside the factory as drinking water for the 200 workers.7

Wednesday, 30 August 1854

Mrs. Lewis’s little daughter was worse. Early in the day the baby had rather abruptlystopped passing stools and vomiting. Dr. Rogers had noted no fever or cramps, nordid the infant seem blue or cold. Even so, she appeared thoroughly listless and ex-hausted, and overall the doctor was not at all optimistic (CIC, 164).

Nearby, on Berwick Street, Rev. Henry Whitehead was returning to St. Luke’sChurch after a series of visits and errands. To reach it he had to wend his wayamong stalls and barrows selling fish and eels, fruit, cat’s meat, old rags, and bones.

Broad Street 285

The twenty-nine-year-old clergyman, son of a Kent schoolmaster, had taken hisB.A. at Lincoln College, Oxford, in 1850 and the following year had been ordaineda deacon. His first appointment as an assistant curate was at St. Luke’s, a postwhich, according to the vicar, Mr. Stooks, was “for such as care more for the ap-proval than the applause of men.” Unmarried, Whitehead was sharing lodgingswith his brother in nearby Soho Square.8 He was considered an intelligent anddiligent young man, devoted to his clerical work, a good companion, and a livelystoryteller.

Thursday, 31 August 1854

The atmosphere was unusually hazy, although the sky was clear. In the latter part ofthe day the wind shifted from southwest to northeast.9

The day was much the same as the previous one for Mrs. Lewis. Her little girl re-mained largely free of diarrhea and vomiting but would take no food.

The day was quite different for Henry Whitehead. Early in the morning he hadhad an urgent call to one of the houses in his parish, where four people had beenseized with an attack of cholera during the night. As he left the house he found sim-ilar scenes wherever he turned. By noon he had returned to the vestry hall of St.Luke’s and there learned from the other curate and the scripture-reader that eachhad spent the morning in a similar fashion. Whitehead hastened out in response tofresh calls, and it was evening before he had completed his round.10

One of the many residents of the neighborhood who fell ill was Mr. G., the tailorwho lived on the first floor at 40 Broad Street. His economic situation was much likethat of the Lewis family, although he and his wife did not share Mr. Lewis’s aversionto the water of the street pump.

Friday, 1 September 1854

Mrs. Lewis’s little girl continued to sink into lethargy, although her diapers were stillstained with urine every so often (CIC, 164). Mr. G.’s illness progressed rapidly, andhe died of cholera approximately twenty-four hours after he was first seized. Thispattern of disease was being repeated throughout the neighborhood:

The people in this district were, no doubt, reading in the newspapers, or learn-ing from others, that cholera had reached London, but felt . . . that they werethemselves safe. On Friday morning, however, . . . people might be seen be-fore the break of day running in all directions for medical advice. “The angelof death had spread his wings over the place,” and by midday, groups werestanding in the street, looking the picture of wonder and consternation.11


Henry Whitehead spent another exhausting day rushing the length and breadthof his parish visiting the sick and dying. He was hardly less busy than the medicalpractitioners of the area, “whose labours day and night in behalf of the sufferers werebeyond all praise,” he later wrote.12 As he went past the top of Berwick Street, wherea yellow flag now hung to warn the populace of cholera, and observed the dead cartsremoving the bodies, Whitehead reflected that virtually all of those he had visitedthe previous day were now dead.13

Cholera was raging in Golden Square. Hampstead, by contrast, with its higher elevation and more spacious and well-ventilated homes, was free of the dread disease—almost, for Susannah Eley, alone among her neighbors, had been laid lowwith cholera.

Saturday, 2 September 1854

At 40 Broad Street at 11 A.M., the Lewis infant died (CIC, 164). Dr. Rogers filled outthe death certificate: “Exhaustion, after an attack of Diarrhœa four days previous todeath” (CIC, 159).

There was also mourning in Hampstead. Susannah Eley died after a sixteen-hourillness. Quite a number of the workers at the percussion cap factory also were com-ing down with cholera (MCC2, 43).

Whitehead and his fellow clergy had another hectic and depressing day as the dis-ease seemed to be raging without letup. Even busier than Whitehead was FlorenceNightingale. She had been at the Middlesex Hospital for about a month to superin-tend the nursing of the cholera patients there. “Patients [were] brought in every halfhour from the Soho district, Broad Street, etc., . . . chiefly fallen women of the dis-trict. . . . The prostitutes came in perpetually—poor creatures staggering off theirbeat! It took worse hold of them than of any.” Miss Nightingale was “up day andnight, undressing them . . . putting on [cloths soaked in] turpentine. . . .” She hadreportedly not had any rest all night and was on her feet all day that day as well.14

John Snow had to put aside his south London work when he was called upon byMr. Duffin to administer chloroform to a three-year-old girl from Blackheath foramputation of a toe (CB, 342).

Sunday, 3 September 1854

Snow had no anesthetics to administer, yet for the first time in weeks his attentionwas not focused on his south London study. There was much talk about the greatoutbreak of cholera in Golden Square, which seemed to have begun on Thursday orFriday. Snow knew the area well—it was immediately to the west of the Soho dis-trict where he had lived as a medical student and then practiced while living in Frith

Broad Street 287

Street. It was a mere five minutes’ walk to Broad Street from his current home inSackville Street.

As he heard more details, Snow came to suspect that the pump in Broad Street,the most popular in Golden Square, was the culprit. A sudden, severe outbreakin a relatively localized area meant that a street pump, drawing water directly fromthe ground, had become contaminated. The two companies providing piped wa-ter to the houses in this region, the Grand Junction Company and the New RiverCompany, supplied relatively clean water, and their customers had been almostentirely free of cholera. The current outbreak reminded him of several earlier in-cidents that he had carefully studied: “In the autumn of 1848, when cholera hadjust commenced in London, a number of cases occurred about Bridge Street,Blackfriars; and it was found by Mr. Hutchinson, Surgeon, of Farringdon Street,that the well of St. Bride’s pump had a communication with the Fleet ditch, upwhich the tide flows.”15

There were similar accounts of point-source outbreaks in the official governmentreport on the 1848–1849 epidemic. A sudden, violent outbreak in a street in Man-chester was attributed to a pump well into which a stopped-up sewer had leaked. Inthe thirty houses using the pump, twenty-five people had died, while in sixty nearbyhouses with another water source, there was no cholera at all.16 In Lambeth, in southLondon, an isolated court had several cases of disease, including two of cholera. Thelocal surgeon had examined the court’s pump and found the water discolored andsmelling like a cesspool. The enterprising surgeon removed the piston of the pump,and no further cholera occurred in the court.17

In the evening Snow went directly to the Broad Street pump (Fig. 11.2) and tookwater samples for visual inspection. The water was clear, which surprised him be-cause he expected to find some cloudiness, evidence of organic impurities (CIC,98–99). So he next inspected the water of four nearby street pumps, those in War-wick Street, Bridle Lane, Vigo Street, and Marlborough Street. He found some im-purities, white flocculent particles evident to the naked eye, in each, the greatestquantity in the Marlborough Street pump, and passers-by told him that the neigh-borhood residents usually avoided that pump altogether and used the Broad Streetpump instead.

For Henry Whitehead this day went just like the preceding three. He was con-stantly on the move, going from house to house, everywhere finding scenes of dis-may and devastation. When he ran into any of the local physicians, he heard thesame general comments. The cholera was striking with few premonitory symptoms,the sufferer going from normal health to complete collapse in a matter of hours.Medicine’s usual remedies were proving to be singularly unavailing.18 It was not un-til eleven o’clock at night that Whitehead finally had time to relax. He took advan-tage by treating himself to a drop of brandy with some cold water drawn from theBroad Street pump (CIC, 156).


Monday, 4 September 1854

Mrs. G., the widow of the tailor at 40 Broad Street, developed symptoms of cholera(CIC, 161). The Times reported the happenings in Golden Square in the form of anotice from the General Board of Health.

Henry Whitehead continued on his dismal rounds, but despite the grim scenes hewitnessed, more hopeful thoughts occupied his mind. He was impressed with thecalm among most residents in the neighborhood. He had heard of numerous actsof great generosity and courage as people tended to the sick, in some cases totalstrangers caring for others with complete disregard for their own safety.19

John Snow thought matters over and was not satisfied with the results of his pumpwater inspection of the previous evening: “Further inquiry . . . showed me thatthere was no other circumstance or thing common to the circumscribed locality inwhich this sudden increase in cholera occurred, and not extending beyond this

Broad Street 289

Figure 11.2. Broad Street pump, modern replica; Broadwick Street, London

(photograph by authors).

locality, except the water of the [Broad Street] pump.”20 After administering chloro-form for Mr. Cartwright while that dentist extracted two teeth (CB, 343), Snow wentback and reexamined water from the Broad Street pump. Again he saw the whiteparticles, and this time he did a chemical test and detected a large quantity of chlo-rides, which he took to be evidence of impurity. Not trusting his own microscopicskills, he took a sample of the water to the eminent microscopist Dr. Arthur HillHassall.21 Hassall reported that he saw a good deal of organic matter and some oval“animalcules” that seemed of no importance except to signal the presence of the or-ganic matter on which they fed. Perhaps there were more organic impurities in thewater than Snow had originally assumed.

Snow returned to the Broad Street neighborhood and began to ask more ques-tions of the inhabitants. No one had seen a change in the character of the water justbefore 31 August, when the outbreak had begun. One of the Eley brothers said hehad noticed for quite a while that the water became offensive if it sat for about twodays. Farther afield, on Poland Street, an informant claimed that the water wouldform a film if it remained motionless for a few hours (CIC, 99).

Tuesday, 5 September 1854

Mrs. G. died around 10 a.m. at 40 Broad Street having lasted only a little longerthan her husband once her attack began (CIC, 161). The clergymen at St. Luke’shad much to talk about when they met for their regular noontime gathering.There had been a definite decrease in the number of deaths, and the new casesof cholera were both fewer and less severe.22 As Whitehead reflected on the casesof recovery he had seen in the past several days, he was struck by the victims’ in-tense thirst and how often some had sent to the Broad Street pump for fresh wa-ter. He had visited a servant woman daily who had had a severe attack on Fri-day, soon was in a state of near-total collapse, but had ultimately rallied, drinkinggreat quantities of the pump water all through the illness. On Sunday one boywho recovered had drunk ten quarts, and a girl in similar straits drank seven-teen (CIC, 136).

The president of the General Board of Health, Sir Benjamin Hall, visited BroadStreet that morning as part of a tour of the affected areas to inspect the “sanitaryand preventive measures” that had been taken. The next day’s Times reported,“Groups of people formed themselves in the streets, and evinced much gratitude athis presence.”23 The Board of Health had just been through a serious shake-up. Ed-win Chadwick, the main force behind the board since it had been formed in 1848,had stepped on too many toes in the business and medical communities in his zealfor sanitary reform. On 31 July Parliament had used the expiration date of the au-thority of the previous board as an opportunity to dismiss Chadwick and his allies.Hall, a member of Parliament, had been put in charge of the newly reorganized


board, with a smaller staff and reduced authority to ensure that the board did notstray from its Parliamentary mandate.24

John Snow had no anesthesia work and went back to interviewing the residentsof Broad Street. His patient inquiries turned up Mr. John Gould, “the eminent or-nithologist,” who lived just up the street from the pump and routinely drank thewater. He had been away from home, had returned on Saturday, and immediatelysent for some of the water, but despite it being freshly drawn and perfectly trans-parent, he noticed an offensive smell. His assistant noticed it, too (CIC, 100). De-spite the great amount of negative testimony, this one positive assertion from a sci-entific observer of a recent change in the water was enough to spur Snow forward.He decided that his inquiry now required statistical methods rather than chemistryor microscopy.

He hastened to the General Register Office to ask for a list of cholera deaths inthe districts of St. James’s and St. Anne’s, Soho. William Farr’s staff were then tabu-lating the week that ended on Saturday, 2 September, during which they had recordedeighty-nine deaths from cholera in that quarter of London. The daily distributiontold the same story that Snow, Whitehead, and others had already observed—sixdeaths occurred during the first four days of the week, followed by four on Thurs-day, 31 August alone, and seventy-nine on Friday and Saturday. Snow decided toeliminate the first six deaths as not properly being part of the great outbreak and fo-cused his attention on the remaining eighty-three.

Armed with the list of cholera deaths showing the address of each victim, Snowreturned to Broad Street. He did a mental calculation to determine the point on eachstreet from which it would be closer to walk to another street pump than to thepump in Broad Street. He observed from the addresses that seventy-three of theeighty-three deaths had occurred in residents of houses closer to the Broad Streetpump than to any other. Snow next made inquiries at the houses on his list locatedoutside of the area of the Broad Street pump. He discovered that eight of these tendeaths occurred among people known or thought to have drunk the Broad Streetwater. Some went to that pump by preference, others were children who went toschool near the pump.

Snow then turned to the addresses located inside the pump’s area as he hadcalculated it. He found in sixty-one cases that the deceased person drank thepump water. In another six cases every possible informant had either died or fled. In only six cases was Snow informed that the victim was known not to have used the pump water. Snow concluded from his data that if he eliminatedthose known to have drunk the water from the pump, the number of cases ofcholera could easily represent the background level of sporadic cases occurringelsewhere in the metropolis. It seemed clear to him that there had been “no par-ticular outbreak or prevalence of Cholera in this part of London except amongthe persons who were in the habit of drinking the water of the above-mentionedpump well.”25

Broad Street 291

Wednesday, 6 September 1854

The Times published the Weekly Return of the Registrar General, which included theeighty-nine deaths of which Snow had been informed the previous day. The sum-mary noted, “On the north side of the Thames there has been a remarkable outbreakin the St. James’s district.”26

The staff at St. Luke’s held their customary daily meeting in the vestry at noon.There were still many visits to be made, even though the cholera thankfully seemedto be waning. Whitehead was concerned: the scripture-reader, James Richardson, aScotsman and retired grenadier guard, was not there. He hastened to Richardson’shouse and found the sergeant in bed with cholera. “I knew you would come,” saidRichardson.“And I knew how I should find you when I did come,”Whitehead replied.

The sergeant was calm in the face of the threat: “I shall look up to my God, andthough he slay me, yet I will trust in him.”27 Whitehead learned that the sergeanthad been suffering premonitory symptoms for the past day and a half, which he hadnot mentioned to anyone. The sergeant also recalled that on 2 September, quite con-trary to his usual custom, he had drunk half a pint of water from the ladle at theBroad Street pump.28

Snow was busy with his practice, first administering chloroform to a linendraperin the Edgware Road for ligation of hemorrhoids. The man had lost a good deal ofblood and had a bounding pulse. Nonetheless, Snow was relieved to report that thechloroform produced no faintness or depression. The next operation, a tooth ex-traction in Hanover Square, was much simpler (CB, 343).

He then returned to his detailed inquiries near Golden Square. He visited one ofthe small coffeeshops near the pump, frequented by mechanics, where the pump wa-ter had been the main beverage supplied with dinner. The proprietor mentioned thatshe knew of nine of her regular customers who had so far died of cholera (Fig. 11.3)(CIC, 103–04).

Thursday, 7 September 1854

The General Register Office had not yet received the death returns for the week af-ter 2 September, but local observers knew that the cholera around Golden Square,though now declining, had exacted a very high toll. The numbers meant little untilone realized how very few city blocks made up the affected area. A walk of less thanthree minutes sufficed to take one from the epicenter of the outbreak to a regionmostly free of cholera.29 Whitehead could stand at the front door of St. Luke’s andpoint to four houses, at an average distance of fifteen yards, that had collectively lostthirty-four inhabitants in four days.30

The official body most directly responsible for local health matters in St. James’sparish in 1854 was the Board of Governors and Directors of the Poor, rather than


12 residents, 3 deaths

Lion BreweryEdw. G. & John Huggins

80 workers, 0 deaths

MARSHALL STREET

#29

Pum

p-w

ell

CAMBRIDGE STREET

Cambridge St.; Newcastle-on-Tyne pub6 residents, 1 death

#7

#40

#30

#31

#32

#33

#34

#35

#36

#37

#38

#39

Mary Hooper; Grocer10 residents; 1 death

Henry Cooke; Straw bonnet maker15 residents, 3 deaths

Eliza Grimmond, Baker14 residents, 2 deaths

William Peel, Grocer19 residents, 3 deaths

Edmund Tisdall, Saddle tree mfr.7 residents, 0 deaths

Edwin Bell, Engraver7 residents, 1 death

Eliz. Main, Ironmonger11 residents, 2 deaths

William Pollit, Trimming seller29 residents, 5 deaths

Eley Brothers, Percussion cap mfrs.150 workers, 16 deaths

John Haws, Wardrobe dealer19 residents, 3 deaths

Theo. Hammond, Boot tree mfr.20 residents, 5 deaths

BR

OA

D S

TR

EE

T

NEW STREET

#50

#6

#41

#42

#43

#44

#45

Cambridge St.23 residents, 2 deaths


Engraver, carpenter, dyer15 residents, 2 deaths


Alexander Jeffrey, Veterinarian29 residents, 2 deaths

Arthur Abbott & Sons, Builders28 residents, 5 deaths

POLAND STREET

DUFOURS PLACE

#28 Edw. Malton, Surgeon; Wm. Ridley, Furrier5 residents, 0 deaths

#27Patrick Quigley, Tailor;Robert Bonner, Bootmaker7 residents, 0 deaths

#22 Crown pub, J. F. Hallatt? residents, 0 deaths

#21 Griffiths, Lodging House? residents, 0 deaths

#14 20 residents, 2 cholera cases, 0 deaths

#13 Francis Stringer, Undertaker0 residents, 0 deaths

#6 William Dutton, French water gilder20 residents, 1 death

#26

#25

#24

#23

Robert White, Billiard table maker18 residents, 2 deaths

Edward Brown, Blacking mfgr.? residents, 0 deaths

Anne Ersser, Lapidary14 residents, 1 death

Thomas Bennett, Plumber & painter18 residents, 1 death

#12

#11

#10

#8

#7

McAuliffe & Ross, Leather case mfrs.20+ residents, 5 deaths

#9C. Ash & Sons, Mineral teeth mfrs.42 workers, 6 deaths⎧

⎨⎩

William Beal, Timber dealer11 residents, 1 death

John Greenfield & Son, Machinists23 residents, 3 deaths

James Smith, Umbrella maker10 residents, 1 death

#20

#19

#18

#17

#16

#15

John Gould, FRS5 residents, 0 deaths


William Stannard, carver/Gilder;John Williams, Tailor16 residents, 3 deaths

Samuel Carlson, Jeweler25 residents, 2 deaths

Thomas Davis, Die sinker20 residents, 6 deaths

Angelo Pontecorboli, Warehouse3 residents, 1 death

N➲

Figure 11.3. Diagram of the western portion of Broad Street showing principal businesses at

each address, number of residents, and cholera deaths (adapted from GBH, Appendix to CSI,

343–46; Watkin’s London Directory for 1855, 695).

a Board of Guardians. The parish had been exempted from implementation ofthe New Poor Law. Instead of in-door relief provided in a union workhouse, St.James offered its poor a combination of out-door relief or admission to a smalllocal workhouse. The Board of Governors handled day-to-day affairs and reportedto the parish vestry. The governors and directors were concerned about the threatof cholera and on 14 August 1854 had voted to abandon their usual meeting pro-tocol and form themselves into a special emergency response committee to dealwith the it. It seemed during the past week as if their worst fears had been real-ized. As they considered at their weekly meeting what course of action to pursuenext, they were notified that Dr. John Snow had respectfully requested an inter-view with them. He was admitted and presented an account of his investigationso far. As a result the committee issued an order that the handle be removed fromthe Broad Street pump.31


The order was carried out, and the pump handle was removed. The event passed to-tally unnoticed by the newspapers and journals of the day,32 but it was certainly no-ticed by the local populace, who were not pleased. The butts and cisterns in whichpiped drinking water was stored (because the water companies typically providedrunning water only a few hours each day) were coated with dirt, uncovered, and of-ten located in “close, unwholesome, and disgusting propinquity” to the water clos-ets and garbage cans.33 Small wonder that many supplied with piped water still pre-ferred the Broad Street pump.

Mr. Thomas Lewis, the policeman living at 40 Broad Street whose infant daugh-ter had died on 2 September, developed unmistakable symptoms of cholera. Hissymptoms, however, did not seem to be progressing as fast as those of his late neigh-bors, the G. family (CIC, 161).

The General Board of Health took the action promised earlier by Sir BenjaminHall and issued instructions for a house-by-house medical inspection by Dr. DavidFraser, Mr. Thomas Hughes, and Mr. J. M. Ludlow. The inspectors were instructedto focus on the areas of St. James where cholera was most prevalent. While Chad-wick and his reformist allies on the old Board of Health had been dismissed, the fur-ther instructions to the inspectors showed that the new board was equally devotedto a miasmatic theory of cholera. The inspectors were told to investigate atmosphericconditions, the ventilation of streets and buildings, the presence of nuisances andnoxious trades, bad smells in the streets (especially from sewers) and houses, priv-ies and cesspools, the state of the basements, the floor of the house where each casehad occurred, the condition and habits of the inhabitants, and the quantity and qual-ity of water supply.34


The General Board of Health was not alone in adopting a miasmatic view. Theneighborhood was rife with rumors that recent sewer works had disturbed the soilof an ancient pit, just northwest of Broad Street, where bodies had been buried dur-ing the plague of 1665. As a local resident wrote to the Times, “Is it not thereforereasonable to suspect that . . . when the new sewer was constructed . . . , it musthave most injuriously disturbed the soil, saturated with the remains of persons de-posited here during the great plague . . . , and that a deadly miasmatic atmospherehas been for some months arising through the gully holes connected with this sewer,poisoning the surrounding atmosphere . . . ?”35

It was Rev. Whitehead’s turn to speak from the pulpit at St. Luke’s. There was no pointin trying to talk about anything other than the cholera. Enumerating instances of God’sprovidence, Whitehead congratulated the poor old women, who made up a substantialproportion of the congregation, on their relative immunity from the great outbreak. Pri-vately, he was puzzled by the disproportionate exemption of these elderly women.36

Saturday, 9 September 1854

Once again Mrs. Lewis was occupied emptying pails of water into the cesspool inthe area at 40 Broad Street. Instead of her now-dead baby’s diapers, this time shewas washing her husband’s soiled bedclothes. There was less noise outside her housewith the handle of the pump removed.37


Dr. Fraser, Hughes, and Ludlow, the Board of Health inspectors, had located manysources of noxious odors. A charwoman had died of cholera at 44 Silver Street; shehad kept a total of seventeen dogs, cats, and rabbits. The inspectors found mosthouses overcrowded, with people forced to wash, cook, and sleep in the same room.They were surprised to note that a number of deaths had occurred among temper-ate people of clean habits.

They also found that they were not the only official inspectors in the neighbor-hood—they ran into Edmund Cooper, an engineer from the Commission of Sew-ers.38 Since the Golden Square outbreak began the commission had been besiegedwith criticism. As long as bad smells were held to be a cause of cholera, the sewersystem was a natural suspect. Some residents, like the author of the letter to the Timeson 8 September, blamed the disruption of the ancient plague pit. Others alleged thatcholera deaths had been especially numerous in houses next to gully holes, the open-ings through which sewer gases were vented to the surface.39 Cooper had been dis-patched to look into these allegations.

Broad Street 295


Thomas Lewis still clung to life in the front kitchen at 40 Broad Street.40 Residentsof the neighborhood read about themselves in the Times:

The outbreak of cholera in the vicinity of Golden-square is now subsiding, butthe passenger through the streets which compose that district will see manyevidences of the alarming severity of the attack. Men and women in mourn-ing are to be found in great numbers; and the chief topic of conversation isthe recent epidemic. The shop windows are filled with placards relating to theall engrossing subject; and, if it be true that in a multitude of counsels thereis wisdom, the good people of this parish ought to be so wise in the matter ofcholera as to be quite beyond the chance of a second attack. At every turn theinstructions of the new Board of Health stare you in the face. In shopwindows,on church and chapel doors, on dead walls, and at every available point ap-pear the parochial handbills, directing the poor where to apply for gratuitousrelief. The homoeopathists are not behindhand, but energetically assert theircapability of putting a stop to the epidemic. An oil-shop puts forth a large caskat its door, labelled in gigantic capitals “Chloride of lime.” The most remark-able evidence of all, however, and the most important, consists in the contin-ual presence of lime in the roadways. The puddles are white and milky withit, the stones are smeared with it; great splashes of it lie about in the gutters,and the air is redolent with its strong and not very agreeable odour. You mightat first imagine that a vast amount of building was going on, but not so. Thefact is that the parish authorities have very wisely determined to wash all thestreets in the tainted district with this powerful disinfectant; and, accordingly,the purification takes place regularly every evening. The shopkeepers have dis-mal stories to tell—how they would hear in the evening that one of their neigh-bours whom they had been talking with in the morning had expired after afew hours of agony and terror. It has even been asserted that the number ofcorpses was so great that they were removed wholesale in dead-carts for wantof sufficient hearses to convey them; but let us hope this is incorrect.41

The extensive use of lime in the streets (to eliminate bad smells from decaying or-ganic matter) showed that the Board of Governors was adopting a local miasmatistposition. They apparently saw no conflict between that theory of cholera spread andSnow’s hypothesis on the wisdom of removing the pump handle.


Thomas Lewis died of cholera after eleven days of illness (CIC, 161).


Thursday, 21 September 1854

Snow’s letter to the Medical Times and Gazette summarizing his work on the BroadStreet outbreak and the positive response he had received from the Board of Gov-ernors was in the hands of the editor awaiting publication.42 Perhaps Snow thoughthe was finished with Golden Square and could turn all his research attention to southLondon again, but he found himself back doing “shoe-leather epidemiology” in St.James.

Snow now realized that the original figures he had obtained from the General Reg-ister Office on 5 September had seriously undercounted the deaths in Golden Square.He had thought that there had been seventy-nine deaths on the first two days of Sep-tember, but a recount the following week, as well as information from surroundinghospitals to which Golden Square victims had been taken, raised the actual total to197. This spurred Snow to return to do more detailed inquiries, but he immediatelyfound himself stymied by the general flight of the population in the aftermath ofthe epidemic.43 Many of the houses and shops where he had hoped to ask questionswere empty: “In less than six days from the commencement of the outbreak, themost afflicted streets were deserted by more than three-quarters of their inhabitants”(MCC2, 38). Nevertheless, the people he was able to interview provided much newinformation to support his original conclusion that the pump was the source of theoutbreak. The new data took the form of both positive and negative evidence.

On the positive side he found a number of ways in which residents of the areacould have drunk the pump water without being aware of it. The local pubs usedthe water freely for mixing with spirits, and it was similarly served in coffee shopsand restaurants. Several little shops put an effervescing powder in the water and soldit as “sherbet.”44

Eighteen of the 200 workers in the Eley percussion cap factory, where the pumpwater was made available in tubs for drinking, had died. Mr. Peter Marshall, Snow’smedical friend and associate who resided nearby on Greek Street, told Snow aboutseven workmen at Ash & Sons, a manufacturer of dentists’ materials located at 8–9Broad Street. All of these men had died in their homes nearby. Marshall said that allof them had regularly drunk pump water, usually half a pint once or twice a day.Two others who worked at that factory but did not drink any pump water had onlymild diarrhea. Marshall also passed along the case of an army officer who lived welloutside the district but came to dine at a house in Wardour Street and had somepump water with his dinner. He developed cholera and died in a few hours.

Marshall had some other interesting cases to recount, all implicating the pump,but Snow was especially fortunate to run into Dr. Fraser, one of the medical in-spectors for the General Board of Health.45 Fraser told him about the case of Su-sannah Eley, the “Hampstead widow” who had the water from the pump brought toher every day (CIC, 102–107; MCC2, 40–45). On investigating that case further, Snowfound that Mrs. Eley’s niece had been visiting her at the time of her attack and had

Broad Street 297

also drunk some of the pump water. The niece went home to Islington, which wasat that time free of cholera, developed the disease, and died. A servant in Mrs. Eley’shouse drank a small quantity of the water, developed diarrhea (diagnosed by thephysician as not being cholera), and lived.

Snow was also indebted to Dr. Fraser for the report of the case of:

a gentleman in delicate health [who] was sent for from Brighton to see hisbrother at No. 6, Poland Street, who was attacked with Cholera and died intwelve hours on the 1st of September. The gentleman arrived after his brother’sdeath and did not see the body. He only staid [sic] about twenty minutes inthe house, where he took a hasty and scanty luncheon of rump steak, takingwith it a small tumbler of cold brandy and water, the water being from theBroad Street pump. He went to Pentonville, and was attacked with Cholera theevening of the following day, September the 2nd, and died the next evening.

CIC, 106

Snow was accumulating one case after another in which people whose only contactwith the Golden Square neighborhood was the pump water and who had contractedcholera. The association seemed strong enough to postulate a cause-and-effect relationship.

However, he was not content to accumulate only positive evidence in support ofhis hypothesis. He devoted particular effort to looking into negative evidence thatat first glance appeared to discount it. In several instances further investigation ofthe negative evidence actually gave him additional support. For example, one un-likely sanctuary was the workhouse in Poland Street—only five of 535 inmates haddied, while the houses on the adjacent streets had been hit severely. A miasmatistwould have had a hard time explaining this, especially because the workhouse resi-dents, being poorly nourished, sickly, and probably of indifferent morals, might bethought to be more predisposed to disease. Snow found that the workhouse had itsown well and also took piped water from the Grand Junction company. He calcu-lated that had the death rate at the workhouse been equal to that of the adjacentstreets, there would have been more than fifty deaths.46

Another interesting sanctuary was the Lion Brewery in Broad Street. Miasmatiststhought that alcohol increased susceptibility to cholera, yet none of the seventy-oddworkers at the brewery was known to have died. The proprietors, Edward and JohnHuggins, told Snow that they supplied their workers with New River Company wa-ter and also had their own deep well on the premises. However, that hardly mat-tered; to their knowledge, because the men were allowed an allotment of malt liquor,they did not drink any water at all, in apparent defiance of the third precautionagainst cholera published by the General Board of Health on 4 September. Thus, intwo important instances Snow found that the factors identified as important by miasmatists—breathing the supposedly contaminated epidemic atmosphere of the


neighborhood and suffering from various predisposing factors—were much less im-portant in explaining freedom from cholera than the fact of not drinking the pumpwater.

Whitehead, for his part, was at work on a pamphlet about the outbreak, which hetitled The Cholera in Berwick Street, perhaps not unnaturally concluding that his ownchurch had been the true epicenter of the calamity. He described the reactions of thepopulace, especially the general lack of panic, in order to put an end to rumors fromother quarters.47 He also indulged his mathematical bent by constructing a table toshow the relationship between the day on which the victims contracted cholera andhow fast that person’s disease progressed to document his assertion that it was muchmore virulent during the first days of the epidemic. He showed that people who con-tracted cholera in the earlier days of the outbreak were more likely to die even thoughthe duration of their illness was shorter.48

Whitehead learned of Snow’s hypothesis that had led to the removal of the pumphandle. Perhaps thinking back to his own drink of brandy and water on 3 Septem-ber, but especially remembering the residents who had survived the cholera specif-ically by drinking huge quantities of the pump water, Whitehead rejected Snow’s the-ory. He told “a medical friend” that all it would take would be a careful investigation(as contrasted with Snow’s quick visits during the period 3 to 7 September) to con-clusively disprove Snow’s idea. Moreover, Whitehead himself was the ideal person todo this study. With his intimate knowledge of the people of the district and the factthat his church work took him up and down Broad Street almost every day, he couldtrack down all the information that was needed.49 No matter if much of the popu-lation had fled, he knew how to trace them much better than did Snow. Plus, heknew the friends and families of those who had died, who could give him accurateinformation on the habits of the deceased.

Monday, 25 September 1854

With the inspection of houses in Poland and Marshall Streets, David Fraser, T.Hughes, and J. M. Ludlow finished their investigations on behalf of the General Board of Health, so that in the preceeding two weeks there had been three inde-pendent but simultaneous inquiries (by Snow, the Commission of Sewers, and theboard) in the neighborhood, with the investigators periodically running into one an-other as they made their rounds. Dr. Fraser and his colleagues had visited 800 housesand smelled and duly noted an incredible variety of bad odors. They had looked atthe Broad Street pump to be sure that no drainage from the sewer had percolatedinto the water. They found no evidence of this when they inspected the brick liningof the well under the pump, and a local surveyor, Mr. York, informed them that thesewer ran ten feet away from the well anyway and was twenty-three feet below ground.They had found two cases (both of which Dr. Fraser had described to Snow) that

Broad Street 299

implicated the pump; but they had found a greater number of cases in which thosedrinking the water had either never been attacked or had recovered. They completedtheir work by inquiring into the death at 37 Marshall Street, said to be due to cholera,but discovered that the victim was a drunkard who had been in a fight the day be-fore and was just as likely to have died from his injuries.50


Edmund Cooper, engineer for the Commission of Sewers, had completed his inves-tigation. To apprise the local populace of his findings, the commission held a spe-cial “court” in their offices in Greek Street, Soho. Cooper had prepared a detailed re-port accompanied by a map (see Fig. 12.4) that showed all details of the sewer systemand the location of each house in which a death from cholera had occurred.51 Hepointed out that the houses nearest the gully holes had no greater number of deathsthan did houses farther away. He also drew attention to an old plague pit at a farcorner of the cholera district. Very few deaths had occurred nearby. The sewers thatdrained the plague pit area flowed northward to Regent Street, where few, if any,cases of cholera had occurred.

Cooper put forth a miasmatist account of the cause of the outbreak. The sewersof the area where most of the deaths had clustered were in quite good condition.The drains of the houses of the region were in generally bad condition, with manycesspools and deteriorating brickwork, and most of the owners had not taken ad-vantage of the opportunity to connect their drains to the recently constructed sew-ers. Bad air was without doubt the cause of cholera, but it came from within thehouses and not from the commission’s well-kept sewers.52

The chairman of the commission concluded accordingly that “the sewers were notthe cause of the cholera; that they were not in any way connected with the disease;but that the real cause of the calamitous occurrences in the locality . . . was thefilthy and undrained state of the houses.” The commissioners expressed their hopesthat these facts would be widely circulated so as to allay public fears.53

Looking at a carefully and accurately drawn map showing the location of the deathsdid nothing to dispel the power of miasma theory. Apparently, none of the manypeople who studied Cooper’s map that day thought to wonder about the concen-tration of deaths around the corner of Broad and Cambridge Streets—the approxi-mate location of the pump.54

Wednesday, 25 October 1854

Snow administered anesthesia for the repair of an infant’s harelip and for the ex-traction of seventeen teeth and stumps. He was relieved that the dental anesthesia


led to no ill effects despite the long duration of the procedure (CB, 347). This wasan average day in his practice.55

He then returned to his cholera research. He was engaged in revising his mono-graph On the Mode of Communication of Cholera (MCC2). Since he had publishedthe slim volume of thirty-one pages in 1849, he had amassed much additional datato support his theory of water-borne transmission. The centerpiece of the new edi-tion would be the detailed statistical analysis of his south London study, but he alsowanted to include a full account of the Broad Street outbreak. This would requirefurther data on cholera deaths and the water drunk by each individual, especiallythose who had died at some distance from the pump. Some of those who had fledwere now returning to the district, making it easier to pursue his inquiries.56

Thursday, 23 November 1854

The vestry of St. James’s was holding one of its regular meetings. On the table forfinal action was a motion by Dr. Edwin Lankester: “That a Committee of this Vestrybe appointed for the purpose of investigating the causes arising out of the presentsanitary conditions of the Parish of the late outbreak of cholera in the districts ofGolden Square and Berwick Street.”57 After some discussion the motion was passed,and a committee of eight, Dr. Lankester included, was formed.58

Lankester thought at first that eight members would suffice. He imagined thatmost of the information needed could be secured from two sources: written ques-tionnaires distributed throughout the parish and a review of the data laboriouslygathered for the General Board of Health by Fraser, Hughes, and Ludlow. Lankesterwas soon disabused of his optimism. The first questionnaires distributed producedno useful returns. The approach to the president of the General Board of Health forcopies of data resulted in a blunt refusal on the grounds that “investigations of thiskind were more valuable when independent.”59 Perhaps this was a polite way of say-ing that the amateurs in St. James had better stand aside while government profes-sionals did the work properly.

Faced with the need to conduct its own personal interviews house by house, thecommittee added eight more members. Dr. Snow was now asked to join as well asthat earnest young clergyman who had written a pamphlet.60

Monday, 27 November 1854

At the instigation of the parish authorities, the Paving Board (which had authorityover the street pumps) conducted a survey of the interior of the well under the BroadStreet pump. Snow wrote, “I was informed by Mr. Farrell, the superintendent of theworks, that there was no hole or crevice in the brickwork of the well, by which any

Broad Street 301

impurity might enter . . .” (MCC2, 52). This was something of a setback as heworked to complete the revision of his cholera monograph. He was pointing his fin-ger at the pump as the source of the outbreak yet was unable to prove or even showhow it could have become contaminated with cholera evacuations.

Monday, 4 December 1854

Snow produced an exhibit for the evening meeting of the Epidemiological Societyof London, a cholera spot map of the Broad Street area.61 By now he had gathereddata on 616 deaths and displayed these data in tabular form. Where he could dis-cover the address, he showed these deaths as black bars on the map (see Fig. 12.5).He wanted to use his new map to illustrate the Golden Square outbreak in his re-vised monograph. Churchill, the publisher, needed a copy of the map immediatelyto prepare the plate, but it was still two weeks before Snow was to submit his reporton the water supply of Golden Square to the St. James Cholera Inquiry Committee.Perhaps he could continue to tinker with the map in the meantime.

Tuesday, 12 December 1854

Snow had a light day—only a tooth extraction (CB, 353)—and so was able to completehis work for Dr. Lankester’s Cholera Inquiry Committee. He had been asked to reporton the water supply to the affected district, but he used the report as a platform for histheory of the cause of the outbreak as supported by his investigations. After just a fewparagraphs in which he generally described the water supply, he simply copied the rel-evant portions of the text of his cholera monograph. However, having sent that text offto Churchill a few weeks earlier, he was able to make some corrections and additions.

In particular, he had continued to refine his map. He found that he had shownthe Broad Street pump in the wrong place, at the corner by the public house insteadof in front of the house at number 40. His new map relocated it correctly (see Fig.12.7). His most important addition was a dotted line that graphically depicted themental process Snow had carried out on site in September. It showed the points ofequal walking distance between the Broad Street pump and all other street pumps.Snow wanted his readers to be struck visually by the fact he had deduced initiallyfrom inspecting the list of addresses of deaths from the Registrar-General—that thenumber of deaths fell off dramatically as soon as one reached the point where it wascloser to walk to another street pump than to the pump in Broad Street. (Since 4December Snow had gone back and carefully measured the distances along the streets[CIC, 109].) Moreover, he now had much more data on those who had died butwhose residences lay outside the dotted line, showing that in most cases they wereknown to have used the Broad Street pump.


He accompanied the map with a table accounting for all 616 deaths by date. Heenumerated his data on how many of those who died were known to have drunkthe water from the pump. He mentioned the workhouse, the brewery, and the per-cussion cap factory as well as a number of other instances. He also included the caseof the “Hampstead widow.”62

Even so, Snow could hardly regard his case as open-and-shut. He had no direct evi-dence of any contamination of the Broad Street pump water with cholera evacuations.It was true that Dr. Hassall’s microscopic examination had shown organic impurities,but while the miasmatists might be satisfied with vague accounts of putrefying organicmatter of any sort, Snow’s theory required that one specific sort of organic matter bepresent. In addition, lacking any knowledge of an “index case,” he had no explanationof how the cholera evacuations could have found their way into the pump well.63

Thursday, 14 December 1854

The St. James Cholera Inquiry Committee was in jeopardy. The vestry had weighedin and objected strongly to the creation of the committee, which would have to bepaid for by the Poor Law funds for which it was responsible. The area was just start-ing to recover; people were moving back and customers could be seen in the shops.All that was needed to drive people away again was some sort of official reminderof recent calamities. The poor rates were already far below what was needed to meetthe extra expenditures necessitated by the cholera. All the placards and the lime inthe streets had cost a lot of money. Dr. Lankester, however, was not one to be putoff easily.64 He offered a spirited defense, and after considerable discussion the vestryreluctantly allowed the committee to continue its work.65

Tuesday, 19 December 1854

The latest issue of Gazetta Medica Italiana Toscana, from Florence, featured a leadingarticle by Filippo Pacini, a prominent microscopist and professor at the local medicalschool. Pacini reported on the results of his microscopic inspection of the mucous mem-branes of the intestines from postmortem exams of cholera patients. He called partic-ular attention to a bacterium, which he called a “vibrio,” with a distinctive “comma”shape, and he postulated that this organism was the specific causative agent of cholera.66

Saturday, 27 January 1855

The Medical Times and Gazette published the notice on its front page that J. Churchillof New Burlington Street had released the revised and expanded edition of On the

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Mode of Communication of Cholera, by John Snow. It could be purchased for sevenshillings.

Among the complimentary copies Snow gave out was one to his new acquaintanceon the Cholera Inquiry Committee, Henry Whitehead. Whitehead discovered onreading the book that he had originally misunderstood Snow’s theory regarding thepump:

I found, moreover, that he attributed [the cholera-causing properties of thepump water] not to general impurity in the water, but to special contamina-tion of it from the evacuations of cholera patients, which he conjectured musthave reached the well from a sewer or cesspool. In thanking him for the book,whilst I could not help admitting the weight of many of his recorded facts, Istill clung, as a last resource, to an a priori objection to his theory—urgingthat, if special contamination of the water in the way suggested had begun themischief, the outbreak ought not so soon to have subsided, when much largerquantities of cholera excretions must have been continually pouring into thewell through the same channel . . . of communication with the sewers. Asfor cesspools, I at that time supposed they had mostly been abolished.67

Tuesday, 20 February 1855

The previous September Henry Whitehead had told his medical friend that he couldeasily disprove Snow’s theory of the pump. The young clergyman reflected that henow knew a good deal more about the complexity of a thorough inquiry into a dis-ease outbreak. The vestry’s Cholera Inquiry Committee had assigned to Whiteheadthe special task of reporting on Broad Street and its residents, and he wanted the re-port to be as complete as possible. A later acquaintance wrote that during this pe-riod Whitehead would combine his church duties with gathering evidence on thecholera and after a long day’s work would then sit up writing till 4:00 A.M. to recordall of his data.68

While Whitehead had originally set out to disprove Snow, Snow had become histeacher. Three on the committee—Snow, Lankester, and Dr. King—had drawn up alist of questions for the house-to-house surveys, and Whitehead adopted their ques-tionnaire. In effect, Whitehead found himself replicating more thoroughly Snow’snecessarily hasty investigation carried out during the first week of September 1854.That investigation had an important flaw. Snow studied the use of the pump onlyamong those who had died and did not examine two other groups, those who haddeveloped cholera but recovered and, most important, those who did not havecholera at all. If it had turned out, for example, that the same percentage of thosewho had no cholera had drunk the pump water as those who had died, then Snow’scase would have fallen to the ground.


Whitehead had now set out to complete his appointed task properly, limiting him-self to Broad Street in particular. The denominator would be the number of peopleliving in the street, not those who had died of cholera. He soon discovered that thestreet had been decimated—of 896 residents, 90 had died. As Snow had found, a fairnumber of the living had moved away, and Whitehead patiently followed many ofthem to their new addresses, some far across town. He was able to accumulate de-tailed information on about 500 of them.

Whitehead also discovered that repeated questioning was often needed to arriveat the facts he sought. Among the anecdotes he eventually included in his report wasthis illustration:

I next went to the top of the house where lived a family consisting of father,mother, a little girl about ten years old, and an infant. They had moved out ofthe district September 4th, but had recently returned. I asked whether any ofthem had been attacked with Cholera or Diarrhœa? No. Were they in the habitof using the pump water? Yes. Who fetched it? The little girl. Was she not afraid(I then asked the child), going through the streets to see the shutters all up andso many hearses about? Didn’t go through the streets. Why not? Was ill in bedwith a cold. I asked the mother whether that was the case. She called to mindthat it was so. Who fetched the water when the child was unable to go for it?Why then they got it from the cistern.

CIC, 146–147

Whitehead concluded that his predecessors, both Snow and the General Board ofHealth inspectors, probably received many unreliable answers because of their timeconstraints.

Whitehead still had much to do to complete his study. So far, the numbers he hadassembled seemed more likely to confirm Snow’s theory than to disprove it. He nowunderstood the mystery that had perplexed him on 8 September. It was no wonderthat the old women of the parish were often spared from the cholera. They were in-firm, often lived alone, and most had no one to fetch water from the pump.

Tuesday, 27 March 1855

Whitehead had nearly completed his report. Far from rejecting Snow’s pump hypoth-esis, his data supported it in the most conclusive way possible. Of those who drank thepump water, 58 percent developed cholera while 42 percent escaped. Of those who didnot drink the water, only 7 percent were attacked while 93 percent were unaffected.Or, to put the matter a different way, among those who developed cholera, 80 percenthad drunk the water while 20 percent had not. Among those who were free of the dis-ease, only 17 percent had drunk the water while 83 percent had not.69

Broad Street 305

Whitehead had also narrowed down the window of infectivity of the pump wa-ter. The earliest cases he could attribute to the pump began on 31 August, and hecould not implicate the pump in any deaths after 6 September. Indeed, the pumpwater seemed to have become considerably less infectious just about the time thathe took some of it himself with his brandy on 3 September.

His work, it seemed, was finally done. It was, he explained, “for a purpose uncon-nected with this matter” that he was studying the returns of the Registrar General whenhis eye fell upon an entry from the week ending 3 September 1854: “At 40, Broad Street,2nd September, a daughter, aged five months, exhaustion, after an attack of Diarrhœafour days previous to death.” Whitehead continued: “I knew the case, and had recordedthe date of death, but somehow had neglected to inquire about the date of attack, hav-ing passed it by lightly, I suppose, because it was the case of an infant. Neither had it oc-curred to me that the child might have been ill all the week” (CIC, 159).

Whitehead immediately went to the address and spoke to Mrs. Lewis. As he heardher describe how she emptied the pails into the front area cesspool, he realized thathe finally had what he and the rest of the committee had been searching for—a caseof choleralike disease occurring close enough to the pump to point to a likely sourceof contamination and at precisely the time when the water must have acquired itsinfectious properties.70

Monday, 23 April 1855

With Whitehead’s discovery it seemed to the Cholera Inquiry Committee that theinvestigation of the pump well the previous November had been too superficial. Je-hoshaphat York, a surveyor, was also the secretary to the committee, so it seemednatural to delegate the task to him. York superintended the excavations of thecesspool, drains, and pump well at 40 Broad Street and wrote up a formal report forthe committee dated 1 May, with an accompanying plan (Fig. 11.4).

York found that the cesspool in the area was “intended for a trap, but miscon-structed” so as to create a dam across the drain, forcing sewage to back up ratherthan flow out. Both the cesspool and the drain into which it emptied were lined withdecaying brickwork, the bricks being so loose as to be easily lifted out of their bedswithout applying any force (CIC, 171).

A mere two feet and eight inches away from the house drain was the brick liningof the well under the Broad Street pump. The state of the surrounding soil and gravelmade it clear that there had been a steady percolation of waste from the cesspooland drain into the well (CIC, 173–74). York’s excavation showed the great impor-tance of Whitehead’s discovery of the case of the infant. Beginning with the cesspooland working toward the well, York found clear evidence of the route of contamina-tion. The Paving Commission, looking only within the well itself in November, hadthought that nothing was amiss.


Wednesday, 25 July 1855

The St. James Cholera Inquiry Committee had finally completed its general report,to which separate reports from Snow, Whitehead, and York were attached. The re-sult was a partial victory for Snow. The committee commended Snow’s and White-head’s investigations and concluded, “The Committee is unanimously of the opin-ion that the striking disproportionate mortality in the ‘Cholera area,’ as comparedwith the immediately surrounding districts, which . . . constitutes ‘the sudden, se-vere and concentrated outbreak,’ beginning on August 31st and lasting for the fewearly days of September, was in some manner attributable to the use of the impurewater of the well in Broad Street.”71 However, after reviewing Snow’s specific theoryof the nature of the causative agent in cholera and alternative theories of what pre-cise form the contamination of the pump water took, the committee expressed noopinion one way or the other.72

The committee had a problem with the case of baby girl Lewis at 40 Broad Street.On the one hand, Whitehead had received a detailed letter from Dr. William Rogersexplaining why he thought the case was not one of cholera and emphasizing that theinfant never had the typical rice-water stools, which Whitehead dutifully quoted infull in his own report (CIC, 163–65).73 He, for one, was loath to question the diag-nosis of the medical attendant who had been personally involved in the case,74 yetneither Whitehead nor his fellow committee members could avoid the conclusion

Broad Street 307

AB

C

A

B

Figure 11.4. J. York’s plan of the drain from 40 Broad Street and its position relative to the

well under the Broad Street pump. Left: plan view, from above. Right: side view. A: well un-

der pump; B: main drain from house; C: sewer (adapted from CIC, 170–71).

308

Choleradeaths

Diarrhoeadeaths

Thames River:Mean dailywater temperature

Average airtemperature

Mean dailyair temperature

Golden Sq.outbreak

Mean dailywind direction

Max airpressure

Dailyrainfall

Mean dailycloud

Relative amountsof fog or mist

July August10 2030

September October November30 10 20 30 1010 20 30 10 20

Figure 11.5. Cholera deaths per day in London, August–September 1854. The peak reflects a

doubling of deaths during the ten-day outbreak in Golden Square. Meteorological data was

entered on the graph for miasmatic analysis (adapted from GBH, Appendix to CSI, opposite

106).

that the days during which the diaper water was emptied into the cesspool coupledwith the results of York’s excavations provided a compelling reason for the contam-ination of the pump.

Despite Sir Benjamin Hall’s earlier refusal to release the inspection data, theSt. James Cholera Inquiry Committee eventually was given leave to use for itsown report a copy of the Golden Square map prepared by the General Board ofHealth’s Committee on Scientific Inquiries, which was published in the officialboard report on the cholera epidemic.75 When they reprinted the board’s map,

Broad Street 309

Figure 11.6. Number of deaths at 40 Broad Street: (top) Snow’s MCC2 map, detail—number

of bars identical in CIC map; (bottom) General Board of Health map, detail.

however, the committee made one modification. The “official” theory remainedfirmly miasmatic, and the board saw no reason to focus attention on the BroadStreet pump (Fig. 11.5). However, the St. James committee, at Whitehead’s in-stigation, drew a circle on its map with a radius of 210 yards, with the BroadStreet pump at the center (see Fig. 12.8). Whitehead had noted to the commit-tee that this circle included the “cholera area” in which almost all the deaths hadoccurred (CIC, 17–18).

Ironically, while the General Board of Health dismissed Snow’s and Whitehead’shypothesis completely, they concurred with one critical piece of confirmatory evi-dence. While Whitehead and the committee had hesitated to disagree with Dr. Rogersand declare that the little girl at 40 Broad Street had died of cholera, the governmentinspectors showed no such compunction. Their house-to-house survey listed fivecases of cholera at that address, including “policeman and child,” and their mapshowed five black bars adjacent to number 40. Snow’s map, completed before White-head’s discovery, showed only four bars (Fig. 11.6).76

Wednesday, 26 September 1855

The commissioners of paving of St. James’s again received a petition from the in-habitants of Broad Street and environs. There was much complaint in the neigh-borhood that the Broad Street pump remained without its handle. Back in June theparish medical officer, John G. French (a friend of Snow’s since 1849 and a memberof the Cholera Inquiry Committee), had warned of the increased threat of cholerawith the warm weather and had advised strongly that all the street pumps be closeddown.77 The pumps remained popular, however, compared to the filthy cisterns thatnormally held the piped water. Besides, it was now autumn, and the cholera seemedto be gone from London. On a 10–2 vote the commission decided to reopen theBroad Street pump.78

Notes

1. Dr. W. R. Rogers to Rev. H. Whitehead, 30 May 1855, reprinted in CIC, Report, 163–65.Hereafter, citations to CIC are given parenthetically when possible. Henry Whitehead referredto the family as “L.” in a table in his CIC report (161). The General Board of Health (here-after GBH) house-by-house report did not use any names or initials, and the street and postoffice directories list only principal businesses at each address (see Figure 11.3). The 1851 Cen-sus enumerator, however, listed seven households at 40 Broad Street, only one beginning with“L”: Thomas Lewis, head, age 46, police constable; Sarah Lewis, wife, age 40; and two chil-dren, Thomas (age 13), and Anne (age 8). See UK HO 107/1485/232. Because the head’s vo-cation matches what was recorded by the GBH, we are confident that Whitehead’s “L” werethe Lewis family.


2. UK GBH, Report of CSI, appendix, 345.3. On the history of Broad Street and its buildings, see Sheppard, St. James Westminster, 2:

221–23. The Survey of London is silent on the early history of the house at 40 Broad Street.The row of houses directly across Broad Street (north side) had been built originally in1722–23.

4. The data on the house at 40 Broad Street and its inhabitants were later gathered duringa house-to-house survey undertaken by the GBH; see UK GBH, Report of CSI, appendix, 345,reprinted in Paneth et al., “A rivalry of foulness,” 1551.

5. Years later a commentator recalled the local custom of keeping cows on the top story ofthese houses. The animals were hoisted up by windlass and remained shut up in the attics solong as they gave milk; Rawnsley, Henry Whitehead, 34. On the other hand, the inspectors forthe GBH were most industrious in rooting out any possible source of bad smells in the re-gion during their house-to-house visitations from 11 to 25 September. They reported no cowsin any attics, although they did describe the noxious cow yards. According to the report ofthe medical officer of health, Edwin Lankester, a decade later there were eight cow houses inthe parish with a total of 205 cows. “The nuisance of the cow house in Marshall Street is no-torious throughout the whole parish. . . . The herding together of 25 or 30 cows in a roomof a dwelling house, in a row of other houses. . . . These cow houses, though probably notmore injurious to health than slaughter houses, are very great nuisances to the neighbour-hood in which they are situated”; Saint James, Annual Reports, 1864–65, 24–25.

6. Snow, “Further remarks on the mode of communication of cholera” (1855).7. On the “Hampstead widow,” see MCC2, 44–45, and Whitehead’s report, CIC, 139–40.

The Eley’s percussion cap factory was apparently quite a successful concern. Years later thename was well known—Sherlock Holmes told Dr. Watson in “The Adventure of the Speck-led Band,” “I should be very much obliged if you would slip your revolver into your pocket.An Eley’s No. 2 is an excellent argument with gentlemen who can twist steel pokers into knots”;Doyle, Adventures of Sherlock Holmes, 184. Doyle confused the name “Eley,” for the cartridge,with “Webley,” for the revolver. The firm survives today, although relocated to Birmingham.

8. Rawnsley, Henry Whitehead, 29, 32–33.9. These atmospheric details were carefully noted later by the official inspectors for the UK

GBH, Report of CSI, appendix, 139–40.10. Whitehead, “Broad Street pump,” 113.11. Editorial, “The life and death question. The outbreak in Berwick-Street—A word or two

on protective measures,” Builder 12 (9 September 1854): 473.12. Whitehead, “Broad Street pump,” 113.13. Another local clergyman, Harry Jones, later recalled: “Whitehead fought like a hero night

and day, with hand and lips and brain, helping to strengthen the living, heal the sick, andcomfort the dying. . . . I can’t say I saw much of Whitehead then, for we both had our handsfull; but one thought of the man in the thickest of the fight . . .”; Rawnsley, Henry White-head, 41–42.

14. Mrs. Gaskell to Emily Winkworth, recounting the story Mrs. Gaskell had heard fromMiss Nightingale, in Woodham-Smith, Florence Nightingale, 79–80. The CIC took issue withaccounts such as Nightingale’s: “It is remarked by Mr. Sibley, the registrar of the MiddlesexHospital, that a large number of the persons brought there for treatment presented a very un-cleanly appearance. . . . This may doubtless be explained, partly by the circumstances thatthe patients so admitted were probably the most destitute of those who were attacked, andpartly by the fact of their being suddenly seized by the disorder whilst engaged in the usualoccupations of their trade”; CIC, 31–32. Both Snow and the CIC documented that cholerastruck all occupations and social classes in the district with equal severity.

Broad Street 311

15. Snow, “Cholera near Golden Square” (1854): 322. In addition to this letter to the edi-tor, he wrote two more accounts of his Broad Street investigations: “Dr. Snow’s report” to theCIC (1854) and a segment of MCC2, 38–56. A detailed word analysis shows that MCC2 wassubmitted to the publisher before Snow wrote his report for the CIC. Copies of MCC2 wereavailable in late December 1854 despite a date of publication of 1855; see G[eorge] Budd toSnow, 3 January 1855, Clover/Snow Collection, VIII.4.i, in which Budd acknowledges receiptof a copy. The three accounts agree on all major points and help to indicate the order in whichSnow obtained new information as his investigations proceeded. When Snow revised mate-rial, he tended to add more text instead of altering the existing text. For example, in MCC2and CIC he repeats almost verbatim from the MTG article the account of the first eighty-three deaths he investigated and then adds later that the true number was 197, not eighty-three, as he learned from the later returns (see below).

16. UK GBH, Cholera of 1848 & 1849, 62.17. UK GBH, Cholera of 1848 & 1849, 61–62. We are indebted to Professor Pamela Gilbert

for calling our attention to this incident. It is much less likely that Snow had seen a letter sentto the GBH to report a suspicious occurrence: “A few days ago some friends of mine residingin Regent St. (No. 181) wishing to take some brandy & water, sent the servant to a neigh-bouring pump in Warwick St. hoping to obtain water fresher and purer than that which thehouse furnishes, but, to their astonishment, when they came to mix it with the brandy it in-stantly turned black: a second experiment being made with the same result, it was [taken] toa chemist to be examined & his assertion was that the Sewer had entered the well and dete-riorated the water which, in appearance, is perfectly lucid”; John Clarke Rowlatt (?) to GBH,10 September 1849, “Metropolitan nuisances,” 1849, MH 13, 261, PRO, Kew. Rowlatt, a cler-gyman, resided at 32 Lower Belgrave Street, from which the letter was sent.

18. Whitehead, “Broad Street pump,” 113.19. Rawnsley, Henry Whitehead, 203–04.20. Snow, “Cholera near Golden Square” (1854), 322.21. Hassall eventually was called upon by the GBH to conduct microscopic studies of this

cholera outbreak.22. Whitehead, “Broad Street pump,” 113.23. “The Board of Health and the cholera,” Times (6 September 1854). Sir Benjamin Hall

later became commissioner of works and in that capacity in 1859 superintended the installa-tion of the great bell in the tower of the Houses of Parliament. Hence the bell, and eventu-ally the clock, were called Big Ben.

24. The end of July and the beginning of August was a particularly inauspicious time forParliament to be tinkering with the GBH, as the cholera epidemic was just then gaining mo-mentum. During July cholera deaths in London had increased from one to 133 per week. Theabolition and recreation of the GBH in July–August 1854 is recounted in more detail in Panethet al., “A rivalry of foulness.”

25. Snow, “Cholera near Golden Square” (1854): 322. Nearly identical passages appeared inSnow’s report, CIC, 101–02, and MCC2, 39–40. Snow’s circumstantial account of his rea-soning and investigation up to this point makes no mention of any map or graphical repre-sentation of the data. For the role that mapping did (and did not) play in Snow’s and otherinvestigations, see Chapter 12 and Brody et al., “Map-making and myth-making in BroadStreet.”

26. “The public health,” Times (6 September 1854). The public impact of such a news an-nouncement can scarcely be appreciated by readers today. St. James and the neighboring parishto the east, St. Giles, had long been paired in the popular mind as the extremes of what wasgood and bad about London. While St. James had tenements, it also had St. James’s Palace,


St. James’s Park, and Pall Mall. St. Giles, by contrast, was a particular haunt of poor Irish im-migrants and had been the site of “The Rookery,” a particularly notorious slum and criminalden. For cholera to afflict St. James, while St. Giles was mostly spared was therefore to turnthe natural order of the world on its head, much as if Dr. Jekyll had been caught stealing candyfrom tots while Mr. Hyde was canvassing for donations for the church bazaar; Gilbert,“‘Scarcely to be described.’” Gilbert goes on to speculate,“The outbreak in St. James’s [by dash-ing the existing folk theories of cholera causation] probably did far more to advance Snow’scredibility with the public than his meticulous research did” (161).

27. Whitehead, “The experience of a London curate,” 203. This anecdote was in his farewelladdress on leaving London in 1874.

28. Whitehead, “Remarks on the outbreak,” 102.29. UK GBH, Report of CSI, appendix, 161.30. Rawnsley, Henry Whitehead, 203.31. We know little about what actually transpired at the meeting. On 14 August 1854 when,

acting in response to “an apprehended visitation of Asiatic Cholera,” the Governors and Di-rectors of the Poor again formed themselves into a “general Sanitary Committee,” they agreedto keep a separate minute book, which is no longer extant; St. James, Minutes of the Gover-nors and Directors of the Poor (D2151), 455. They had formed a similar Sanitary Committeein April 1853 and submitted a report on 3 October 1853; Ibid., 151. Snow’s account of whathappened is terse: “I had an interview with the Board of Guardians of St. James’s parish, onthe evening of the 7th inst., and represented the above circumstances [i.e., the results of hisinvestigation] to them. In consequence of what I said, the handle of the pump was removedon the following day”; “Cholera at Golden Square” (1854): 322. Identical language appearedin MCC2, 40, and “Dr. Snow’s report,” CIC, 102, except that “the 7th inst.” was changed to“Thursday, 7th September.” Snow’s confusion of Guardians for Governors may reflect unfa-miliarity with Poor Law regulations in St. James, compared to most parts of the metropolisthat were organized into unions. The vestry did not meet on 7 September; St. James, VestryMinute Book (D1777), and Rough Minutes of the Vestry (D1810).

32. We have been unable to find any contemporary accounts.33. UK GBH, Report of CSI, appendix, 151.34. UK GBH, Report of CSI, appendix, 138.35. “A Resident of Broad-street” (letter to the editor), Times (8 September 1854). The GBH

inspectors scouted the plague pit theory and suspected that it had “been prominently put forthby interested persons, who were desirous of diverting the current of popular indignation fromtheir own particular nuisances.” The owner of the “monster slaughter-house in MarshallStreet,” they suggested, might have been one such interested party; see UK GBH, Report ofCSI, appendix, 151.

36. Whitehead, “Broad Street pump,” 120.37. Whitehead specifically called attention to the efficacy of removing the pump handle in

possibly preventing a new outbreak of cholera, even if it were true, as he and Snow later wrote,that the original outbreak was already on the wane before 8 September. Whitehead suggestedthat the discharges from the infant’s father, thrown into the same cesspool, would surely havecontaminated the well again on the days following 8 September. Henry Whitehead, “Remarkson the outbreak,” 99–104.

38. UK GBH, Report of CSI, appendix, 142, 145, 150–51, 336.39. For example, “I was accidentally accosted by a friend in passing along the highway. . . .

After a few minutes I was surprised and somewhat alarmed to find a feeling of great sicknessand faintness suddenly coming over me. . . . [M]y friend called my attention to the fact thatwe were in close proximity to one of [the] untrapped gully-holes, from which, now that my

Broad Street 313

attention was directed to the circumstances, I soon found that a most deadly effluvium wasarising. I immediately moved from the vicinity of the grating and felt almost instantaneousrelief”; Times (15 September 1854).

40. When Whitehead interviewed Mrs. Lewis in the spring of 1855, she was living in theback parlor of 40 Broad Street; “Rev. Whitehead’s report,” CIC, 159. During the 1854 epi-demic, however, her ill husband and infant had lain in the front kitchen, which was why itwas easier for her to pour the dirty water from rinsing bedding and diapers into the cesspoolin the front area rather than carry it to the privy at the back of the house; Whitehead, “Re-marks on the Outbreak,” 104. The GBH only listed the two cholera cases as having occurredon the ground floor of 40 Broad Street; UK GBH, Report of CSI, appendix, 345.

41. “The cholera in Golden-square,” Times (15 September 1854).42. Snow, “Cholera near Golden Square”(1854). This letter appeared on 23 September.43. It is difficult to reconcile Snow’s account of the flight of the population with White-

head’s assertion in the summer of 1854 that there was a notable calm and lack of panic. LaterWhitehead admitted that a flight had occurred, and he had an advantage over other investi-gators because he knew the families better and so could more easily track them down in theirnew locations; “Broad Street pump,” 116. Perhaps Whitehead, in his earlier pamphlet, exag-gerated the calm so as to defend what he took to be the reputation of his community (TheCholera in Berwick Street, 14–17), or perhaps the population fled calmly.

44. “Dr. Snow’s report,” CIC, 103–04. The popularity of the pump water was partly due tothe fact that the chemical by-products of organic impurity, carbonic acid and nitrates, gavethe water a sparkling quality, as was noted by many observers; see CIC, 72–74.

45. Snow refers to “Dr. Fraser, of Oakley Square” in his writings, but he does not mentionFraser’s official connection with the GBH; see CIC, 106; MCC2, 44.

46. “Dr. Snow’s report,” CIC, 104. Earlier Snow had written that 100 would have died, butthis would have produced a mortality rate twice that of the one in ten that Whitehead laterfound in Broad Street; MCC2, 42. The corrected figure is further evidence that Snow’s CICreport was completed after MCC2.

47. Whitehead’s point was not whether people had fled the neighborhood, but that sickpeople were cared for compassionately by their relatives and neighbors rather than being ruth-lessly abandoned out of fear of contracting the disease.

48. Whitehead, The Cholera in Berwick Street, 13. Whitehead reprinted this table in his re-port to the CIC, 155. Fraser, Hughes, and Ludlow of the GBH found it useful in their reportto quote extensively from Whitehead’s pamphlet (by “the exemplary and indefatigable curateof St. Lukes’”), especially in regard to the floors of the houses on which the most deaths oc-curred, the ages and conditions of the victims, and the small area within which the choleradeaths were concentrated. UK GBH, Report of CSI, appendix, 158–60.

49. Whitehead, “Broad Street pump,” 116. The notion of conducting an investigation of hisown to disprove Snow’s theory of the pump seems to have occurred to Whitehead after hehad finished work on The Cholera in Berwick Street, which makes no mention of Snow’s the-ory or his own doubts about it.

50. UK GBH, Report of CSI, appendix, 139, 153–55, 351.51. Cooper, “Report.” Whether Snow attended this meeting is not recorded. Between 22

September and 2 October his casebooks show no anesthesia work; CB, 344. During this pe-riod he was undertaking additional investigations in Golden Square.

52. “Since the outbreak, six men have been employed in these lines of sewers getting up in-formation on this subject, all of whom, I am glad to state, are quite healthy, and entirely freefrom disease”; Cooper, “Report.” Consequently, he suggested that sewer gases per se were un-likely to spread cholera.


53. Times (27 September 1854). While the GBH inspectors agreed with Cooper about theplague pit, they disagreed on the role of the gully holes. Their report eventually blamed theoutbreak mainly on the “multitude of untrapped and imperfectly trapped gullies and venti-lating shafts constantly emitting an immense amount of noxious, health-destroying, life-destroying exhalations” made worse by a stagnant atmosphere; UK GBH, Report of CSI, ap-pendix, 161. Dr. Fraser and his team claimed that many of the houses closest to the gully holeshad been most severely hit by cholera (143), whereas the corner houses, being in the best ven-tilated positions, often escaped (161). Neither Cooper nor the board inspectors provided anystatistical analysis to back up their respective (and contradictory) claims.

54. The point is worth noting because of some of the later inaccurate and mythical accountsof Snow and the pump. Many of today’s authors speak as if merely glancing at the map, withits distribution of bars (or dots, as most modern versions have it), would be sufficient to con-vince the most skeptical observer that the pump water was the source of the outbreak. Coopernoted that of all the local streets, Broad Street had been most heavily visited by the cholera,but he focused only on the sewers in his inquiry as to why this was so. Broad Street was servedby two nonconnecting sewers, one of recent vintage and one rather old, but the numbers ofdeaths appeared equally divided between the portions of the street served by the two differ-ent sewers.

55. For most of October Snow attended one or two cases a day, with a high of five cases on28 October; CB, 348.

56. The late October date for these inquiries is given in “Dr. Snow’s report,” CIC, 114.57. Chave, “Henry Whitehead,” 94.58. Chave, “Henry Whitehead,” 94. Chave states that the original committee had nine mem-

bers, but CIC, iii, lists eight.59. CIC, v.60. Chave notes that this was probably the occasion for the first meeting between Snow and

Whitehead; “Henry Whitehead,” 95. We do not know why Edwin Lankester, who had servedas a fellow officer with Snow of the Westminster Medical Society and was a vestryman of St.James’s at the time when Snow made his appeal regarding the pump, delayed so long in ask-ing Snow to join the committee. Perhaps ill will lingered over Snow’s association with A. B.Garrod, who had been selected over Lankester for a medical school professorship in 1846; seeEnglish, Victorian Values, 44–45. On the other hand, in 1849 Snow had credited Lankesterwith an idea regarding the transmission of cholera in bodies of water; PMCC, 928.

61. “Epidemiological Society,” Lancet 2 (1854): 531.62. The “Hampstead widow” case was the one that even his severest critics later found most

difficult of all his facts to dismiss. For example, Edmund Parkes, in a review of MCC2, re-jected Snow’s views on cholera and dismissed the map as being precisely what one would ex-pect to see in the case of a concentrated, noxious miasma causing an epidemic of disease.There were so many pumps in that neighborhood, he noted, that no matter where the epi-demic had its center, there was sure to be one of them close by, yet he admitted that the caseof the Hampstead widow was, “if there is not some fallacy, . . . certainly unanswerable”;Parkes,“Review: Mode of Communication of Cholera by John Snow,” British and Foreign Medico-Chirurgical Review 15 (1855): 449–63; quotation from 456.

63. “Dr. Snow’s report,” CIC, 97–120. He revised his report to the CIC as late as 14 June1855, but he did so in a footnote that was explicitly dated and kept separate from the mainbody of text (CIC, 116). The lack of firm data on the contamination of the pump did notstop Snow from speculating: “The reason why the water of this pump produced the great out-break is, I feel confident, that the evacuations of one or more Cholera patients found theirway, by some means, into the well. There were fatal cases of Cholera, a few days before the

Broad Street 315

great outbreak, not far from the well, and there may have been other cases, not fatal, whichare not recorded”; “Dr. Snow’s report,” CIC, 119. In MCC2 he noted that as the well waterpassed with almost all observers as being perfectly pure, “the quantity of morbid matter whichis sufficient to produce cholera is inconceivably small” (54).

64. Chave, “Henry Whitehead,” 94.65. Ibid.66. Pacini, “Osservazioni microscopiche,” 1. This article remained unknown and unre-

marked upon by the vast majority of British physicians. See also Bentivoglio and P. Pacini,“Filippo Pacini.” By the time Robert Koch took credit for discovering the bacillus Vibriocholerae in 1883, Pacini’s work had been forgotten, and it was many decades before Pacini’spriority in the discovery was officially recognized.

67. Whitehead, “Broad Street pump,” 116.68. J. Netten Radcliffe, quoted in Rawnsley, Henry Whitehead, 40.69. Whitehead expressed his numbers as more difficult to interpret ratios rather than per-

centages; “Rev. Whitehead’s report,” CIC, 132–33.70. Whitehead dated this portion of his report “April 3rd” and stated that the event here

described occurred “one day last week”; CIC, 159. We have arbitrarily chosen the date exactlyone week before April 3.

71. “General report,” CIC, 83 (italics in original).72. “General report,” CIC, 84–91. Lankester seems to have been closer to Budd’s position

on cholera than to Snow’s, and while acknowledging the role played by contaminated water,was unwilling to deny a possible role for atmospheric spread; English, Victorian Values, 104.For the view that the CIC report “finally . . . substantiated” Snow’s theory, see S. Snow, JS-EMP, 244.

73. Dr. Rogers even showed up personally at the meeting of the Epidemiological Society on4 July 1855, when Snow was giving a paper on the Broad Street outbreak that included men-tion of Whitehead’s identification of the index case. Rogers objected that because Snow’s the-ory apparently hinged on cholera evacuations getting into the well and because his own casewas being cited as the “cholera” case, he remained unconvinced by Snow’s presentation as heknew that his case was not one of cholera at all: “Epidemiological Society,” Lancet 2 (1855):11–12.

74. Years later Whitehead expressed himself somewhat more forcefully on that issue: If theinfant’s discharges, thrown into the cesspool that communicated with the pump well duringthose exact days, did not cause the outbreak, then it was “indeed a very remarkable coinci-dence”; Whitehead, “Broad Street pump,” 122.

75. UK GBH, Report of CSI, frontispiece. The GBH map (according to CIC) was based tosome extent on Cooper’s earlier map and was similarly sophisticated from a cartographicstandpoint. Thus, the CIC Report contained two maps—the GBH map (with the circle added)accompanying the general report and Snow’s revised map accompanying his own report.

76. Confirmation of Whitehead’s theory of how the pump came to be contaminated be-came generally known in the summer of 1855, when the GBH Report was published. The ac-tual raw data from which the number of bars at each house were derived were gathered byDr. Fraser’s team in September 1854, which means that the GBH inspectors (who knew of noconnection between the drains at no. 40 and the well) believed that infant girl L[ewis] haddied of cholera. They presumably arrived at this conclusion from the mother’s testimony be-cause there is no record that they consulted the infant’s physician.

77. St. James, Board of Commissioners of Paving, Rough Minutes (D1941), 20 June 1855.78. St. James, Board of Commissioners of Paving, Rough Minutes (D1941), 26 September

1855. A sanitarian minded local resident sarcastically described the scene when the pump was


reopened: “High festival was held that day in Broad-street. . . . Full many a copious stream,arrears of libation to offended Cloacina, did the pump send forth. Loud and long the exult-ing shouts of children working the handle in wantonness of exuberant joy . . .”; Mens Sanain Corpore Sano [pseud.], “What has been done in St. James’s, Westminster?” Builder (27 Oc-tober 1855): 510. By then repairs at 40 Broad Street were finished: “All [the] old drainage hasbeen removed; the cesspool destroyed, and new tubular pipe drains with cemented joints, anda syphon trapped closet have been substituted”; “Mr. York’s report,” CIC, 172–73. However,the sievelike brickwork of the nearby pump well remained unchanged. The Broad Street pumpwas not permanently closed until the cholera epidemic of 1866, when Edwin Lankester wasmedical officer of health for the parish; see Chave, “John Snow, the Broad Street Pump, andafter,” 349. In the 1864–1865 report he had noted, “The wells in this Parish are gradually be-ing abandoned, as the longer they stand the more liable they are to impurities from the leak-age of drains through rat-holes and the percolation of street gutters and cesspools”; SaintJames, Annual Reports, 1864–65, 52. With respect to Thames water, he thought it had im-proved since the last epidemic, “and a supply is now afforded to London free from the inju-rious influence of organic contamination. It is to be regretted that this supply is still inter-mittent, and is stored in leaden cisterns and wooden butts, which when neglected to becleansed, render the water impure”; Ibid., 51.

Broad Street 317

318

ON THE EVENING OF 3 June 1851 Snow delivered the secondpart of a paper on the propagation of cholera at the monthly meet-

ing of the London Epidemiological Society. The society had again rented the libraryof the Royal Medical and Chirurgical Society in Berners Street.

Snow began the paper by offering a general principle of “epidemic diseases, thewhole of which I look upon as communicable from one patient to another, this com-munication being probably the real feature of distinction between epidemic and otherdiseases,” and he reviewed several local outbreaks that conformed to this principle.1

He proposed to show that “cholera was often communicated through the water, ona more extensive scale, by means of sewers which empty themselves into variousrivers, from which the population of many towns derive their supply of water” (610).A map extracted from the second Report on the Health of Towns, suspended in theroom, indicated which water companies supplied particular districts in London.Snow then pointed to another map (Fig. 12.1), produced by Mr. Richard Graingerfrom the Board of Health, that depicted the “relative prevalence of the late [1849]epidemic in different parts of London” in varying shades of blue.2 A comparison ofthe two maps showed that “cholera was most prevalent . . . in those districts sup-plied with water vitiated by the contents of sewers and cesspools” (610).

This presentation is the first recorded instance of Snow using a disease map. Inthe past he had frequently used data tables when presenting papers at medical

Chapter 12

Snow and the Mappingof Cholera Epidemics

319

Figure 12.1. Mr. Grainger’s “Cholera Map of the Metropolis. 1849. Exhibited in the Registra-

tion Districts” (detail). There were four districts south of the River Thames that might have

interested Snow—#25, St. Saviour, Southwark; #26, St. Olave, Southwark; #27, Bermondsey;

#28, St. George, Southwark; and #29, Newington. The dotted lines indicated where cross-

sections were taken for showing elevation above the high-water mark on the River Thames.

Places with “bad ventilation,” “no drainage,” “open sewer,” and “overcrowding” were also

marked on the map (GBH, Report on Cholera, 1848–49, appendix B, opposite 200).

society meetings and in his published writings.3 He had limited his other graphicaldevices to demonstrations and drawings of apparatus. Why, then, did he make useof two maps in this presentation? Perhaps it was because they were readily available,cost him nothing to display, and, in the case of the Board of Health map, carried atouch of irony by employing a device prepared by sanitarian opponents to supporthis contrary explanation of what had caused the 1848–1849 epidemic.

Although many epidemiologists and public health figures today consider him apioneer in disease mapping, Snow published only two disease maps, of which thespot map in MCC2 of the Golden Square outbreak in 1854 is the better known.4 Itwas an afterthought to the investigative process. That is, he had not used this mapinductively, collecting data, putting a mark by the address of each case, and eventu-ally developing a theory to explain the cluster of cases around the Broad Street pump,nor had he used the map deductively, hypothesizing at the outset that the cause wascontamination of the Broad Street pump, then plotting cases to confirm his hy-pothesis or falsify an alternative. Instead, the spot map in MCC2 is an example of il-lustrative mapping, a visual enhancement of the descriptive narrative of his investi-gation in Golden Square.

Snow wrote the passage on his Golden Square investigation for a revised editionof MCC a few weeks after the outbreak had ended, and textual analysis suggests thathe had decided from the outset to include a map showing most of the cholera cases.5

At a meeting of the Epidemiological Society on 4 December 1854, he displayed anadvance copy of this spot map that would be published in MCC2 in a few weekstime.6 Something must have happened that evening to make Snow believe the GoldenSquare spot map he had constructed to illustrate his theory would not have the in-tended effect. Until then, spot maps were generally the preserve of anticontagionists,and it is possible that a member of the Epidemiological Society interpreted Snow’smap as showing local miasmatic causes. It was too late for Snow to remove the spotmap from MCC2, but there was time to alter it for a report on the outbreak he waspreparing for the parish of St. James. In a matter of ten days he had collected newdata and had expanded an aside in MCC2—“It may also be noticed that the deathsare most numerous near to the pump where the water could be more readily ob-tained” (47)—into an analytical exercise in disease mapping. Snow methodically plot-ted equidistant walking points between pumps for every street on his spot map inorder to refute counterclaims that the geographical clustering of cases supported mi-asmatic explanations of the outbreak rather than his hypothesis of a water-bornesource (CIC, 109). Nonetheless, the Golden Square map most frequently reproducedor redrawn to the present day is the illustrative one in MCC2, not the CIC map thatreflects Snow’s deductive reasoning and innovative mapping.

Besides Snow, other contemporary observers constructed three spot maps of thehorrific cholera outbreak in Golden Square. One involved deductive reasoning, likeSnow’s CIC map, although this author was testing a miasmatic hypothesis. Two oth-ers were illustrative accompaniments to committee reports on the outbreak.7


Origins of Cholera Mapping

Humoralism had stressed the role of “airs, waters, and places”—the title of an oftenreferenced Hippocratic essay—in causing epidemics, and long after the heyday ofhumoral theory medical authorities continued to describe the topography and cli-mate where epidemic diseases prevailed. They included no disease maps, however,as distinct from purely topographical maps, until the latter part of the eighteenthcentury.8

By the mid-nineteenth century, however, the German geographer Augustus Pe-termann (1822–1878) believed medical cartography had developed to the point thatit could play a significant role in elucidating the “general laws” underlying the spreadof cholera.9 He lived in London between 1847 and 1852, during which time he pro-duced a map of the 1831–1833 cholera epidemic in the British Isles. In an accom-panying text he trumpeted the importance of inductive and illustrative disease map-ping. One prepares a map “to obtain a view of [that is, illustrate] the Geographicalextent of the ravages of this disease, and to discover [that is, induce] the local con-ditions that might influence its progress and its degree of fatality.” Petermann ar-gued that,

For such a purpose, Geographical delineation is of the utmost value, and evenindispensable; for while the symbols of the masses of statistical data in figures,however clearly they might be arranged in the Systematic Tables, present buta uniform appearance, the same data embodied in a Map, will convey at once,the relative bearing and proportion of the single data together with their po-sition, extent, and distance, and thus, a Map will make visible to the eye thedevelopment and nature of any phenomenon in regard to its geographic distribution.

In other words, Petermann considered disease maps both an essential part of the dis-covery process for the medical topographer and an illustrative enhancement of dataand description for the reader.10

The first recorded instance of a spot, or dot, map being used to record the geo-graphical distribution of individual cases of a disease was in 1798. Dr. Valentine Sea-man (1770–1817), a surgeon at the New York Hospital, published a detailed paperabout the 1796 yellow fever outbreak in New York City. His article was illustrated bytwo carefully drawn disease spot maps.11 Seaman mapped two areas along the har-borfront, New Slip and Burling Slip, with a symbol to indicate the residence of eachperson who had suffered from yellow fever. Based on these maps he inferred that thedisease was caused by putrefying substances in the nearby wetlands and stagnant wa-ter, factors he described in the article but did not indicate on the maps.

While yellow fever remained a feared disease in the New World, it was soon overshadowed in Europe by the specter of epidemic cholera. To a large extent the

Snow and the Mapping of Cholera Epidemics 321

history of disease cartography during the years 1820 to 1850 is the history of choleramaps. These fell into two general categories, progress maps and spot maps. Progressmaps depicted the temporal spread of cholera across large areas such as nations orcontinents. A solid circle or similar symbol on a progress map represented a city ortown, and the date adjacent to the dot indicated when the first cases of cholera hadappeared in that place. Some progress maps used arrows or lines to show the se-quence of towns in which cholera broke out. One example is the “Chart Shewing theProgress of the Spasmodic Cholera” that accompanied a report compiled by A.Brigham in 1832 (Fig. 12.2).12 Along with dated points, the solid reddish “flow” linesillustrate the diffusion of cholera from southeast Asia, through the Middle East andEurope, to England, and across the Atlantic Ocean to the eastern seaboard of Canadaand the United States.

The contagion–anticontagion debate was in full swing at the time of the 1831–1832epidemic. Both camps often agreed that progress maps showed that cholera first ap-peared, for example, in town A in July, town B in August, and so on, but contagionistsconsidered that such progress of cholera across a country was evidence of person-to-person contact along established trade and travel routes, whereas anticontagion-ists interpreted the same data as disease being spread by the prevailing winds. Thus,


Figure 12.2. A portion of the “Chart Shewing the Progress of the Spasmodic Cholera.” Solid

reddish lines (shaded in this figure) indicated the movement of cholera from southeast Asia

to western Europe and England and then on to the eastern seaboard of Canada and the United

States (Brigham, Treatise on Epidemic Cholera, frontispiece).

progress maps were used by contagionists and anticontagionists alike to illustratetheir own preconceived theories. James Jackson and his committee at the Massa-chusetts Medical Society prepared a progress map of the spread of “cholera morbus”from Hindustan to England based on the published literature, dispassionately listedthe arguments for and against contagion and anticontagion, and concluded that in-sufficient evidence existed to come down definitely on one side or the other.13

The other category of cholera map was the spot map. Such a map typically cov-ered a much smaller geographical area than the progress map, such as a village, acity, or a part thereof, and represented each case of cholera with a symbol such as adot. In the accompanying texts medical cartographers generally associated clustersof dots with topographical or other physical features, including housing, regardlessof whether such features were noted on the maps. Many early spot maps followedSeaman’s example, showing cases of cholera but not the purported causal factor, butdots without dates, whether of morbidity or mortality, conveyed an impression ofsimultaneity that favored anticontagious causal explanations, such as the rapid spreadof a noxious miasma from a nearby marsh or effluvial emanations from an over-crowded and filthy district. Contagionists could have added specific dates to spotmaps showing how an epidemic began in a particular location and spread in grad-ually widening ripples, but we have found none. Like Seaman, some cartographersused spot maps inductively, formulating hypotheses of probable causal factors whileactually plotting the cases. For others the spot map was purely illustrative, playingno role in the investigative process.

For example, Dr. Thomas Shapter (1808–1902) constructed a spot map purely toillustrate his narration of events during the cholera epidemic in Exeter during1832–1834 (Fig. 12.3).14 In order to depict the geographical distribution of individ-ual cholera deaths for each year, he employed a different red symbol of uniform size:a thick line, or bar, for 1832, a cross for 1833, and a solid dot for 1834. He publishedhis book in the 1840s, after major renovation and sanitary projects had altered thetown significantly from what it had been during the epidemic. Shapter did not be-lieve that cholera was contagious and referred to his map to support his view thatthe disproportionate number of deaths that occurred in the low-lying southeasternquarter of the old walled city were primarily caused by stagnant river miasmas car-rying “zymotic” particles.15 As an additional causal factor, Shapter pointed to “a fewisolated spots in which a remarkable and undue amount of mortality took place, . . . the very places in which . . . a large amount of mortality had been an-ticipated, and of whose bad drainage and unwholesome state, complaints had beenmade” (224). The effects of low elevation and bad drainage could be mitigated byother factors. For example, St. Edmund’s parish was “situated at the bottom of thehill,” on low-lying ground, “densely people,” inhabited “chiefly by the poor,” and had“no particular sanitary arrangements”(224). But the death rate was only one-thirdthat of the worst-affected parish because the area’s “sole peculiarity” was “being freelyintersected by running streams of water”(224).16 That is, Shapter was a sanitarian


who believed his narrative vindicated the aggressive approach of the local Board ofHealth. In the words of one reviewer writing in 1849, “When cholera visited Exeterin 1832, it found a city close, confined, badly drained, and still worse supplied withwater. . . . These things are different now, and so likewise . . . is the progress ofthe present epidemic.”17

Later Developments in Spot Mapping Techniques

Cholera maps appeared during the first three major epidemics in Europe (Table12.1). The later progress maps were not substantially different from the earliest. Spotmappers, by contrast, evolved new cartographic techniques and expanded the use ofdisease maps in investigating the causes of cholera outbreaks. A significant changein spot mapping came with the realization that the mere display of dots within a


Figure 12.3. Cholera mortality in Exeter between 1832 and 1834 (Shapter, Cholera in Exeter

in 1832, frontispiece).

Table 12.1. Examples of cholera maps published between 1832 and 1855. These examples are listed according to how they were used (denoted by a “✓”): (1) illustratively (without any analytic purpose), (2) inductively (seeking causative associations), and (3) deductively

(whereby a hypothesis or theory was tested).

Type of map analysis:

Date Date Date ofAuthor(s) published constructed Location of epidemic epidemic Illustrative Inductive Deductive

Spot maps

Gaulter 1833 1833? Manchester, England 1833 ✓ — —Shapter 1849 ? Exeter, England 1832–34 ✓ — —Hatton 1854 1854? Chorlton-Upon-Medlock, England 1853–54 — ✓ —Shattuck 1850 1850? Boston, Mass. 1849 ✓ — —Cooper 1854 1854 Golden Square, London 1854 — — ✓

Snow/MCC2 1855 1854 Golden Square, London 1854 ✓ — —Snow/CIC 1855 1854 Golden Square, London 1854 — — ✓

Board of Health 1855 1855? Golden Square, London 1854 ✓ — —St. James CIC 1855 1855 Golden Square, London 1854 ✓ — —von Pettenkofer — 1854 Kingdom of Bavaria 1854 ✓ — —von Pettenkofer 1857 1854 Aubing, Germany 1854 — ✓ —

Shaded and cross-hatched maps

Baker 1833 1833? Leeds, England 1832 ✓ — —Rothenburg 1836 ? Hamburg, Germany 1832 ✓ — —Chadwick 1842 ? Leeds, England 1831–32 ✓ — —Gavin 1848 1848? Bethnal Green, London 1848 ✓ — —Sutherland 1850 1849 Glasgow, Scotland 1848–49 ✓ — —Petermann 1852 1848 England 1848 — ✓ —Farr 1852 ? England 1849 ✓ — —Administration Générale 1855 ? Paris, France 1852–54 ✓ — —

(continued)

Table 12.1. Examples of cholera maps published between 1832 and 1855. These examples are listed according to how they were used (denoted by a “✓”): (1) illustratively (without any analytic purpose), (2) inductively (seeking causative associations), and (3) deductively (whereby a

hypothesis or theory was tested). (Continued)

Type of map analysis:

Date Date Date ofAuthor(s) published constructed Location of epidemic epidemic Illustrative Inductive Deductive

Progress maps

Brigham 1832 1832? India–North America 1817–32 ✓ — —Jackson, et al. 1832 1832? India–England 1831–32 ✓ — —General Board of Health 1850 ? China, England, North America 1817–48 ✓ — —

Source: Gaulter, after 207; Shapter, Hatton; Shattuck; E. Cooper; Snow, MCC2, between 44 and 45; Snow, “Report,” CIC, between 107 and 08; GBH, Report, Committee for Sci-entific Inquiries, 1854; Pettenkofer (Bavaria) in Barrett, 501; Pettenkofer (Aubing) in Barrett, 501; Baker; Rothernburg; Chadwick; Gavin; Sutherland, in GBH, Report on Cholera,1848–49, appendix A; Petermann; Farr; Administration Générale, in Kudlick, 16; Brigham, facing title page; J. Jackson, 170; GBH, Report on Cholera, 1848–49, facing title page.

geographical area could be highly misleading unless the population density was rel-atively constant over the same area. Suppose that there are twice as many dots onthe left-hand side of a spot map as on the right. It might be that some environmentalfactor that predisposes toward cholera exists on the left side. It might also be thattwice as many people live in the left of the region than in the right, so that the ac-tual rate of cholera cases per unit of population is identical.

In a retrospective map of the 1831–1833 epidemic, Petermann accounted for vari-ations in population density by adapting Quetelet’s method of continuous tonalshading to depict the differential rates of cholera mortality in various parts ofBritain.18 This cartographic change was made possible when census authorities in1841 distributed an official “household schedule” to every house, and enumeratorstransferred data from these schedules into books subsequently available from theRegistrar-General’s Office.19 The concentrations of cholera deaths (shown by dots)“seemed to lie all in the lower ground and valleys,” which would confirm Farr’s the-ory that residing at low elevations increased the risk of cholera,20 but Petermann wasnot convinced. He engaged in a “minute investigation” of the relationships amongterrain, demography, and cholera deaths, concluding from this inductive exercise that“of all of the local causes of the spread of the disease, altitude is one of little com-parative influence . . . it is much more affected by the density of the population.”21

Because more large cities were located at lower than at higher altitudes, lower ele-vation was associated with both population density and various unsanitary featuressuch as overcrowding, making it hard to blame elevation alone for increased choleraincidence. The Lancet acknowledged receipt of this “cholera map . . . the ingen-ious production of Mr. A. Petermann,” and suggested “that a map of a similar char-acter, coloured weekly, agreeably to the report of the Registrar-General, so as to in-dicate the localities successively invaded by cholera at the present time, would not bedestitute of public interest.”22 No such combination of spot and progress maps ofcholera appeared during the 1848–1849 epidemic, however.

Other cartographers also expanded the spot map’s potential for showing associa-tions among variables. John Hatton, working contemporaneously with Snow in Lon-don, displayed a spot map in his lecture on the sanitary condition of Chorlton-Upon-Medlock, a district in the city of Manchester, in 1854.23 He incorporated shadingand various circular symbols to show a broad array of data. He distinguished be-tween “fevers” and actual cholera cases, mapped such cases and deaths, included de-tails about local sewers, and indicated “unhealthy districts” as shaded areas. A sani-tarian, Hatton constructed the map to feature a striking concordance between clustersof cholera cases and the “unhealthy districts.” A star denoting the first recorded caseof cholera, which epidemiologists now term the “index case,” suggests that he mayhave been a contingent contagionist and that he added an inductive, discovery di-mension to an otherwise illustrative map. Although Hatton assumed that the effi-cient cause of this epidemic disease was a local miasma, plotting the index case onthe map was part of the investigative process he used to determine the spread of the


epidemic through the inhalation by others of effluvial emanations from the earliervictims.

Max von Pettenkofer (1818–1901) joined a commission investigating the lethal 1854cholera epidemic in Bavaria. His reading of medical literature on cholera, includingSnow’s MCC, left him unconvinced by any current theory. Each one, be it contagion,noncontagion, contingent contagion, or communication by water, could account foronly some of the available evidence about the propagation of this disease; there hadto be a causal factor that existing theories had not considered. During surveys in Bavariahe produced at least two spot maps that reflected his understanding of new carto-graphic techniques. One was a three-color map superimposed on a military map ofthe kingdom that showed various geographical features. The spatial distribution pat-tern of cholera deaths was depicted by three levels of intensity: epidemic (red), spo-radic (green), and scattered (blue).24 This map appears to have been an inductive ex-ercise, designed to help Pettenkofer develop a hypothesis about the causal factorsproducing cholera. The color shading of varying disease prevalence indicated that peo-ple residing in moist, low-lying areas were more often and more severely affected thanthose who lived on drier and more elevated terrain. He speculated that peculiar envi-ronmental features of the soil, groundwater, and organic pollution might explain thisvariation, but he still had no working hypothesis.25

Later in the summer of 1854 he studied cholera outbreaks in ten Bavarian cities,including Munich and outlying villages. For an outbreak in Aubing, west of the city,he plotted the location of cholera deaths by households on a topographical map andadded numerical identifiers for each death. When analyzing the map he was struckby certain associations between deaths and high groundwater levels in partly satu-rated gravel soil at low elevations.26 The following year his inductive mapping ex-perience in Aubing may have been critical in formulating the soil (Boden) theory ofcholera he would articulate in a succession of papers thereafter.

Disease Mapping in Golden Square

At least five spot maps were constructed of the most deadly, localized cholera out-break in London during the epidemic of 1853–1854. The first was made by EdmundCooper, an engineer at the Metropolitan Commission of Sewers. The commissionsent him to Golden Square early in September 1854 to mollify vociferous residentsof St. James Parish, who believed that new sewers, including one that ran through aseventeenth-century plague burial ground, vented cholera poison into their neigh-borhoods, which had experienced few cases in the two previous epidemics. Cooperthought otherwise. Although he shared the residents’ anticontagionist assumptionthat offensive odors could carry epidemic disease particles, it seemed highly unlikelythat the corpses of plague victims buried almost two centuries earlier would still be decomposing. Moreover, any disease particles introduced into the sewer mains


during construction would have been flushed into the Thames long before the cur-rent outbreak, which had commenced at the end of August. A sanitarian himself, likethe commissioners for whom he worked, Cooper’s hypothesis was that the outbreakwas caused by incomplete sanitary renovations in the parish—cesspits still collect-ing wastes from latrines—together with insufficient drainage in certain houses, over-crowded and filthy living conditions, and so on. The only way to exonerate the SewerCommission from public accusations was to show, somehow, that cholera deaths inthe parish were clustered in local effluvia hot spots rather than along the offendingline through the plague pit or near grates and shafts to the connecting sewer lines.That is, Cooper had to devise a way to confirm his own hypothesis and refute theresidents’ counterclaims.

He decided to undertake a study that involved deductive mapping because theproblem was inherently geographical. First, he consulted the Registrar-General’sWeekly Reports through 9 September, from which he compiled a table of 316 deathsat addresses for each street in the area. He then inspected every house in the table.On a detailed engineering map of the parish that showed all sewer lines, gratings,and gully holes, he drew a thick line along the street frontage at each address whereat least one death was listed; behind the street numbers he drew individual bars rep-resenting each case listed at that address (Fig. 12.4). The thick lines are the map’sstriking feature that Cooper used as scientific evidence to disprove the residents’complaints: “It will be seen by the Plan [map], that the houses in which the greatmajority of deaths have taken place, are not situate opposite to gullies or ventilatingshafts.”27 The map and sanitary details from the data table permitted him to provehis own hypothesis:

Throughout the neighbourhood, it is important to observe, that the housesare, for the most part, let out in lodgings; a separate family, and in some caseseven two, are living on one floor, whereas but one water-closet, or privy in theyard or area, exists for the use of the whole house; consequently, in the roomsabove the ground floor, portable cesspools or slop pails are kept, into whichnight soil, dirty water, and all refuse are thrown, and these are emptied aboutonce a day, either down a sink, or into the water-closet or privy; and not un-frequently into a gully in the street. On the top or attic floor, the occupantsgenerally make use of the gutter for the emptying of these accumulations,which find their way down the rain water pipe on to the paving in the yard atthe back of the house, and sometimes on to the footway in the street front.27a

He concluded that local unsanitary conditions had caused the outbreak.Cooper was an engineer, not a medical cartographer. His map combined the tra-

ditional use of marks for each case—solid black bars like Shapter’s rather than dots—with the addition of thick black lines at street frontages for every house with at leastone case of cholera. The combination of bars and lines indicate the deductive


Figure 12.4. Edmund Cooper’s map of the Broad Street cholera epidemic made for the Metropolitan Commission of Sewers, September

1854. Inset: the Broad Street pump and surrounding addresses. Cooper designated each affected house by a large solid bar, and the cholera

deaths occurring in each house by thin lines.

nature of this mapping enterprise. His goal was to disprove public criticism of thecommission for which he worked, not to medically map the epidemic. Consequently,his map and report made no use of advanced cartographic features such as tonalshading to represent variations in mortality by population density or a symbol tonote the index case.

Snow prepared the second and third known maps of the Golden Square choleraoutbreak several weeks after the brief investigation that eventuated in his recom-mendation that the Board of Governors remove the handle of the Broad Street pump.His investigative process involved spatial visualization rather than mapping:

As soon as I became acquainted with the situation and extent of the late out-break of cholera in Broad-street, Golden Square, and the adjoining street, Isuspected some contamination of the water of the much frequented street-pump in Broad-street, near the end of Cambridge-street: but on examiningthe water, on the evening of the 3rd inst., I found so little impurity in it of anorganic nature, that I hesitated to come to a conclusion. . . . I requested per-mission, therefore, to take a list at the General Register Office of the deathsfrom cholera registered during the week ending September 2, in the sub-districts of Golden-square, Berwick-street, and St. Ann’s, Soho. Eighty-ninedeaths from cholera were registered during the week, in the three sub-districts.. . . On proceeding to the spot, I found that nearly all the deaths had takenplace within a short distance of the pump. . . .

I have not thought it necessary to inquire into the very large number ofdeaths that occurred in the week ending Sept. 9, as I deem the above inquirysufficient to establish the cause of the outbreak.28

This is Snow’s first account of his investigation, published on 23 September 1854.He arrived on the scene with a hypothesis in mind and, based on anecdotal infor-mation about the outbreak, prior knowledge of sudden, violent local outbreaks, andpersonal understanding of neighborhood preferences for drinking water, intuited thecause as contamination of the pump in Broad Street by cholera dejecta from an un-known victim. He sought a list of addresses only after an inspection of the pumpwater showed no evidence of sewage. The subsequent investigation involved house-to-house questioning of residents, which revealed that seventy-seven of the victimshad unquestionably taken water from that pump, only six probably had not, and forsix others there was no information about their drinking habits. “The result of thisinquiry, then, is, that there has been no particular outbreak or prevalence of cholerain this part of London except among the persons who were in the habit of drinkingthe water of the above-mentioned pump-well” (322). Later in September Snow re-alized that the GRO list he had used grossly under-reported the number of deaths.He conducted a second house-to-house investigation, received new data from theRegistrar-General’s office, and expanded his letter to the editor of 23 September into


a full descriptive section of the projected MCC2. For some reason he decided at thatpoint to prepare an illustrative map of the Golden Square outbreak and made briefreferences to it in the manuscript.

This disease map (Fig. 12.5), which Snow subsequently displayed at the Epidemi-ological Society early in December, is a modification of an existing street map. Snow’stemplate did not show the location of sewer lines, grates, or vent shafts. It lackedprecise house boundaries and numbers, so that the addresses at which deaths oc-curred could only be approximated. Snow added symbols (circled dots) to locatestreet pumps, although he misplaced the pump in Broad Street, and used individ-ual black bars to represent the 574 victims for whom his new investigation could es-tablish an address.29 The text connected the onset of cholera in most of those vic-tims to drinking Broad Street water. The bars clustered around the Broad Street pumpon the accompanying map illustrated his argument; it played no part in his investi-gations either early in September or during the weeks after the outbreak was over.


Figure 12.5. Snow’s spot map of the Golden Square outbreak, 1854 (MCC2, between 44 and

45).

The map (Fig. 12.6) he prepared for the St. James Cholera Inquiry Committee wasonly partly illustrative of the accompanying text. For the CIC report Snow importedas much as he could of the Golden Square section of MCC2, retaining many pas-sages verbatim, correcting street names in the text to match those on the map, oc-casionally refining the language, and editing some examples, particularly the case ofthe Hampstead widow. There is no indication of a major departure in the argumentuntil the opening reference to the spot map (Table 12.2). After making a few minorchanges to clarify how he had obtained addresses where cholera deaths occurred and“the pump in Broad Street . . . indicated on the map” (correcting the location onthe revised map as well), Snow introduced new wording that showed that he had


Figure 12.6. Detail from Snow’s spot map of the Golden Square outbreak showing area en-

closed within the Voronoi network diagram. Snow’s original dotted line to denote equidis-

tance between the Broad Street pump and the nearest alternative pump for procuring water

has been replaced by a solid line for legibility. Fold lines and tear in original (adapted from

CIC, between 106 and 07).

undertaken additional investigations involving deductive mapping to strengthen hishypothesis (Table 12.3).30 Details from the two maps (Fig. 12.7)31 indicate an illus-trative revision (repositioning the Broad Street pump to its proper location) and thedeductive addition of an “inner dotted line”—a line demarcating equal walking dis-tance between the Broad Street pump and the nearest alternative pump.32 The newline meant that 380 of the 574 cases on the map lived closer in pedestrian terms tothe Broad Street pump than to any of thirteen other pumps within the study area.Establishing such an irregular catchment area for the pump strengthened the prob-ability that many victims whose drinking habits Snow could not determine by in-terrogating survivors may have taken Broad Street water. This new line also coun-tered possible noncontagionist interpretations that the MCC2 spot map showedprecisely the clustering of deaths that one would expect from effluvial vapors dif-fusing from the pump in an ever-widening circle.33 Snow could neither have addedfurther confirmation to his original hypothesis nor falsified a noncontagionist read-ing of the MCC2 map without this exercise in deductive mapping.34

The fourth spot map of the Golden Square outbreak was produced under the aus-pices of the Committee for Scientific Inquiries of the General Board of Health (GBH).This illustrative map charted the locations of 697 deaths determined by an extensivehouse-to-house survey conducted by Fraser, Hughes, and Ludlow in September1854.35 The cartographer consulted Cooper’s map and incorporated its engineeringprecision in the GBH map, but the committee did not agree with Cooper’s conclu-sion. The committee believed that the preponderance of evidence indicated that theoutbreak was caused by an unknown atmospheric influence emanating from putre-fying organic matter, and contrary to Cooper’s report and map, the Fraser team


Table 12.2. Snow’s text illustrates changes in the Golden Square spot mapa

MCC2 CIC “Report”

The dotted line on the map surrounds thesub-districts of Golden Square. . . . Allthe deaths from cholera which wereregistered in the six weeks from 19thAugust to 30th September within thislocality, as well as those of personsremoved into Middlesex Hospital, areshown in the mapb by a black line inthe situation of the house in which itoccurred, or in which the fatal attackwas contracted (46).

The outerdotted line on the mapsurrounds the sub-districts of GoldenSquare. . . . All the deaths from Cholerawhich were registered in the six weeksfrom August the 19th to September the30th within this locality, as well as those ofpersons removed into Middlesex Hospital,are shown by black lines in the situation ofthe houses in which they occurred, or inwhich the fatal attacks were contracted(108).

a We italicize every difference and boldface those significant to the maps.b “The particulars of each death connected with this outbreak were published in the “Weekly Returns” ofthe Registrar General to 16th September, and I procured the remainder through the kindness of theRegistrar-General and the District Registrars”; MCC2, 46.

included sewer gases escaping from new sewer lines in the parish among the un-questionable factors possibly responsible for the local outbreak.36

The Cholera Inquiry Committee in the parish obtained a copy of the GBH mapand was given permission to reproduce it in its report, published late in the sum-mer of 1855.37 The CIC as a whole concluded that impure water from the BroadStreet pump had caused the outbreak: “Contamination of the water in the well inBroad Street by filtration from a cesspool during the time of the Cholera outbreakis rendered certain by the result of Mr. York’s investigations made in April” (75). Inaddition, Reverend Whitehead discovered the likely index case, the infant listed asdying from diarrhea at 40 Broad Street. Snow had not included her death among thefour bars he placed at that address on both of his spot maps. The GBH investigatorsmust have decided that her diarrhea was premonitory of cholera and added a fifthbar on their map. Whitehead reached a similar conclusion and requested anotherexcavation (the earlier one, undertaken at Snow’s request, had found no evidence ofcontamination). This time, York’s team had found decayed brickwork between thepump well and the drain into which water from soiled diapers had been emptied.Although Whitehead had come to accept Snow’s water-borne hypothesis, the CICwaffled: “All the facts seem to point to the introduction, importation, or invasion [of the pump] of a material agent, either gaseous, liquid or solid, having specific


Table 12.3. Snow’s deductive addition to the CIC spot map.a

MCC2 CIC “Report”

It requires to be stated that the water ofthe pump in Marlborough Street, at theend of Carnaby Street, was so impure thatmany people avoided using it. And Ifound that the persons who died near thispump in the beginning of September, hadwater from the Broad Street pump. Withregard to the pump in Rupert Street, itwill be noticed that some streets whichare near to it on the map, are in fact agood way removed, on account of the cir-cuitous road to it.

These circumstances being taken into ac-count, it will be observed that the deathseither very much diminished, or ceased al-together, at every point where it becomesdecidedly nearer to send to another pumpthan to the one in Broad Street (46–47).

It requires to be stated that the water ofthe pump in Marlborough Street, at theend of Carnaby Street, was so impure thatmany people avoided using it; and I foundthat the persons who died near this pump,in the beginning of September, had waterfrom the Broad Street pump. The innerdotted line on the map shews the variouspoints which have been found by carefulmeasurement to be at an equal distanceby the nearest road from the pump inBroad Street and the surroundingpumps; and, if allowance be made for thecircumstance just mentioned respectingthe pump in Marlborough Street, it willbe observed that the deaths either verymuch diminish, or cease altogether, atevery point where it becomes decidedlynearer to send to another pump than tothe one in Broad Street (109).

a We italicize every difference and boldface those significant to the maps.

poisonous properties” (85). At Whitehead’s suggestion the CIC modified the GBHmap by inscribing a circle with a radius of 210 yards around the Broad Street pump(Fig. 12.8) to depict the “Cholera area” within which the vast majority of the caseswere clustered (16).38

What sort of medical cartographer was Snow? Today a considerable part of hisreputation hinges on his role in mapping the Broad Street outbreak, so it is essen-tial that the historical assessment be accurate. When Snow modified his original mapfor the CIC, he introduced a substantial cartographic innovation by explicitly indi-cating the line of equidistance among the pumps. (Ironically, his CIC map is muchless well known today than the more common and less accurate version of the mapin MCC2.) Overall, however, Snow viewed his mapping activities as a minor aspectof his investigation of cholera. He never used his map as a true investigative tool,unlike Cooper and von Pettenkofer, whose theories of cholera transmission are to-day discredited. The structure of MCC2 makes clear that Snow intended his southLondon study to be the centerpiece in supporting his theory. In essence, the BroadStreet investigation was merely preparation for the main event. It is due largely tothe connection between Broad Street and a visually appealing icon, the map, that


Figure 12.7. (left) Snow’s spot map, detail of area around the Broad Street pump (from MCC2).

(right) Snow’s spot map, detail of area around the Broad Street pump. The finely dotted

Voronoi line is in the lower half; the symbol for the Broad Street pump—circle around black

dot—has been repositioned to its correct location opposite no. 40 Broad Street (from CIC,

between 106 and 107).

today’s reader often gets it backward and attributes to the Broad Street investigationan importance that Snow never assigned to it in comparison with the much moreextensive and conclusive study of the south London data.

Notes

1. Snow, “On the mode of propagation of cholera,” 559.2. UK GBH, Cholera of 1848 & 1849, appendix B (by R. D. Grainger), map opposite 200.

In Grainger’s “tinted cholera map” the “depth” of the “tinting” showed the “amount of mor-tality”; Ibid., 31–32. Grainger was an anticontagionist; see “Mr. Grainger and the cholera,”Lancet 1 (1849): 106–07, issue of 27 January 1849.

3. Also suspended in the room at the meeting of the Epidemiological Society was a statis-tical table, copied from the 12 January 1850 Weekly Report of Births and Deaths, depictingcholera mortality in the 1848–1849 epidemic.

4. “Map 1. Showing the deaths from cholera in Broad Street, Golden Square,” MCC2, viii;inserted between 44 and 45. Map 2 was a boundary map showing districts south of the Thamesand their water supply, akin to the one from the Health of Towns Report he displayed beforethe Epidemiological Society.

5. Although MCC2 was not printed until late December 1854 or early January 1855, theopening passage reads as follows: “The most terrible outbreak of cholera which ever occurredin this kingdom, is probably that which took place in Broad Street, Golden Square, and the


Figure 12.8. The General Board of Health map used by CIC, with Whitehead’s “cholera area”

indicated by a circle (CIC, between 96 and 97).

adjoining streets, a few weeks ago” (38)—actually, the first two weeks of September. Furtheron Snow wrote, “The deaths which occurred during this fatal outbreak of cholera are indi-cated in the accompanying map, as far as I could ascertain them. There are necessarily somedeficiencies . . . [although they] probably do not detract from the correctness of the mapas a diagram of the topography of the outbreak” (45).

6. “Epidemiological Society,” Lancet 2 (1854): 530–31; MTG 9 (1854): 629.7. We offered a slightly different interpretation of these maps in Brody et al., “Map-

making and myth-making in Broad Street,” Lancet 356 (2000): 64–68.8. See Barrett, Disease & Geography; A. Robinson, Early Thematic Mapping; Jarcho, “Yellow

fever, cholera, and medical cartography”; and Gilbert, “Pioneer maps of health and disease.”9. Petermann, Cholera Map, “Statistical notes,” 1.10. Ibid., 2. Petermann had traveled to Scotland in 1845 to assist in making an atlas. The

Royal Geographical Society elected him a fellow in 1846, before he moved to London. In 1852Queen Victoria gave him an appointment as physical geographer and engraver in stone at hercourt.

11. Seaman, “Inquiry into yellow fever in New York.”12. Jackson, Spasmodic Cholera.13. Ibid., 170.14. Shapter, Cholera in Exeter in 1832.15. He allowed for person-to-person transmission as a contingent factor; Ibid., 230.16. Later Snow used the parish of St. Edmund as evidence that a pure water supply would

protect residents from cholera despite elevation and cholera’s prevalence in nearby districts(MCC2, 99–100).

17. “Reviews,” Lancet 2 (1849): 317. The reviewer added that “an admirable map of the city,indicating the points at which the disease prevailed, . . . add to the value of the work.” Manydecades later Underwood called attention to the existence of Shapter’s book—”a mine of in-formation, and it must be one of the best descriptions extant of an historical epidemic”; BritishMedical Journal (1933): 620. Unlike the Lancet reviewer, Underwood did not mention the map.

18. Petermann, Cholera Map. The inset for London represented varying percentages ofcholera deaths in six tints, from pink to red. Grainger also used this tonal shading method(see Fig. 12.1); UK GBH, Cholera 1848 &1849, appendix B, 200. Both had adapted AdolphQuételet’s system of continuous tonal shading, with increasing mortality represented by in-creasingly darker shades; see A. Robinson, Early Thematic Mapping, 160–61.

19. Mills and Pearce, Victorian Census, 1; Glass, Numbering the People, 94. Petermann alsoproduced two demographic maps of England, one in 1848 that made use of 1841 census ma-terial and the second to illustrate the 1851 census.

20. Petermann, Cholera Map, “Statistical notes,” 4; Farr, Cholera in England, 1848–1849,lxi–lxv.

21. Petermann, Cholera Map, “Statistical notes,” 4.22. Lancet 2 (1848): 595.23. Hatton, “Sanitary condition of Chorlton-Upon-Medlock.”24. Blue was used to indicate places where cholera was present in only one or two houses.

This map was probably destroyed during the aerial bombing of Munich in July 1944; see Bar-rett, Disease & Geography, 375.

25. Hume, Max von Pettenkofer, 58.26. Barrett brought this map to our attention and supplied a copy.27. Cooper, “Report,” 3.27a. Ibid., 3–4.28. Snow, “The Cholera near Golden Square, and at Deptford” (1854).


29. Shapter’s map of cholera in Exeter may have influenced Snow to substitute bars for dotsto represent cases. In 1849 Snow noted that Shapter “kindly furnished me with informationconcerning the sewers, and maps of their position,” in Exeter; PMCC, 751. However, Snownever cited Shapter’s spot map. In addition, Cooper employed bars, and there is no indica-tion he was influenced by Shapter.

30. Snow, “Dr. Snow’s report,” CIC, 109. Some of the alterations are also noted by McLeod,“Our sense of Snow,” 931–32.

31. The revised spot map in CIC, between 106–07.32. Such an equidistant line dividing a map into areas is today called a Voronoi diagram.

McLeod considers Snow the first disease cartographer to use such a device; “Our sense ofSnow,” 932; see also Brody et al., “Map-making and myth-making in Broad Street.”

33. E. A. Parkes made this point in a review of MCC2 for British and Foreign Medico–Chirur-gical Review 15 (1855): 458. Parkes also noted that there were so many street pumps in thisneighborhood that no matter where the noxious vapors had originated, there was certain tobe a pump nearby, but Parkes’s review appeared after Snow had written his report for the CICand reconfigured the map of Golden Square.

34. Of the 194 cases (33.8% of the total) outside the equidistant demarcation line, Snowmade additional inquiries early in December 1854 and was able to show that at least a quar-ter of them either drank Broad Street water or contracted cholera at a point nearer to thatpump than the alternative closer to where they lived; “Dr. Snow’s report,” CIC, 110–16. In hisearlier investigations he had shown this to be the case for only four victims; MCC2, 47–48.

35. UK, GBH, Report of Committee for Scientific Inquiries, 1854.36. Ibid., appendix, 143.37. CIC, map between 96–97. The virtual identity of the GBH and CIC maps—the CIC

added a circle at Henry Whitehead’s behest—was established via a point-by-point compara-tive analysis.

38. This circle was Whitehead’s second effort to represent the “cholera area” in spatial terms.In the fall of 1854 he had drawn an irregularly shaped polygon to indicate what he took tobe the boundaries of the area most afflicted; Cholera in Berwick Street, 1–2.


SNOW’S WORK AS A SCIENTIST and physician in the 1840s wasconcurrent with some significant formulations of sanitary theory.

Edwin Chadwick’s Inquiry into the Sanitary Condition of the Labouring Population ofGreat Britain (1842) and two reports by the Parliamentary Commissions on theHealth of Towns (1844 and 1845) proposed that the endemic and epidemic diseasesravaging the poor of Great Britain could be controlled only by government action.The ultimate results of the sanitary reform movement—publicly-financed water sup-plies and sewerage in cities, disposal of garbage, and a public health infrastructure—produced profound public health benefits, but not during Snow’s lifetime.1 Later inthe century, when the sanitary reform movement eventually adopted the insightsfrom epidemiology that it had initially spurned, and also accepted the new bacteri-ology that it had been slow to acknowledge, great improvements in public health didtake place. Sanitary reform would have borne fruit much sooner, however, had itlinked disease to class distinctions, slum housing, and industrial exploitation of theworking classes.2

Sanitarianism in Snow’s time retained the humoral notion that health was the re-sult of a harmonious relation between every body’s unique internal components andthe external environment. As such, the sanitary reform movement was based on acomprehensive view of the relationship of humans to their natural and social envi-ronments rather than a theory of fever causation.3 The immediate consequence of

340

Chapter 13

Snow and theSanitarians

such views was to reject narrow or specific theories such as Snow’s. It seemed to defycommon sense experience for him to insist that cholera, always and everywhere, wascaused by one particular method of transmission: the fecal–oral spread of the spe-cific cholera particle or agent. It seemed equally obvious to his critics that cholerawas sometimes caused by one factor, sometimes by another, depending on local con-ditions and the history of the individual patient. To a sanitarian Snow’s simple re-forms for the prevention of cholera were pure nonsense; why bother to institute re-forms that might not prevent other disorders?4 By comparison William Budd’s claimsthat cholera was usually spread by contaminated water, although inhaled effluvia wasa possibility, were more readily acceptable to a multifactorially inclined audience.5

The Sanitarian Establishment

The participants in the GBH’s several investigations and committees included a cross-section of London’s leading physicians, surgeons, apothecaries, scientists, and pub-lic health officials. The professional leadership of all three medical corporations inLondon, the queen’s physicians Clark and Arnott, the paleontologist Richard Owen,the public health leaders Farr and Simon, Hassall the microscopist, Babington, pres-ident of the Epidemiological Society of London, and many others supported theboard’s miasmatic interpretation of cholera. They shared a common understandingof the etiology of epidemic disease, even though they differed at times as to theproper ways to achieve particular sanitary goals.

Snow’s views on the nature and spread of epidemic diseases such as cholera dif-fered fundamentally from those of the leading sanitarians of his time. The essenceof the disagreement was the all-encompassing nature of Snow’s cholera theory andits dependence on two singularities. First, cholera was a singular disease; only a caseof cholera could give birth to another case of cholera. Cholera bred as true as anyspecies of animal or plant. Local impurities, whether acting by themselves or in con-cert with atmospheric conditions, and no matter how foul, could not produce a caseof cholera. Second, cholera had a singular route of transmission. With minor andrare exceptions, the only way the cholera agent could be introduced into the bodywas by swallowing the dejecta of another case of cholera.

Even to think of “routes of transmission” was to conceptualize the agent of cholerain a radically different way. By late 1854 Snow assumed the cholera agent had to bea form of live matter and suggested that it probably took the form of a cell, analo-gous to the morbid material that caused smallpox and cowpox (MMC2, 15). It couldproduce its pathology only by interacting with a specific tissue, the intestinal lining,and therefore needed to be transported to that location. He did not see the choleraagent, as the sanitarians did, as a local atmospheric phenomenon that in the pres-ence of common toxic gases arising from putrefaction was inhaled and absorbed intothe bloodstream, where it chemically combined with unspecified human material to

Snow and the Sanitarians 341

produce its pathology. Snow emphasized the singularities of the nature of choleraand its fecal-oral and waterborne route of transmission. But this advocacy includeda negative dimension—an intense skepticism of the alternative explanation, thegaseous-miasmatic concept of cholera origin. His skepticism of miasma theory,which stemmed in part from his understanding of anesthetic gases, ultimately provedmore troubling to sanitarians than did his cholera theory and its link to water supplies.

Both Snow and the sanitarians recognized that their differences in the theoreticalconstruction of the nature of cholera and its agent were not idle speculations in purescience about which gentlemen could disagree. Their divergent theories had profoundimplications for public health action. Snow believed that the sanitarian focus on theelimination of fictitious air-borne cholera agents was either useless in the preventionof cholera or inadvertently promoted spread of the disease. He believed the sanitar-ians were especially mistaken in their desire to rid cities of sewage by flushing it intothe same waterways that served as the sources of municipal water supplies. This prac-tice was a major plank in the sanitary program of the Metropolitan Commission ofSewers (MCS) in London.6 One of the commission’s recommendations was to elim-inate London’s estimated 200,000 cesspools, replacing them wherever possible withwater closets directly connected to the sewers. In Snow’s mind such a program es-sentially meant that cholera evacuations would be routed into the Thames and thenrecirculated in the piped water supply to be ingested by an unsuspecting populace.Chadwick was one of the twenty-three original commissioners appointed in 1848,and it seems clear that the MCS was influenced by the recommendations on drainagehe had formulated earlier in the decade when writing Sanitary Condition of the Labour-ing Population. Chadwick believed that substituting water closets for latrines andcesspools, laying sewer drains, and then using great volumes of water to flush urbanfilth and refuse into nearby rivers would eliminate the foul smells he considered pre-disposing for epidemic diseases. Joseph Bazalgette, the chief engineer of the MCS andthe designer of the nineteenth-century sewage system that continues to serve Lon-don, noted that, “within a period of about six years, thirty thousand cesspools wereabolished, and all house and street refuse was turned into the river. . . .”7 Success inachieving this goal was largely due to an MCS recommendation that all new housingbe outfitted with flushable water closets,8 but the “arrival of the water closet was agiant step forward for personal hygiene and two steps backward for public sanita-tion.”9 Snow’s theory predicted that unless the water supply was protected from re-cycling raw sewage, the new system, appealing though it might be to the olfactorysense, would exacerbate the severity of future cholera outbreaks.

Despite their theoretical disagreements, Snow maintained cordial personal rela-tions with most of the sanitarians, participating amiably, for example, in meetingsof the sanitarian-dominated Epidemiological Society, of which he was a foundingmember. In return they generally accorded him a respectful hearing, seldom reject-ing his arguments out of hand. In turn Snow avoided ad hominem attacks when he


considered it necessary to criticize the sanitary agenda. During the 1849 epidemic,for example, he was gently ironic in commenting on high mortality in Rotherhithe,where many inhabitants obtained their drinking water directly from ditches ofThames water that were refilled at each high tide: “Rotherhithe is less densely pop-ulated than many parts of the metropolis which have been comparatively free fromcholera, and those ditches, it should be remembered, are not very offensive to thesmell; being only Thames water rendered a little richer in manure; being, in shortprobably equal to what Thames water would be if certain of our sanitary advisorscould succeed in having the contents of all the cesspools washed into the river”(PMCC, 748). However, five years later his criticism had an edge to it:

There is one circumstance, however, that ought to prevent any expression ofblame or recrimination for the propagation of cholera in this way; it is this—that the persons who have been more instrumental in causing the increase incholera, are precisely those who have made the greatest efforts to check it, andwho have been loudest in blaming the supineness of others. In 1832, there werefew water-closets in London. The privies were chiefly emptied by night men,a race who have almost ceased to exist; or a portion of the contents of thecesspool flowed slowly, and after a time, into the sewers. By continued effortsto get rid of what were called the removable causes of disease, the excrementof the community has been washed every year more rapidly into the river fromwhich two-thirds of the inhabitants, till lately, obtained their supply of water.While the fæces lay in the cesspools or sewers, giving off a small quantity ofunpleasant gas having no power to produce specific diseases, they were spo-ken of as dangerous and pestilential nuisances; but when washed into the drink-ing-water of the community, they figured only in Sanitary Reports as so manygrains of organic matter per gallon.10

In his mind it was obvious that cholera epidemics in London were getting worse,and he held misguided sanitarian reformers chiefly responsible.

The Nuisance Trades

On 5 March 1855 Snow provided his testimony to Parliament on the proposed Nui-sances Removal and Diseases Prevention Act. This act sought to control factory pro-cesses, such as tanning and soap making, which depended upon animal productsand were associated with unpleasant smells. For miasmatists such as Chadwick, whoadhered to the notion that all stink is disease, the smells emanating from these fac-tories were exciting or contributory causes of epidemic disease. But Snow believedthat medical concern about such odors was a complete waste of time, so he agreedto present his views on epidemic disease in support of the manufacturers whose


factories were threatened by the pending legislation.10a The testimony sparked edi-torial denunciation from the Lancet, accusing Snow of joining forces with filth anddisease and abandoning the sanitary cause.11 Had Snow been thinking solely of pol-itics, he would surely have avoided presenting this testimony. Had he wished to winthe sympathies of the sanitarians, he would have avoided taking the side of the nui-sance trades. He was later characterized by his friend and fellow student Joshua Par-sons as someone who cared solely about truth and gave not a jot about what othersmight think of him. Still, the Snow who loved truth must have been bothered by theLancet editorial. After giving his testimony Wakley accused him of “riding his hobby. . . down a gully-hole” and being unable to extricate himself.12 He assumed thatSnow was so enamored of his theory of the diffusion of gases that he could not smellwhat was right under his nose and so failed to reach the common sense, sanitarianconclusion that anything as patently offensive as the nuisance trades would have tohave an injurious impact on health. In Wakley’s view, Snow had deviated from hisusual scientific practice. He had presented conclusions without experimental evi-dence or statistics to back them up.

Snow seems to have taken that portion of Wakley’s criticism to heart. The fol-lowing year he submitted a paper on the nuisance trades to the Lancet.13 He madeno reference to the harsh words meted out by Wakley, nor did he attempt to justifyhis decision to testify on behalf of a consortium of manufacturers. Instead, he pre-sented evidence that workers in offensive trades did not suffer more ill health thandid other urban workers. Snow presented mortality rates by occupation derived fromWeekly Returns published during the previous eighteen months. The overall mortal-ity for men over twenty was 241 per 10,000, while for men over twenty in the of-fensive trades it was 205. If the category was enlarged to include all who worked withdead animals (i.e., poulterers, butchers, and fishmongers) the mortality rate was 201.Snow listed fifteen offensive trades in which at least one death occurred, trades thatgive a wonderful sense of the early industrial world of urban London—tripedealer/dresser, tallow chandler, comb maker, soap boiler, music string maker, bonegatherer, bone worker, carrier, tanner, fellmonger, grease dealer, cat meat purveyor,skinner, parchment maker, glue and size maker.14 Snow was aware that age distri-butions above twenty might well vary in the several occupations and cited Farr tothat effect when discussing the data from which his numbers came, but Snow dis-missed age as an explanation for his findings. Compared to the total population ofmen over twenty, Snow reasoned, the ages of men in any specified occupation oughtto be greater because the trades might be joined at any age over twenty, thereby ex-cluding younger men from the occupational tally. The higher average age of any oc-cupational group ought to have produced higher mortality, and thus the lower ratefound in the offensive trades was yet more impressive evidence of their healthiness.By way of comparison, Snow mentioned that the mortality rate among keepers ofbeer shops was a relatively high 373. However much Snow the teetotaler might havebeen tempted to attribute this high death rate to the evils of alcohol, Snow the sci-entist pointed out that it was common for older men who had become unfit for


more active occupations to take up the beer trade. The higher mortality rate reflectedthe average age and earlier health of the workers and not the inherent danger of thetrade. He thought that the nuisance trade figures should be reasonably accurate withregard to health hazards because he knew of no biasing tendencies for men of anycertain age group to enter or to leave those trades. Although his argument restedmainly on numerical data, he reiterated the view that the laws of diffusion of gasesdirectly contradicted miasmatic theory: “As the gases given off by putrefying sub-stances become diffused in the air,” he noted, “the quantity in a given space is in-versely as the square of the distance from their source. Thus, a man working withhis face one yard from offensive substances would breathe ten thousand times asmuch of the gas given off, as a person living a hundred yards from the spot.”15

Mention of gas laws drew Wakley from his den. A week later the Lancet respondedwith an editorial that also drew on data and conclusions published by the Registrar-General. The editorial noted the documented hazards to the respiratory systemcaused by the air of London, contaminated as it was by “mechanical impurities inthe shape of fine dust, composed of a variety of organic and inorganic matters.” Al-though the public health issue in question was not quite the same as that dealt withby Snow in his article and testimony, the Lancet used this tangible evidence of theill effects of air to cast aspersion, once again, on Snow’s science. Speaking of the “va-riety of noxious gases and vapours” in the London air, the editorial suggested that,“There can be no doubt that they exert a most efficient and malignant influence inthe causation and aggravation of disease. They are evolved so fast in many districts,that the ordinary rate of circulation of the air and the action of that beautiful lawof the diffusion of gases are altogether insufficient to dilute them rapidly enough todeprive them of their poisonous properties.”16 Snow did not respond to this edito-rial, or to a letter that appeared the following week from a Dr. John W. Tripe, themedical officer of health for the borough of Hackney. Dr. Tripe could not agree withSnow’s conclusions about the offensive trades, arguing that the census figures Snowused were not adjusted for the increase in population since the 1851 census and thatthe problem of age differences might not have favored Snow’s view. One neededyouth and strength for these kinds of work, so the deaths of older, retired workersfrom these trades might not be classified with them.17 Dr. Tripe was considering apossibility that Snow had dismissed, that diseases caused by constant exposure tonoxious gases would be either delayed in onset or else slow to develop and chronicin nature. But Snow’s testimony had focused only on acute fevers and epidemic dis-ease, while his paper included deaths from all causes and concluded that there wasno elevation in mortality.

Responding to the GBH

Snow turned next to a critique of government reports on the cholera epidemic of1853–1854. The Committee for Scientific Inquiries of the GBH had concluded that


cholera was the result of an atmospheric ferment that interacted with the existingorganic impurities in the residences and neighborhoods of the poor.18 In a series ofreports published in mid-1855 and illustrated with the map developed from the la-borious house-to-house survey conducted by Fraser, Hughes, and Ludlow, the com-mittee dealt with concerns about impure water by incorporating them into their gen-eral miasmatic framework. They attributed the epidemic to the accumulation ofdecaying animal and vegetable matter interacting with the “epidemic influence” (aseasonal change in atmospheric conditions). They described the unknown cholera-causing agent as acting “after the manner of a ferment,” so that “the stuff out of whichit brews poison must be air or water abounding with organic impurity. . . . Eitherin air or water, it seems probable that the infection can grow. Often it is not easy tosay which of these media may have been the chief scene of poisonous fermentation;for the impurity of one commonly implies the impurity of both; and in consider-able parts of the metropolis (where the cholera has severely raged) there is a rivalryof foulness between the two. But, on the whole evidence, it seems impossible to doubtthat the influences, which determine in mass the geographical distribution of cholerain London, belong less to the water than to the air.”19 The Committee was aware ofSnow’s writings but were unpersuaded by his theory or the evidence he presentedthat the pump in Broad Street was the source of the Golden Square outbreak : “Af-ter careful inquiry, we see no reason to adopt this belief. We do not find it estab-lished that the water was contaminated in the manner alleged; nor is there before usany sufficient evidence to show whether inhabitants of that district, drinking fromthat well, suffered in proportion more than other inhabitants of the district whodrank from other sources.”20

Snow responded with a paper presented to the London Epidemiological Societyin May and June of 1855. After reiterating themes (sometimes using the very samewords) made in MCC2 and his report for CIC, he noted specific points of disagree-ment with the GBH reports.21 He considered Dr. John Sutherland’s contribution es-pecially problematical. Sutherland, too, had implicated bad water, but only as a pre-disposing cause; it weakened the constitution, making people more susceptible tothe effects of cholera-carrying effluvia than they would be otherwise. He did not ac-cept Snow’s theory that a specific cholera agent must be in bad water for a personto come down with the disease. Snow warned his listeners at the EpidemiologicalSociety that his views on water-borne transmission of cholera required the presenceof a transmissible agent: “The division of my views on cholera which refers to itscommunication through the means of drinking water, has apparently obtained agreater amount of attention from the Profession, than my views respecting its moreimmediate communication by the cholera poison being swallowed without the wa-ter. While I speak on this division of the subject, however, I must beg the Society tobear in mind also the other part of my views, first alluded to, for I am well awarethat the part which relates to polluted water will not of itself explain the wholeprogress of the disease as an epidemic.”22 Nevertheless, Sutherland, the board’s chief


sanitary inspector, took a pragmatic view of the influence of impure water. He be-lieved that it did not really matter whether one viewed water as containing the “spe-cific poison of cholera” as long as it was recognized that “impure water is injuriousto the public health.”23 Even so, Snow was not tolerant of this apparent tilt towardhis theory: “It seems very curious that Dr. Sutherland should not have perceived thatthis question, as to whether or not the water contains the specific cause of cholera,involves the entire question of the cause and prevention of the malady, and also theapproval and condemnation of nearly all the so-called sanitary measures which havebeen adopted with respect to cholera, since it was first expected in 1830.”24 Only wa-ter rendered impure by the admission of cholera evacuations could cause the dis-ease, so the central question was whether sanitary reforms reduced or exacerbatedthat possibility.

Snow found errors in several parts of the board’s work, errors that generallystemmed from a lack of knowledge of the water supply. He alleged that the board’sanalysis of mortality from cholera in Christchurch, the model lodging houses in Lam-beth Square and Park Road, and Jacob’s Island was either mistaken or misleading.The board credited sanitary improvements for lower than expected mortality at eachof these locations, whereas Snow argued that the information he had collected dur-ing his analysis of metropolitan water supply showed precisely the opposite. For ex-ample, he argued that lower mortality in the new lodging houses, with their waterclosets and good ventilation, was artificial because the board had not taken into ac-count that some cholera victims were removed to distant hospitals. Snow also crit-icized the board for using the concept of disease predisposition too loosely. In hismind “a predisposing cause is one which is supposed to prepare the patient to beacted upon by some more direct cause; and it must, therefore, require a certain timefor its operation.”25 The information he had gathered in south London and GoldenSquare clearly showed that some individuals who had not been in the habit of drink-ing water from a contaminated source did so on one occasion and promptly camedown with cholera. “[These] circumstances show that the water did not act as a pre-disposing cause, but must have contained the real and efficient cause of the cholera.”26

Snow and Simon

The differences between Snow and the GBH on the causes of cholera epidemics weremore subtle than his disagreement with local miasmatists like Milroy, because theboard agreed that impure water could pose health hazards. Hence, Snow’s responsein the immediate aftermath of the 1853–1854 epidemic was a series of emphatic clar-ifications that his theory required fecal–oral transmission of the cholera agent; itmust be swallowed, and the vehicle could be food as well as impure water. The dif-ferences between his views and the GBH’s became even blurrier when, in mid-1856,the latter published a “Report on the cholera epidemics of London as affected by the


consumption of impure water,” written by the medical officer to the privy council,John Simon.27 This report virtually replicated Snow’s analyses of London water sup-ply in MCC2. Moreover, Simon practically appropriated his description of the nat-ural experiment offered by the comingled water supply in south London.28 The re-port was well received in the medical and popular press,29 but Snow bit his tongue.He wrote a letter to the Times at the end of June in which he summarized his viewsand then embarked on a scientific paper for the journal of the Epidemiological So-ciety published in October 1856. He began the former with a laconic assessment:“This report, although valuable in some respects, contains, from the nature of it,only an approximation to the truth.”30 Next he told the truth, as he saw it: “The pop-ulation supplied with the impure water of the Southwark and Vauxhall company suf-fered a mortality from cholera in the late epidemic not [as Simon would have it]merely three and a half times as great as that supplied by the Lambeth Company,but six times as great; and even this fact expresses the influence of the impure wa-ter in an inadequate manner, unless the different periods of the epidemic are con-sidered separately.” Snow then gave a brief history of his own investigation, the as-sistance he had received from Farr’s office, and his conclusions. It was a letter toestablish his priority. It was also an opportunity to tout the validity of his theory anddistance himself from the sanitarians: “I should like to say, in conclusion, that manyother diseases, beside cholera, can be shown to be aggravated by water containingsewage, and that since the Southwark Water Company has obtained a supply almostequal in purity to that of the Lambeth Company the mortality of the south districtsof London had greatly diminished.”

The centerpiece of Snow’s article in the JPH&SR was the predictive mathematicalmodel of south London mortality by subdistricts (discussed in Chapter 10), which Si-mon’s report enabled him to complete, for it contained what he had been hoping to seesince August 1854: a breakdown by subdistricts of the number of houses supplied bythe Lambeth and Southwark and Vauxhall companies.31 He also used the article to out-line four problematical aspects in Simon’s report that diminished the mortality differ-ences between customers of the two water companies. Snow pointed to

1. Imperfectly drawn subdistrict boundaries resulting in a misclassification of thewater supply to some houses

2. Failure to enumerate streets in which no death took place, resulting in an un-derestimate of the risk of death from cholera

3. Apparent failure to ascertain the correct address for each death4. Failure to account for the transfer of cholera patients to workhouses and other

locations

Although each error was relatively minor, their net effect was to dilute the differencein mortality among customers of the two water supplies—from six-fold to three-and-a-half throughout the entire epidemic, as he had already noted in the letter to


the Times. In essence, Snow was arguing the statistical principle that random mis-classification biases towards the null.32 He thought it worth emphasizing this differ-ence in calculated cholera mortality because sanitarians could point to Simon’s lowerfigure as confirmation that impure water was only a predisposing factor. A six-folddifference overall (and even higher during the early weeks) was more consistent withtrue causation.

Although Snow never objected in public to Simon’s unwillingness to credit himfor the original investigation of the south London water supply, a handful of Snow’sfriends in the sanitary movement did so on his behalf. At the 1856 meeting of theBritish Medical Association held in Birmingham, Dr. T. Bell Salter presented an ad-dress, “A summary of our present knowledge of the laws of epidemics.”33 BenjaminW. Richardson created an opportunity to support his friend, proposing (as recordedin the minutes)

“That the cordial thanks of the meeting be given to Dr. Bell Salter for hislearned address.”

In proposing this vote, Dr. Richardson was anxious to state that the au-thor of the paper had, as he thought, made an accidental omission in speak-ing of the Report of the Board of Health on the influence of the Southwarkand Vauxhall water supply on cholera, in the last epidemic of that disease inLondon. It was well known to all who were acquainted with the subject inits fulness, that the discovery of the connexion between water supply andcholera in no way belonged to the Board of Health, but exclusively to one ofour own associates—Dr. John Snow. [Hear, hear.] The Board of Health had,indeed, up to a late period, ignored to a great extent this important ques-tion; and it was not until Dr. Snow had, with unwearied industry, with thattrue genius for observation which so characterises his labours, and at greatpecuniary cost, placed the question beyond dispute, and had been secondedin this respect by Dr. Budd of Bristol, that the Board took up the mat-ter. . . . The Report itself was nothing more than a corroboration of Dr.Snow’s important and original views; and he (Dr. Richardson) thought it byno means fair that, while the views of other men were referred to, the claimsof our associate were entirely overlooked. [Hear, hear.] He thought it was buthonest to put the meeting fully in possession of these facts; and regrettedthat he should have been obliged to digress from the simple business of pro-posing the resolution placed in his hands.

Dr. Lankester seconded the resolution. . . .Dr. Budd said he could not let the occasion pass without expressing his en-

tire concurrence in the remarks . . . from Dr. Richardson. . . . He consid-ered the [GBH] Report decidedly unfair. He had himself laboured at the sub-ject of the diffusion of cholera by means of water, and by the excreta of cholerapatients; but he was proud to have that opportunity of stating, that the entire


priority of this inquiry rested with Dr. Snow. [Hear, hear.]. . . . Certainly, inregard to the spread of cholera by water, [the GBH] had only declared an opin-ion when the question had been satisfactorily proved by others; and he re-gretted exceedingly to see that Dr. Snow’s great labours had been so completelyunrecognized. [Hear, hear.]

The motion was carried unanimously.34

This occasion may have been the only time in Snow’s lifetime that his study of cholerareceived a “Hear! Hear!” from a medical audience.

Later Cholera Writings

After the 1856 article that finalized his south London study and commented on Si-mon’s report, Snow published seven more items on cholera. One article (and a follow-up letter) discussed a neighborhood-level cholera outbreak in Abbey-row, West Ham.He made personal inquiries into the layout of the dwellings, water supply, and drainage.At the time of the outbreak, 115 inhabitants received their water supply from one pumpin the middle of the row of houses. According to the inhabitants, “The impurity of thewater of this pump-well was a chronic affair, and therefore, as mere impurity, wouldnot account for the remarkably sudden and circumscribed outbreak of cholera whichhas occurred around it. Moreover, mere impurity in the water was never known tocause, or even aggravate, cholera. In all the sudden outbreaks of cholera which I havebeen able to connect with impure water, and have related in previous volumes of thisJournal [MTG], and the two Journals from which it sprung [LMG and MT], there hasalways been either absolute proof or strong presumption that the evacuations of acholera patient had entered the water.”35 In addition to this aside at the expense of thesanitarian obsession with all impure water, Snow explained how the evacuations froma cholera patient in one of the houses could have seeped into the pump-well and spreadit to other inhabitants of Abbey-row. He counseled patience to anyone who expecteda documented index case and cited an example of delayed confirmation: “In the fear-ful outbreak of cholera near Golden-square, . . . I could myself only bring forwardstatistical and other evidence of the effect of the water, not having the power to openthe well and adjoining drains; but when this was done by the parish authorities, at thesuggestion of the Rev. Henry Whitehead, six months afterwards, the pump-well whichcaused the outbreak was found to be the recipient of the overflow from a cesspool,into which the evacuations of a child ill of cholera had been emptied within three daysbefore the great irruption of the disease.”36 Nonetheless, the British Medical Journalpublished an article in which the author accused Snow of presenting a tendentious in-terpretation of the outbreak. Snow responded firmly: “I should like to say,” he wrotein a letter to the editor, “that I have not clipped or shaped this outbreak of cholera tofit the bed I had made for it; on the contrary, it came and shaped itself exactly to the


conclusions which I had drawn from the observance of previous epidemics.”37 There-after, he clarified facts relating to this incident that he considered indisputable, re-hearsed parallel examples he had described in earlier writings, and noted the recentchanges in the water supply of London that made future epidemics at the metropoli-tan level unlikely: “At present no water company draws its supply from any part of theThames which is within reach of pollution by the shipping, or the sewers of the town.”38

Consequently, any cases of cholera introduced from outside London were unlikely tocascade to epidemic proportions. Nonetheless, he “beg[ged] the reader to rememberthat, although I find it necessary to write most on that part of the subject which con-cerns the communication of cholera through the medium of water, its propagation byswallowing the morbid poison without this medium, plays a very important part inits progress, more especially in the crowded habitations of the poor.”39

On three occasions Snow used the medical journals to assert his priority overWilliam Budd in developing a new theory about the mode of communication ofcholera. The first (in December 1855) was a letter to the editor of the EdinburghMedical Journal in which he took issue with Dr. William Alison’s statement that “Dr.Budd of Bristol” was the first to propose “the communication of cholera by dejec-tions.”40 Snow noted that MCC was published in advance of Budd’s essay and that Budd had already “made a full and handsome acknowledgement of my priority. . . .”41 However, the editor appended a note to Snow’s letter: “his theorythat it is chiefly or almost exclusively by swallowing that the poison of cholera istaken in, can scarcely be supposed.”42 Alison’s article apparently prompted Sir JamesKay-Shuttleworth to make a similar misattribution in the Association Medical Jour-nal. Snow read it the day it appeared, and he was again quick to respond, sending aletter of correction that included verbatim phrases from the letter he had sent to theEdinburgh Medical Journal. In the process he distanced himself from Budd’s will-ingness to consider multifactorial explanations for “the propagation of cholerathrough the air, by means of the excretions,” and conditional acceptance “that somekind of change or fermentation is necessary in the peculiar excretions of cholera toenable them to propagate the disease.”43 Otherwise, he and Budd were in completeagreement on the pathology and mode of communication.

The last publication of Snow’s life, published only weeks before his death, was atwo-part paper that gives a picture of where Snow’s thinking might have gone hadhe lived longer.44 After reviewing much familiar material on the relation of the wa-ter supply to cholera and repeating his disagreement with sanitarian and local mi-asmatic reasoning, he examined the relation of water supply to overall mortality. Themetropolitan part of the county of Surrey corresponded quite closely to the south-ern reaches of the water supplies of the Lambeth and S&V companies. In July 1855S&V had established a new water intake at the village of Hampton, remote from thesewage of London. Leaving out the cholera years (from July 1853 to December 1854),Snow tabulated total mortality in metropolitan Surrey and in the remainder of Lon-don before and after this change. He found that mortality in Surrey, consistently


higher than in the rest of the metropolis before S&V changed its supply, droppedbelow average in the succeeding two and a half years. Even greater relative reduc-tions were apparent if attention was paid to deaths from diarrhea and typhus.45 Heconcluded the article with a disquisition on water closets, which he considered athreat to public health. Flushing required enormous quantities of water, often forc-ing towns to tap the very rivers into which the sewage was drained. If water closetswere to be continued, Snow advised the development of separate water supplies—one for flushing, in which purity was not an issue, the other for drinking water,drawn from pure sources.46

Snow, Public Health, and Social Class

Whereas most of the London sanitarians came from the middle classes, Snow’s ori-gins were in the laboring classes. Strikingly absent in his writings on cholera is anymention of the ostensibly “vicious habits” of the poor mentioned by some of his col-leagues. Nothing he wrote or said in a medical society meeting approximates Chad-wick’s conclusion that “adverse circumstances [poverty] tend to produce an adultpopulation short-lived, improvident, reckless, intemperate, and with habitual avid-ity for sensual gratifications.”47 Unlike most sanitarians, Snow did not incriminatedrinking as a predisposant to cholera, even though he was a teetotaler. While Snowacknowledged that cholera could spread rapidly through the slum neighborhoods ofLondon and Glasgow, he never attributed this fact to moral degeneracy of the vic-tims. Instead, he pointed out that the residences of the lower classes were poorly lit,making it difficult to notice contamination, and that they lacked sanitary facilitiesfor hand washing. Moreover, cholera could spread like wildfire in a mine not be-cause the miners were poor, but because the owners did not provide them separatefacilities in which to defecate and consume their food. Long shifts forced them toeat some meals underground. One of the simplest ways to prevent cholera in mines,therefore, was to reduce the length of the shifts so food need not be taken below(PMCC, 929).

Snow gave further evidence of his concern for public health problems among thepoor in an article on rickets in children. At his death his thinking on the subject wasstill preliminary, but it is evident that he intended to attack this problem with meth-ods similar to those he had used to study the transmission of cholera. The begin-ning of the article is typical Snow: He established the prevalence of rickets, the suf-fering it was causing, and its tendency to afflict children from the disadvantagedclasses. Next he offered an epidemiological observation: Rickets was less prevalentin urban areas of the north of England than in metropolitan London, even whereovercrowding and sanitary conditions were equally bad. What causative factor, hewondered, was present in the south of England but not in the north. As was his in-clination, he looked first for a chemical explanation: “[I]n rickets the phosphate of


lime in the bones is known to be deficient.”48 One possibility, therefore, was that in-fants in London received less of this vital nutrient (calcium phosphate) in their di-ets, but Snow rejected it because milk was just as often in short supply in the northas in the south. He had suspected for some time that the bread eaten by Londonerswas less than ideal. A report by Liebig in which the chemist showed that phosphoricacid forms a very stable compound with alumina turned Snow’s attention to a com-mon practice among bakers of adulterating bread with alum. In the north of En-gland, however, where coal was cheaper than in the south, many poor and laboringfamilies baked their own bread using flour that contained no alum. Here was a ge-ographical difference that might explain why so many children in London developedrickets: The alum in their bread interacted with phosphate of lime to form sulfateof lime and phosphate of alumina, neither of which provided the necessary nutri-ents for growing bones.

“The subject is capable of being decided by an exact numerical investigation,” andSnow imagined a natural experiment comprised of two large orphanages, or similarinstitutions, one of which served homemade bread and the other serving its wardsadulterated bread from a local baker. So far, every institution he had consulted saidit used only bread containing alum. He had heard, however, of two towns in Corn-wall situated a few miles apart in which the inhabitants of one generally purchasedtheir bread from commercial bakers, whereas townsfolk in the other baked their own.Supposedly, rickets was absent in the latter town but prevalent in the former. “[B]utas my inquiries have been only of a colloquial nature, I hesitate to mention placesand persons.”49 Perhaps with the critics of his cholera theory in mind, he immedi-ately offered a caveat to his hypothesis on rickets in children: “It does not follow, ifmy conclusions are correct, that every child eating bread adulterated with alum oughtto have rickets, or that every child fed with good bread ought to be free from thecomplaint.” Children fed bread containing alum might obtain adequate calcium fromother parts of their diet, while some children fed homemade bread could be sicklyand unable to absorb nutrients adequately. Probabilistic evidence, not certainty,would be the most that anyone should expect. As he had done on several other oc-casions, he decided to publish his hypothesis before he had the desirable confirma-tory evidence in the event that others would find it instructive and pursue it further.On that basis he offered suggestions for testing the alum content of bread.50

Snow in some ways resembles another group of public health reformers of theearly nineteenth century—physicians, mostly Scottish, who sought the causes of epi-demic and zymotic diseases in destitution, factory work, and other evils of the cap-italist industrial revolution rather than in the filthy habits of the poor. William Ali-son of Edinburgh was perhaps the leading advocate of this point of view and hasbeen described by Hamlin as having provided a “medical critique of industrialismand capitalism the like of which did not appear until the twentieth century.”51 InObservations on the Management of the Poor in Scotland, and its Effects on the Healthof Great Towns (1840), Alison was skeptical of a purely miasmatic interpretation of


fever and expressed sentiments similar to Snow’s in 1855, when he dismissed the im-portance of “dead animal and vegetable matter” in his testimony before the selectcommittee investigating the nuisance trades. Hamlin has documented that severalother writers, including William Tait of Edinburgh, Alexander Tweedie of London,and William Budd, expressed similar viewpoints in the 1840s. Hamlin also notes thatChadwick stripped such radical content from the reports submitted by medical menin Scotland and Ireland before including them in his own Report on the SanitaryCondition of the Labouring Population.52 By comparison, Snow never developed asystematic critique of industrialism. His critique of the sanitarians was made on sci-entific grounds only.53

Sanitary Reform in 1858

While the sanitarians of the era from 1830 to 1850 relied on a miasmatic theory ofdisease causation and spread, sanitary reform was not logically tied to it. Actually, anew scientific model was emerging during the last years of Snow’s life, although fullacceptance of his theories by the public health establishment would not come formany years. In part, acceptance of a new model reflected the success of Farr’s zy-motic theory. Farr had gradually shifted toward the view that specific “ferments”could produce specific diseases. As zymotic theory gained ascendency, Snow was nolonger such an outlier in insisting that cholera was caused by a particle or agent spe-cific to that disease. The demise of miasmatic reasoning was also hastened by thesummer of the Great Stink. In June and July of 1858 a horrible stench emanatedfrom the Thames, but there was no outbreak of epidemic diseases. Chadwick’s no-tion that stench equaled disease could not survive such a dramatic disproof. For allthe lack of credit Snow received during his lifetime, his work was part of the evolu-tion in sanitary thinking and hastened the day when sanitary reform could be placedon a more modern scientific footing.54

Notes

1. “The plain truth of the matter is that is that in 1875, the death rate stood at almostexactly the same level as it had in 1838 when civil registration began and Chadwick first sent his poor law medical investigators into the London slums. . . . Infantmortality . . . scarcely began to fall before the end of the century”; Finn, “Introduction”to Sanitary Reform, 7.

2. Hamlin emphasizes the essential conservatism and pro-industrialism of Chadwick andmost sanitary reformers; see Public Health and Social Justice in the Age of Chadwick, and “JohnSutherland’s Epidemiology of Constitutions.”

3. Baldwin, Contagion and the State, 127-29, and Worboys, Spreading Germs, 31–37. “Healthand disease were seen as consequences of the total environment. The conditions of city life—


the stale and vitiated air, the uncleanliness, crowdedness, alcoholism, poor food and foul wa-ter—acted collectively to undermine health; the combined effect of all these ‘predisposingcauses’ was virtually the disease itself”; Hamlin, Science of Impurity, 106. According to W. M.Frazer, the sanitarian idea was rooted in “the principle that the material environment exer-cises a profound effect on the physical, and indeed, the mental well-being of the individual”;Frazer, History of English Public Health, 15.

4. In a speculative vein, in CMC (1853) Snow suggested that several other diseases besidescholera might be spread by the fecal–oral route and by contaminated water. It was not untilthe very end of his life, however, that Snow claimed to have evidence that cleaning up drink-ing water could prevent other diarrheal diseases and not cholera only; “Drainage and the wa-ter supply in connexion with the public health” (1858).

5. Several contemporary historians and epidemiologists believe that the sanitarians’s mul-ticausal view of public health has much to recommend it to a modern temperament, whereasSnow’s focused researches sometimes seem less appealing. This was Pelling’s main point in comparing Snow’s “exclusivity” unfavorably to Budd’s “inclusivity” within the context ofnineteenth-century medicine; Cholera, 275–81. Hamlin generally agrees with this assessment;Science of Impurity, 107. Likewise, Eyler compares Snow unfavorably with Farr: “Judged by thestandards of his time Snow was the dogmatic contagionist and premature reductionist”;“Changing assessments of cholera studies,” 230. Another way to interpret the schism betweenSnow and his sanitarian contemporaries is to note that whereas they argued that the socialenvironment could increase cholera incidence by “lowering general health,” his theory pro-posed that social environments determined “patterns of exposure”; Davey Smith, “Behind theBroad Street pump,” 929.

6. The MCS established in 1848 was an amalgamation of seven autonomous commissionsof sewers (with a total of 1,065 commissioners) in existence since the days of Henry VIII. Par-liament extended MCS authority over drainage and house construction in London and itssuburbs. On the history of London sewage generally, see Trench and Hillman, London underLondon, and Halliday, The Great Stink of London.

7. Bazalgette, Metropolitan System of Drainage, 6.8. The water closet was first invented in the seventeenth century by Sir John Harington, re-

fined in the eighteenth century by Alexander Cummings and Joseph Bramah, and developedinto its modern form by Hopper and Crapper in the nineteenth century. Trench and Hillman,London under London; Halliday, Great Stink of London.

9. Trench and Hillman, London under London, 65. Hamlin has more sympathy for Chad-wick’s sanitary program. Chadwick was no supporter of sewage-contaminated water and even-tually envisioned a London water supply drawn from pure sources other than rivers, as wellas the recycling of sewage. The problem was that one part of the sanitarian agenda could beaccomplished quickly (flushing sewage into the Thames) while the other part (supplying puredrinking water) was still decades away; personal communication. But Hamlin also shows thatin 1850 Chadwick was relatively more concerned with the hardness of London water and lesswith the degree of organic contamination from sewage; Science of Impurity, 108.

10. Snow, “On the communication of cholera by impure Thames water” (1854), 366.10a. UK HoC, “Select committees on medical relief and public health,” 328–30.11. The key portions of Snow’s testimony and the Lancet’s critique are reprinted in Lilien-

feld, “John Snow: The first hired gun?” See also Vandenbroucke, “Invited commentary: Thetestimony of Dr. Snow,” and Sandler, “John Snow and modern-day environmental epidemi-ology.” Interestingly, these modern epidemiologists largely echo the Lancet’s position. The lat-ter two authors see Snow’s opposition to miasmatic effects of disease as evidence of narrow-mindedness, Sandler citing his lack of evidence for the innocuousness of factory fumes and


Vandenbroucke his “unreasonableness.” The three authors fail to distinguish between toxicfactory exposures as causes of chronic diseases of the twentieth century and as agents of theepidemic communicable diseases during the nineteenth.

12. Editorial, Lancet 1 (1855): 635.13. Snow, “On the supposed influence of offensive trades on mortality” (1856). Snow did

express dismay at the manner in which the medical press characterized his Parliamentary tes-timony; [Open] Letter to the Right Hon. Sir Benjamin Hall (1855).

14. A fellmonger was a dealer in skins or hides of animals, especially of sheep.15. “On the supposed influence of offensive trades on mortality,” 96. Snow also could not

resist telling the reader that in two London subdistricts full of nuisance trade establishmentsbut supplied with sewage-free water, there were hardly any cholera deaths in 1853 or 1854,while in two districts almost totally free of nuisance trades but supplied with sewage-con-taminated water, the death rate had been much higher.

16. Lancet 2 (1856): 139–40.17. John W. Tripe was a member of the London Epidemiological Society and is listed, along

with Snow, as having taken part in the discussion of a paper on cholera in the Baltic fleet byBabington; “Influence of offensive trades on health,” Lancet 2 (1856): 177, and Babington, “Onthe cholera which visited her majesty’s Black Sea fleet in the autumn of 1854,” Lancet 2 (1856):225–26.

18. Farr had provided in 1852 an open-minded review of several cholera theories, includ-ing those, such as Snow’s, that were not miasmatically based. Farr on that occasion referredto Snow’s theory as “in many respects the most important theory that has yet been pro-pounded” and endorsed Snow’s preventive recommendations; Farr, Cholera Mortality in En-gland, 1848–49, lxxvi. However, the only theoretical contribution in the 1855 Board of HealthScientific Appendix, by Neal Arnott, considered solely the miasmatic perspective and focusedits recommendations on ventilation and air exchange: “[O]bservation has now clearly ascer-tained that the travelling morbific cause, whatever it may be, can no more produce a truepestilence, unless it meet with much filth of decomposing animal and vegetable matters—ofwhich air which has served for respiration is one kind—than coal gas can produce an explo-sion without being mixed with many times its volume of common air. . . . It thus appearsthat the ravages of Cholera may be prevented, by preventing the local accumulation of or-ganic impurities”; Arnott, “Memorandum on Asiatic cholera and other epidemics as influ-enced by atmospheric impurity,” in UK GBH, Report of the CSI, appendix, 168.

19. UK GBH, Report of the CSI, 48.20. UK GBH, Report of the CSI, 52. The dates of publication suggest that the CSI did not have

access to the St. James Cholera Inquiry Committee report, and especially Whitehead’s findings,when their own report was written, although it is unclear whether that would have changedtheir opinions in any way. For more on the CSI report see Paneth et al, “Rivalry of foulness.” Bycontrast, Snow’s theory received a somewhat kinder reception from another quarter. MCC2 andthe CIC report were reviewed together in the Lancet 2 (1856), 524–25, with the anonymous re-viewer disagreeing on several points with Snow but stating that “these books must exert con-siderable influence on sanitary reform, and in fact prove the position, hitherto scarcely demon-strated, that zymotic diseases are, to a certain extent, removable by sanitary measures.”

21. The paper was later published as “Further remarks on the mode of communication ofcholera” (1855).

22. Ibid., 32. When contrasting the cholera theories of Snow and the sanitarian John Suther-land, Hamlin argues that “to explain cholera among those who have not consumed the wa-ter, one can posit supplementary modes of transmission through person to person contact orfomites,” and attributes this strategy to Snow; Hamlin, “John Sutherland’s Epidemiology,” 918.


In doing so, however, Hamlin reverses the order of Snow’s logic; person-to-person transmis-sion by the fecal-oral route is the fundamental route of transmission, public water suppliesonly one means of its extension. Thomas Snow understood his brother’s theory quite well andasked readers of the Times not to be misled by commentators who claimed that it limited thespread of cholera to waterborne transmission; “Propagation of Cholera,” Times (26 Septem-ber 1885), and “Dr. Snow on the Communication of Cholera,” Times (20 November 1885).

23. UK GBH, Letter of the President (1855), 40.24. Snow, “Further remarks on the mode of communication of cholera,” 84.25. Ibid., 34.26. Ibid., 35.27. Snow’s name for the report; see “Cholera and the water supply in the south districts of

London in 1854” (1856), 245.28. Snow wrote in MCC2, “[N]o experiment could have been devised which would more

thoroughly test the effect of water supply on the progress of cholera. . . . The experimenttoo was on the grandest scale. No fewer than 300,000 people of both sexes, of every age andoccupation, and of every rank and station . . . were divided into two groups . . . one groupbeing supplied with water containing the sewage of London, and amongst it, whatever mighthave come from the cholera patient, the other having water quite free from such impurity”(75). Simon’s language a year later was, “An experiment . . . has been conducted during twoepidemics of cholera on 500,000 human beings. One half of this multitude was doomed inboth epidemics to drink the same faecalized water . . . while another section—freed in thesecond epidemic from that influence which had so aggravated the first, was happily enabledto evince . . . the comparative immunity which the cleanlier beverage could give”; Simon,Report of the Last Two Cholera Epidemics (1856), 9.

29. An MTG editorial reported favorably on Simon’s report and rehearsed conclusions thatalso supported MCC2, but the journal would not give Snow’s “hypothetical views” an un-qualified endorsement because he did not consider effluvial infection a cofactor; “Impure wa-ter a source of disease,” MTG 13 (1856): 15–16. See also the article on Simon’s report; Times(25 June 1856).

30. Snow, “Cholera and the water supply” (26 June 1856).31. While Simon had possession of the subdistrict data that Snow had been unable to ob-

tain for the previous two years, he did not preempt Snow in carrying out any sophisticatedpredictive modeling using those data and made no particular statistical use of them in hisown report.

32. On the random misclassification principle, see McMahon and Trichopoulos, Epidemi-ology, 248; Kelsey, Thompson, and Evans, Observational Epidemiology, 294; Brownson and Pe-titti, Applied Epidemiology, 53. Snow phrased it thus: “For these reasons it follows that, in com-paring the lists of the water supply with the list of deaths, many errors must have occurred;and as the deaths were six times as numerous in the houses supplied by the Southwark andVauxhall company as in those supplied by the Lambeth company, the evident result would bethat out of every six mistakes, five would transfer a death from the former company to thelatter, and only one would transfer a death from the latter company to the former”; “Choleraand the water supply in the south districts of London in 1854” (1856), 249.

33. The Provincial Medical and Surgical Association changed its name to the British Med-ical Association at this meeting.

34. “Twenty-fourth annual meeting of the British Medical Association,” AMJ 4 (1856): 683.Budd took issue with the reporter’s accuracy in a letter to the editor two weeks later. He claimedthat he had not, at the Birmingham meeting, referred to his own work on cholera at all buthad simply wished to assert the priority of “Dr. Snow’s admirable, long prior, and entirely


original researches” over any claims by Simon and the GBH; Budd, “Dr. Snow and the Boardof Health,” AMJ 4 (1856): 730.

35. Snow, “On the outbreak of cholera at Abbey-Row, West Ham” (1857), 418.36. Ibid.37. Snow, “On the origin of the recent outbreak of cholera at West Ham” (1857), 934.38. Ibid.39. Ibid., 935.40. Snow, “On the mode of communication of cholera,” (1856), 668.41. Ibid., 669.42. Ibid., 670.43. Snow,“The mode of propagation of cholera,”(1856). He sent a similar letter to the Lancet

after it published Kay-Shuttleworth’s address; it was published under an identical title to theone in AMJ.

44. Snow, “Drainage and water supply in connection with the public health” (1858).45. Typhus is not water-borne, but Snow points out that cases of typhoid fever were in-

cluded in this category.46. Snow indicated that his preferred solution was rather to recycle the human waste as

agricultural manure, which was impractical if it was diluted with large quantities of water. Heapparently did not consider the possibility that agricultural use might also lead to the spreadof disease.

47. Chadwick, Report on the Sanitary Condition of the Labouring Population, 370.48. Snow, “Adulteration of bread,” 4.49. Ibid., 5.50. To prevent adulteration it was essential to have an accurate chemical test for the pres-

ence of alum in bread. Snow described the method used by his microscopist–sanitarian ac-quaintance Hassall that involved incinerating the bread and testing the ashes and warned thatthe failure to use that method would result in underdetection of alum. Four months after hispaper appeared Snow sent a letter to the Lancet calling attention to evidence by a Belgian re-searcher that supported his hypothesis; “The adulteration of bread as a cause of rickets” (1857).

51. Hamlin, Public Health and Social Justice, 81.52. Ibid. Tweedie was Southwood-Smith’s senior at the London Fever Hospital, while Kay-

Shuttleworth had studied with Alison, who was sympathetic to the water supply hypothesisin the broader formulation he attributed to Budd.

53. Snow’s work could have provided strong support for the more radical public health per-spective then in circulation among the Scottish physicians, but there is little evidence that thetwo streams of thought ever converged.

54. On the importance of the Great Stink and the evolution in the scientific base for sani-tarianism, see Hamlin, Science of Impurity, 128–32. Hamlin seems ambivalent as to whetherSnow actually helped to bring this change about or merely reflected the changes occurringaround him. See also Wohl, Endangered Lives, 81, 247, 251.


JOHN SNOW MAY HAVE BEEN THE FIRST physician to “spe-cialize” in anesthesia.1 In principle if not always in practice, his ap-

proach mandated that anesthesia should be performed by a trained physician ex-clusively dedicated to its safe administration. A surgeon or dentist operating on apatient had too much to do to take on the responsibility of inducing, monitoring,and reviving the chloroformed or etherized patient. In the 1850s surgeons began per-forming longer and more complex procedures that could not have been done with-out anesthetics. Surgery without pain made surgery both more popular and morecommon. Procedures that were formerly an excruciating last resort—amputations,removal of tumors, abdominal surgery—were now offered and performed routinelyand repeatedly. Snow worked frequently with William Fergusson, an early practi-tioner of conservative surgical interventions (such as excision of joints or removalof dead bone tissue) that would have been impossible without anesthesia. During aspan of five Saturdays in the autumn of 1848, Snow gave chloroform four times toone little boy for repeated surgeries on an “un-united fracture” of the humerus re-quiring resection (CB, 22–26).2 Such a series of procedure would have been unimag-inable two years earlier. Looking back on the impact of chloroform on surgery, Snowcommented in On Chloroform that surgeon–patient relations were fundamentally al-tered because the surgeon could now obtain “the ready assent of his patient” formany painful operations in which previously “it would either not be obtained at all,

359

Chapter 14

Further Developments inAnesthesia

or not at the most favorable time.” Chloroform also made pediatric surgery possi-ble: “Many operations take place in children which could not be performed in thewaking state” (OC, 263).3 Snow administered chloroform to children as young aseight days old and participated in dozens of infant surgeries, especially for repair ofharelip.

The symbiotic relationship between surgery and pain relief naturally led to in-creased demand for anesthesia. In 1849, the first full year in Snow’s extant Case Books,he administered chloroform in roughly 250 cases. By 1857, the last full year on record,he logged roughly 550 cases, and he was on track in June 1858, when he suffered hisfatal stroke, to reach more than 600 cases. Today, when we think of specializing weoften imagine a narrowing of medical experience to a more uniform type of patient,but Snow’s specialization brought him into contact with all kinds of patients andconditions. His was something of a superpractice in which he traversed the me-tropolis of London seeing the complete range of patients and conditions, from thequeen to the chimney sweep to the stable-boy, from breast cancer to strabismus tovenereal warts to delirium tremens.

Going Under: The Vagaries of the Organism

Through chloroform Snow had become more intimately acquainted with the natureof pain and its relation to degrees of unconsciousness than any man in London. Painrequires a more or less orderly consciousness. Once the mind becomes disorganizedthe usual signs of pain take on ambiguity. In a waking state cries and flinching aresure signs of discomfort. Under anesthesia these signs might indicate that sensation,neural activity, and consciousness are returning but are not necessarily experiencedas pain. Sometimes chloroform functioned like posthypnotic suggestion, erasing allmemory of the operation; at other times it had no such effect. Some patients, uponrecovering from surgery, inquired as to when the operation would begin. Other pa-tients, although clearly under the influence of chloroform, would, in the most rea-sonable way imaginable, and without flinching or stirring, request that they be givenmore chloroform.

Snow is remembered as a systematic thinker, a man who cleverly calculated bloodsolubility ratios for anesthetics and laid out with great precision the degrees throughwhich the anesthetized body travels. But the study of anesthesia reveals the unpre-dictability of the human organism. In his Case Books, therefore, Snow provides arecord that points not only to the laws of these powerful agents but to the vagariesof human experience. The microphenomena of the hypnagogic states he recordedseem unexplainable by physiology; they can be glossed only as the fugitive reactionsof the disorganized consciousness, the random effects of chloroform on the humansubject. That Snow fashioned a rational system to gauge and categorize the phenomena of anesthesia testifies to his diagnostic acumen and his skill at


building models. That he handled so many cases so well speaks to his ability to handle uncertainty and unpredictability on a practical level, to balance phenomenaand epiphenomena.

Anesthesia also suited his temperament. His utterly sober demeanor was perfectfor the Victorian period, especially as it would become his calling to dispense nar-cotic inhalants and thereby control consciousness. One feels this love of control inSnow’s discipline, in his abstemious habits, in his knowing remarks about a patient’signorance that an operation had taken place, even in his preference for fast-actingchloroform. His temperance sprang from a desire for bodily self-possession unal-loyed by piety or faith, which was relatively unusual for the era. When Snow tookanesthetics or even alcohol (when exploring its anesthetic properties or using it med-icinally), it was in the name of science. Throughout these autoexperiments he staredintently at his stopwatch until the hands disappeared or he lost consciousness. Hemade a point of recording his observations the moment he recovered, exerting theforce and will of his mind over the volatile matter. It was no accident that JamesClark tapped Snow to give chloroform to the queen—there may have been no safer,more prepossessing, more self-controlled individual in all the kingdom.

Snow observed, but did not interpret, the anesthetized mind and body:

There is generally a sense of dizziness, with singing in the ears and tingling inthe limbs. Many persons have a feeling like that of rapid travelling, and as anappearance of darkness sometimes comes on from the failure of the sight,whilst there is also a loud noise in the ears, it not infrequently happens that aperson feels as if he were entering a railway tunnel, just when he is becomingunconscious. . . . In the second degree of narcotism, there is no longer cor-rect consciousness. The mental functions are impaired but not necessarily sus-pended . . . [the patient] usually appears as if asleep . . . but if his eyelidbe raised, he will move his eyes in a voluntary manner. There are occasionallyvoluntary movements of the limbs; and although the patient is generally silent,he may nevertheless laugh, talk, or sing. Persons sometimes remember whatoccurs whilst they are in this state, but generally they do not. Any dreams thatthe patient has, occur whilst he is in this degree.

OC, 36–37

He thought that people tended to react differently to chloroform, and there is classand gender inflection to his explanations for the wide variety of behavior he en-countered as people went under. He felt that “brain workers”—people with culti-vated mental faculties—retained their consciousness longest, whereas “certain navi-gators and other labourers” no sooner took a whiff than they would “get into a riotousdrunken condition.”“Hysterical females” would very quickly start to dream (OC, 36).Chloroform could reveal the nature of one’s upbringing. Snow’s experience indicatedthat patients who had been treated kindly were highly suggestible in the early stages

Further Developments in Anesthesia 361

of chloroform. If such patients grew restless, as they often did, “a few kind words”might calm them and render them “tractable,” but had they been used to harsh treat-ment from birth, they would commonly require “a little restraint.” This differenceseemed often to fall along sex lines. Women were raised with kindness and care; menwere more likely to have been brutalized from a young age (OC, 38). Chloroformmight thus reveal glimpses of the harshness of growing up in Victorian London.

As chloroform seemed to provide a means of identifying, or at least confirming, aparticular type of patient, particularly the “hysterical female,” it could also be used bySnow to delve into obscurities of hysterical paralysis as a diagnostic category. Thismight mean using chloroform to detect feigning. Snow recorded a case from Decem-ber 1851 involving a servant of the marquis of Cholmondley, a young woman whohad been in bed in Charing Cross Hospital for two months. She “kept her left knee ina semi-flexed position, and would not allow it to be moved.” Reluctantly, she inhaledthe chloroform. Once unconscious, she exhibited the telltale symptoms of hysteria, fit-ful breathing and sobbing. As unconsciousness deepened the leg “went down flat onthe bed, the knee being quite moveable.” While the leg was unbent, the doctors boundthe leg with a splint to keep it straight. A few days later the bandages grew slack, butSnow was skeptical. He thought the patient “contrived to get her leg bent again. Shewas the domestic servant of a nobleman. It was evident that there was nothing thematter with her limb, and that it was only influenced by her volition, which was per-verted by the hysteria under which she was labouring” (OC, 339; CB, 209). In anothercase an unmarried woman was suspected of feigning paralysis in the left arm and legand the inability to speak. She communicated by nodding or writing on a slate. Un-der chloroform she, too, “breathed in a sobbing and hysterical manner.” Her right sidemoved a great deal as well as her left side and limbs, but much less so. Her jaws re-mained firmly closed, but Snow opened them with his fingers, prying with “a moder-ate degree of force.” The chloroform was allowed to wear off and was given again withsame results, and a cork was slipped in between her teeth in an attempt to keep hermouth open. Somehow the cork slipped out. The patient did not open her eyes or an-swer questions for six days. When Snow raised her eyelid on the seventh day, “sheturned her eye about, as if endeavouring to hide the pupil under the lid.” The next dayshe answered questions by nodding her head or writing in chalk. Snow concluded thatthe patient truly believed her limbs were actually paralyzed. “I looked on the womanas a sick person, and not a mere impostor; for although she appeared to exaggerateher symptoms, and to have a good deal of pretence and affectation, this circumstancearose, no doubt, from her complaint” (OC 339–41; CB 204). The mixture of skepti-cism and credulity, sympathy and force, in Snow’s dealings with hysterical patients tes-tifies to Snow’s belief in chloroform’s power to reveal bodily states. It offered a way ofdrawing the line between mind and body. He regarded the first patient as deceitful be-cause she willed her body into a deformity, but he considered the second sick because,at the deepest stages of chloroform anesthesia, paralysis remained and provided physical basis for the patient’s belief.


Delirium, Tremors, Spasms

Snow recognized that anesthesia provided a model for other unconscious states. Notsurprisingly, the clinical picture of Snow presented in his Case Books reveals a will-ingness to make connections between narcotism and other physiological and men-tal phenomena. In July 1848 he attended a man in his neighborhood who had beenrun over by a cab. The man appeared to have a concussion, and Snow suggested that“he was in a state resembling the ‘second degree of narcotism’” (CB, 4). In “On nar-cotism” Snow had drawn analogies between anesthesia and alcoholic intoxication;now he used the degrees of narcotism to illuminate the nature and severity of men-tal confusion resulting from concussion.

In the stages of ether and chloroform anesthesia, when voluntary motion hadceased, it was common for some patients to experience trembling, spasms, rigidity,and, in rare cases, convulsions. Snow believed these reactions were especially likelyin “robust” individuals, people who were particularly fit or used to physical labor.Just as brain workers were more likely to retain consciousness longer under chloro-form, he believed that body workers, “where the muscles have been much exercised,”were more likely to exhibit disorganized nervous activity (OC, 39). This phenome-non was more common in men, in the active than in the sedentary, and in the leanthan in the fat. It was never found in infancy, rarely before puberty, and diminishedin frequency with age.

Chloroform seemed to both induce and abolish spasms, tremors, and delirium,and Snow frequently administered it in attempts to counter these symptoms. As earlyas May 1849 he gave chloroform with some success to a girl with epilepsy. The royalphysician, Sir James Clark, and James Todd, a colleague with special expertise intreating seizures, were in attendance. In April 1857 Snow gave ether and chloroformto a middle-aged surgeon and colleague, William Hooper Attree, over a ten-day pe-riod. Attree had been suffering for six years from “a spasmodic affection of the mus-cles of the right side of the neck which draws the head down to the shoulder” (CB,471). The anesthetics eased the spasms and put him to sleep, when Snow “pressedthe head over towards the other side as much as I could,” in an attempt to manuallycorrect what the spasms had deformed.

He gave chloroform to young children with laryngismus stridulus, a spasmodiccontraction of the laryngeal folds, with good success. He also gave it for cases ofcroup, whooping cough, and asthma (OC, 331–33). He tried it on patients in thethroes of delirium tremens. In December 1851 he gave chloroform to a forty-five-year-old silversmith, who had not slept for four days and had been placed in a strait-jacket. The man had become enraged, spitting out medicine, and violently castingabout. Snow took the silversmith’s pulse and found it rapid and weak. The man wasbathed in sweat. When Snow brought out the chloroform inhaler, the man objectedvehemently, but Snow compelled him to take it; soon he was unconscious. When theman awoke a minute or two later he was terrified, delirious, and convinced he was


being injured. Snow continued administering chloroform and kept the silversmithunder for more than a half hour. At the same time the attending doctors gave himspoonfuls of an opiate, which were easily swallowed despite the unconscious state.Snow stayed for another hour and fifteen minutes, observing the straitjacketed man,who was sleeping relatively peacefully. He woke totally free from his delirium but“had a slight relapse 2 or 3 days afterwards” (CB, 208). Snow could resort to forcein order to administer chloroform; it could be an agent of force, sleep, and reason,and in cases of delirium tremens, it was an effective inhaled sedative.

Alleged Fatality

Less than a week after treating the silversmith, Snow gave chloroform to Major Evans,a tall, heavy-set gentleman from Herefordshire. The man was seventy-odd years oldand had undergone the same procedure for lithotripsy three or four times in the pastyear. He had taken chloroform on these occasions, but this time Snow was particu-larly pleased with the outcome: “No sickness or other sequelae. The operation wasperformed before breakfast” (CB, 209). Ten days earlier, however, when Major Evanshad had a lithotripsy performed after breakfast with a different anesthetist admin-istering the chloroform, he “was very much depressed [syncope] a few minutes af-ter it” and vomited. Snow’s better anesthetic outcome seemed to vindicate his meth-ods. His liberal use of chloroform, even in patients like Major Evans, whom Snowsuspected “had disease of the heart,” was justified because the risk of chloroform wassmaller than the risk of performing surgery without anesthesia.4 Four days later,Snow and Caesar Hawkins, the surgeon, repeated the lithotripsy with identical re-sults, and the major returned to the countryside relieved of his stone. It was the samepatient, same surgeon, and same procedure done three times within two weeks. Inthe first instance the patient almost died, but in two others the operations wentsmoothly. The only difference was the anesthetist. It is no wonder Snow had confi-dence in his method.

However, Major Evans redeveloped bladder stones and returned to London for anoperation nine months later. He again consulted Mr. Hawkins, who asked Snow togive chloroform during yet another lithotripsy on this elderly man. This time, how-ever, things did not go well. The patient was anesthetized and all seemed normal un-til Snow observed that the patient’s face and lips were growing pale. Immediately, heallowed him to inhale air unmixed with chloroform for two minutes, at which pointthe major’s face reddened, and he began to strain as if “beginning to feel the oper-ation.” Snow gave him a little more chloroform, the patient taking two or threebreaths of it with the air valve one-third open. “He appeared to be merely holdinghis breath” (this sometimes happened with chloroform), and Snow felt sure he wouldbegin breathing again any second. When he searched for a pulse, however, he foundnone. He put an ear to Major Evans’s chest, but he heard nothing. Suddenly, the


patient took a deep breath, when Snow thought he heard some cardiac activity. Moresilence ensued, punctuated by a few feeble gasps. After thirty seconds all signs of lifeceased. Artificial respiration was performed to no avail. The postmortem examina-tion revealed “a good deal of fat” on the surface of Major Evans’s heart, thinning ofthe ventricular walls, and “a calcareous incrustation in one of the aortic valves.” Mi-croscopy revealed fatty degeneration of the heart’s fibers.5

Snow wrote a detailed case report, which was published in MTG on 10 October1852. The title, “Death from chloroform in a case of fatty degeneration of the heart,”suggested that Snow may have believed chloroform was the cause of death. But Snowwas in fact uncertain, and he signalled his intent in this paper to undertake researchas to “whether, in cases of presumed fatty degeneration of the heart, it is more de-sirable to give chloroform or ether,—to operate without anæsthesia, or to leave thepatient without surgical assistance.”6 Snow revisited the case three years later andsaid that although he had “thought it best at the time [1852] to designate the deathas one from this agent [chloroform],” he was now “by no means sure that this pa-tient died from the effects of chloroform.” He felt that the straining effort of the pa-tient while holding his breath may have caused death. “I am quite unable to tellwhether it was the effort of straining, or the influence of the chloroform,” he con-ceded.7 By the third iteration of this case, he had thoroughly exculpated chloroform.The posthumously published book On Chloroform contains a comprehensive inven-tory of every fatal case of chloroform inhalation reported through mid-1858, butSnow placed the Major Evans case in a section entitled “Alleged fatal cases of in-halation of chloroform.” “I am of opinion that this patient did not die from the di-rect effects of the chloroform” (OC, 208). George Pollock, the surgeon–anesthetistfor the first procedure when the major had fainted and then vomited his breakfast,witnessed the fatal operation. He concurred with Snow’s assessment that deathshould be attributed to heart disease rather than chloroform. In fact, Snow arguedthat the chloroform afforded relief that actually added months to this obviously sickman’s life (OC, 208–09). Snow had overcome his brief uncertainty about the safetyof chloroform.

Amylene

By November 1856 Snow had been working with anesthetics for almost ten years,and he had done almost all that a single individual could imaginably do with themin that span. He had developed inhalers for their controlled administration and cal-culated blood solubility ratios and safe mixtures of gas to air. He had laid out thephysical signs that accompany their use and published guidelines for safe usage ofanesthetics in dental and surgical operations and obstetrics as well as in the thera-peutic treatments of some diseases. He had used these agents in thousands ofcases, yet, although he had placed ether and chloroform among a wide spectrum of


anesthetic agents and had experimented with many other inhalants, from Dutch liq-uid to chlorated muriatic ether (ethyl chloride) to benzene, he had yet to introducean anesthetic agent that might supersede ether or chloroform. While confident inhis abilities to administer ether and chloroform safely in most circumstances, expe-rience and experiment had made Snow painfully aware of their shortcomings. Etherwas readily available and nonfatal in use, but it could be explosive and relatively slow-acting. Its pungency made it hard to inhale, and it generally caused expense, delays,and struggles with difficult patients. It frequently caused excessive salivation, spasmsin healthy athletic patients, and, most distressingly, vomiting, sickness, and disori-entation. Chloroform was much faster-acting than ether and less expensive to use,but it shared some of the latter’s unpleasant effects. Snow had calculated doses thatprovided a margin of safety, but he was increasingly aware that both ether and chlo-roform, especially chloroform, were capable of arresting breathing and paralyzingthe heart. He was determined to find a better anesthetic.

In the early months of 1857, he began to think he had found what he was look-ing for in the pentene hydrocarbon amylene. It had been discovered in 1844 in Paris,but Snow only learned of its existence in the fall of 1856. It had a chemical struc-ture similar to other agents he had studied. Introducing the agent to the Medical So-ciety of London, Snow explained that amylene was made from fusel oil (which con-tains amyl alcohol) and zinc chloride and that the chemical relation between amylene(C5H10) and amyl alcohol (C5H12O) was the same that “olefiant gas, or ethylene[C2H4], bears to common alcohol [C2H5OH].”8 Ethylene and amylene were both al-cohols stripped of a water molecule. Because Snow had long been aware of the anes-thetic properties of alcohol and olefin hydrocarbons, it was a good guess that theamyl form would possess similar properties. As he had done with all the other agentshe investigated, Snow put amylene through his own set of chemical and animal tri-als, establishing boiling points, blood-solubility ratios, and air saturation tables. Verylittle amylene had to be absorbed into the blood to produce insensibility. Snow ex-plained, however, that “when considered in relation to the quantity which is con-sumed during inhalation in the ordinary way, it is very far from being powerful.”Amylene’s “great tension and small solubility” made it difficult for the lungs to ab-sorb. Snow thought it resembled “the nitrogen gas of the atmosphere, with whichthe lungs are always four-fifths filled, while the blood contains but a few cubic inches.”Although amylene was more powerful than chloroform and ether, more of it wasneeded to create its effects. Snow thought this might be an ideal combination: a pow-erful agent that was hard to overdose because it was hard to absorb. Amylene seemedto promise the power of chloroform with the safe absorption levels of ether.9

Amylene possessed other advantages. It smelled like naphtha—some liked thissmell, others did not—but it lacked the pungency of ether and chloroform. Patientsdid not gag or choke upon first inhaling. Almost no rigidity or spasms occurred. InJanuary 1857 Snow administered amylene to a patient having plastic surgery on his nose who, a few weeks before, had received chloroform with a great deal of


“rigidity and struggling.”10 The anesthetic powers of amylene seemed to be strongeras well. Snow wrote that the “absence of pain has been obtained with less profoundcoma than usually accompanies the employment of ether or chloroform.” Patientswould wake up more quickly under amylene. Flinching and crying without any signsof consciousness were common signs that ether and chloroform were wearing off,but with amylene patients “have more frequently begun to look about and to speakbefore showing any signs of pain.”11 Perhaps most promising of all, amylene did notproduce excess salivation or sickness.

Snow was aware that the question of amylene’s safety was far from settled, and muchmore clinical experience would have to be obtained. Nevertheless, bringing it to publicnotice in this way was precisely the means to extend its clinical use; perhaps greater de-mand would spur chemists to produce it in greater quantities, thereby reducing its cost.Whatever doubts he may have had, he was very sanguine in the winter of 1857 thatamylene might answer to the disadvantages of ether and chloroform. He had a sensethat he was inaugurating a new era of medical discovery. He took a step he had nottaken with Dutch liquid or any other anesthetic agent he had worked with since chlo-roform, designing a new inhaler apparatus specifically for use with amylene.12

He began his first paper on amylene in January 1857 by rehearsing the history ofinhaled anesthetics, which appeared to his eyes to be largely an accidental affair. Heobserved that Humphrey Davy had brought the pain relieving properties of nitrousoxide to the public’s attention at the beginning of the nineteenth century, remark-ing that “it may probably be used with advantage during surgical operations in whichno great effusion of blood takes place,”13 but it took forty-four years for HoraceWells, an American dentist, to take up that suggestion. Snow also noted that sul-phuric ether’s “exhilarating effects” had been generally known since 1818 and hadbeen regularly inhaled by medical students. Not until 1846, however, was its surgi-cal applicability established at Massachusetts General Hospital. Snow went on tonote, “A medicine called chloric ether has been in use since 1831.”14 Jacob Bell usedit to prevent pain in early 1847 at several London hospitals. This medicine was ac-tually twelve percent chloroform dissolved in spirits. David Waldie, a Liverpoolchemist, explained these circumstances to the obstetrician James Young Simpson inEdinburgh in 1847, and chloroform in an undiluted state came into use. Snow’s pointwas that all of this had occurred more or less by chance:

Ever since the introduction of chloroform I have been of opinion that otheragents would be met with more eligible for causing anesthesia by inhalation.It seemed improbable that this one, which happened to be standing on theshelf of the Pharmaceutical Chemist for another purpose, should be better thanall the very numerous volatile compounds which organic chemistry is dailybringing to light; and the continued use of chloroform is probably due to thecircumstance, that hardly any one has made anæsthesia by inhalation a sub-ject of constant and protracted investigation.15


All the hubris and wisdom of Snow show in this passage. He is at once the proto-corporate spokesperson for better living through chemistry, and the hard-nosed sci-entist requiring protracted investigation before adopting new anesthetics, but hisclaim that an agent discovered by systematic organic chemistry would be better thanone found on the laboratory shelf reveals both insight and insensitivity. After all,who can say whether or not chance discovery will yield better or worse results? Un-doubtedly, organic chemists have washed down their drains many a compound thatlater turned out to be quite useful, but Snow was confident that when one knew howto set about looking the day would come when a better agent was discovered.

In amylene he thought he had a very good candidate. The desire to find a saferanesthetic may have had its roots in a dream of rational scientific discovery, but itwas also prodded by continuing public concerns about chloroform. Stories of morefatal and near-fatal accidents with chloroform continued to be reported in the press.In February 1857 a nine-year-old boy died under chloroform in the care of Mr. JamesPaget, who laid the case before the medical public in a report published in MTG.16

This was, by Snow’s count, the forty-eighth case of fatality since the use of chloro-form began a decade before. He lashed out at those who used handkerchiefs: “It mustbe quite obvious that a handkerchief, or cotton wool, or lint can afford no adequatemeans of properly regulating the amount of vapour in the inspired air.”17 He doubtedthat “fear on the part of the patient is a cause of death from chloroform. If this wereso, accidents would be extremely common; for many patients inhale it, unfortunately,with great fear, only because they have still greater fear of pain; children, also, areusually afraid of anything so strange, yet accidents have seldom happened to them.. . . Excessive fear and an overdose of chloroform may either of them cause sud-den death, just as infancy and old age both predispose to bronchitis; but they can-not combine to cause an accident in the same case. In fact, as soon as a patient be-comes unconscious from chloroform, the effects of fear on the pulse quicklysubside.”18 Despite Snow’s scoldings, however, accidents continued to occur.

By early April 1857 Queen Victoria was in the last month of her ninth pregnancy,and Snow was well aware that he might be called in any day to administer chloro-form as he had done in 1853. By this time he had amassed more than 140 cases ofamylene administration, with results admirably consistent with his preliminary find-ings. Some sickness had arisen in some cases, but it was hardly of the severity hefound with ether or chloroform. So far, he had only “had leisure to administer amy-lene in two cases of labour.” In both instances the anesthetic removed labor pains,allowed the mother to retain consciousness between pains, and produced “no inter-ference with the progress of the labor. I look forward with some interest to a moreextended experience of amylene in midwifery.”19

On Tuesday afternoon, 7 April, Mr. William Fergusson requested Snow’s servicesat Maddox Street near Regent Street. The thirty-three-year-old Mr. Wellington re-quired repair of an anal fistula. According to Snow, he was in good health, “thoughhe had lived somewhat freely.”20 Perhaps because Wellington was strong and such


patients often flinched during this procedure, Snow opted for amylene and pouredsix fluid drachms (about 21 ml) into the inhaler. At 4:46 P.M., the man lay down onhis right side in bed and they commenced. His “pulse was pretty good” as he startedinhaling, and Snow gradually advanced the valve over the opening in the face-pieceuntil it was 3/4 covered. Within two and a half minutes the patient was unconscious.Fergusson probed Wellington’s backside, testing for any signs of feeling. Findingnone, he picked up the bistoury and began to open the fistula. Patients typicallyflinched in these situations, and Snow held the man’s thigh. The patient did not flinchbut held his legs tense and still. When Snow returned his gaze to the patient’s face,he observed that the oxygen-intake valve was shut. This was not uncommon withamylene. Because the patient was still unconscious, Snow discontinued the inhala-tion as the surgeon completed the operation with a single incision. “Out of constanthabit and from a scientific curiosity,” Snow felt for Wellington’s pulse. He could notfind it, even though the patient’s breathing was good and he seemed to be wakingup. Snow grew alarmed. The patient’s insensibility was deepening and his breathinggrowing slower and deeper. Snow called out to Fergusson, who was washing his handsand preparing to leave after another successful operation. They dashed cold water inWellington’s his face, which caused him to begin gasping for breath. They tried ar-tificial respiration, but it was no use. By 5:02 P.M. the patient was dead. After thepostmortem examination, Snow concluded that he could not “attribute the patient’sdeath to any other cause than the amylene.”21

The following Tuesday Snow was summoned to Buckingham Palace. The Queen’slabor had begun at two that morning, but was progressing slowly. At 10 A.M. Dr. Lo-cock, the royal accoucheur, gave the queen powdered ergot to advance the labor,thereby increasing the pains. Snow began administering chloroform at 11 A.M. Thechloroform was given on a handkerchief in minute quantities. Prince Albert had beenadministering it in this fashion before Snow arrived. The queen was in great pain,and she called out for more of the chloroform. As if to make a compromise betweenthe lay and professional modes of administration, Snow poured half a milliliter ofchloroform onto a cloth and folded it in a conical shape for each pain. Victoria ex-pressed “great relief from the vapour,” and she asked for even more. When the timecame to bear down, she complained that she could not make the effort. Just as Snowhad seen in other cases, and as is commonly known today, the anesthetic was in-hibiting the delivery to some degree. The gas was left off, and three or four painslater a princess was born (CB, 471). This was not the time to test amylene as a sub-stitute for chloroform.

Despite young Wellington’s death and the letters of criticism that ensued, Snowcontinued to use amylene and advocate its use throughout the spring and summerof 1857, even sending a sample to John Gay Orton, a physician in Binghamton, NewYork.22 One bad outcome did not worry him at the time: The “accident [with Welling-ton] happened in the 144th case in which I have administered amylene. It is impos-sible to form an average from a single case. I do not know any reason why an


accident like the above might not have occurred in one of the early cases in whichI was giving chloroform, or, on the other hand, why I might not have been able togo on for four or five years at a time administering amylene, without any approachto an accident.”23 However, in late July 1857 another patient died under amylene ad-ministered by Snow. It was the 238th case in which he had used the agent, and “inthe ninety cases and upwards in which I administered amylene between these twoaccidents, I never had occasion to feel a moment’s uneasiness about it” (OC, 416).After the second death we hear no more of Snow using amylene in clinical practice,but he had not given up on it, noting a few weeks after the death, “I still believe, thatif amylene were exhibited, by measured quantity . . . a sudden accident would nothappen.”24 He had in mind a change in the mode of administering it, not its dis-continuance: “In the future cases in which I employ amylene, it is my intention toadminister it from a bag or a balloon.” (OC, 416).25 As such, Snow anticipated theapparatus and recirculating techniques later developed by Joseph Clover, but Snowdied before he could put them into practice.

Notes

1. Shephard, JS, 9.2. Ellis, Case Books of Dr. John Snow, cited parenthetically in the text as CB.3. Snow, On Chloroform (1858), cited parenthetically in the text as OC. This was Snow’s

posthumously published monograph on chloroform and the entire family of narcotic agents,which included many case reports but did not expand the scientific base of narcotism beyondwhat Snow had published in his ON series in 1848 through 1851.

4. Snow, “Death from chloroform in a case of fatty degeneration of the heart” (1852), 361.Here he explained the “weakness” noted in CB as syncope.

5. Ibid.6. Ibid., 362. For a slightly different interpretation, see Shephard, JS, 112.7. Snow, “On the employment of chloroform in surgical operations” (1855), 361.8. Snow, “On the vapour of amylene” (1857), 61.9. Ibid., 62.10. Ibid., 83; see also CB, 444–45.11. Ibid., 83.12. Snow, “Further remarks on amylene” (1857), 379–80. The apparatus was only slightly

modified from his chloroform inhaler, providing a deeper chamber to allow for the greatervolume of amylene required.

13. Snow, “On the vapour of amylene” (1857), 60, quoting Davy, Researches concerning ni-trous oxide, 556.

14. Ibid., 61.15. Ibid.16. James Paget, “Administration of chloroform was fatal,” MTG 35 (7 March 1857): 236–37.

Paget, whose memoirs were cited in earlier chapters, was then assistant surgeon to St.Bartholomew’s Hospital.

17. Snow, “On the recent accident from chloroform,” (1857), 283.18. Ibid.


19. Snow, “Further remarks on amylene” (1857), 359.20. The description of this operation and its outcome are synthesized from accounts in

Snow, “Further remarks on amylene” (1857), 381–82; and CB, 469.21. Snow, “Further remarks on amylene” (1857), 381.22. Snow, “Mr. A Prichard on amylene” (1857); John G. Orton, “Amylene,” Boston Medical

Surgical Journal 56 (1857): 457.23. Snow, “Further remarks on amylene” (1857), 382.24. Snow, “Case of death from amylene” (1857), 134.25. Richardson thought differently: “These deaths affected him very seriously, and his sud-

den and early demise may, in some measure, be attributed to their effects upon him. . . . Hehad not in amylene accounted sufficiently for its insolubility, and it was not until I venturedto show him separation of amylene in the blood, a separation which looked like the forma-tion of minute plugs, that he fully realized the danger”; Vita Medica, 284. Snow never men-tioned anything about Richardson’s microscopic investigations, although he had at least a yearto have recorded any debt he owed his younger colleague and friend.


372

THE THATCHED HOUSE TAVERN in St. James’s Street was afive-minute walk from Snow’s Picadilly residence. In the eighteenth

century it had been the home of a fine arts society, the Dilettanti. In the nineteenthcentury it was a fashionable meeting place for artists and writers and featured a largeroom for public gatherings, where members and visitors of the Medical Society ofLondon assembled to celebrate its eightieth anniversary on Tuesday, 8 March 1853.The annual oration was scheduled for 5:00 P.M., with a dinner to follow. The oratorfor the year was John Snow.1

His address was cumbersomely entitled, “On continuous molecular changes, moreparticularly in their relation to epidemic diseases” (CMC). Given the standards ofthe time, most of Snow’s communications were narrowly focused, addressing one is-sue or a single set of observations. An oration, however, offered him an unusual op-portunity to speak in a speculative way and with unprecedented breadth “on thechief phenomena of living beings” (CMC, 147).2 This work, therefore, provides a rareglimpse of Snow’s scientific thought as a whole, illustrating connections not dis-cernible in his papers on anesthesia and cholera. It is a deeply interdisciplinary, syn-thetic essay, a focal point at which the rays of Snow’s thought converged and his twospecialities were joined, albeit tenuously. Snow thought serially and by accretion, andCMC was the apotheosis of this style.

Chapter 15

Common Ground:Continuous Molecular

Changes

In the 1850s debates over the fundamental nature of life and living processes werestill quite common. Vitalism, the doctrine that life was sustained by forces distinctfrom chemical and physical forces, was no longer popular in the medical circles inwhich Snow traveled, but fundamental questions remained about what distinguishedliving entities from the nonliving. Some believed it was possible for nonliving ma-terials to become living under certain circumstances, a view with special implica-tions for those who believed that epidemic diseases were caused by immaterial par-ticles in miasmatic or effluvial suspension. This debate found Snow in the familiarplace of straddling a line between life and death. He had investigated this border-land of medical research for at least fifteen years, whether by reanimating asphyxi-ated guinea pigs or by studying the patterns by which chloroform shuts down hu-man consciousness. He had long been interested in the chemistry of respiration and oxidation, subjects of crucial concern to the animal physiology of Liebig andMagendie, upon whom Snow often relied and from whom he occasionally departed.Snow was no vitalist, but he maintained a major distinction: vital molecular pro-cesses were continuous, nonvital were not. He believed in a chain of continuity fromone living being to another and intended his oration to show that apparently dis-parate living phenomena share common properties, common patterns of action, andcommon continuities of action. His ultimate goal on this occasion was to convincelocal miasmatists that one could not conclude from the blurred line between vitaland nonvital that one disease or disease-causing agent could change into another. Inhis mind epidemic diseases should ultimately be understood on a molecular level.

In this way the title was meant to signal the common ground represented by aunification of chemistry and epidemiology. He believed that the molecular action oforganic chemistry, essential to all natural processes, was linked to the biological pro-cesses of individual living beings and to the diseases that attacked whole popula-tions—that is, epidemics, especially cholera. The reach of Snow’s argument was vast,from the interactions of atoms to the interactions of a global populace. In short, hisoration was a “think piece,” inviting his colleagues to consider that the same lawsthat regulate the behavior of molecules also regulate the patterns of epidemic dis-eases. If they agreed, Snow had found a common ground with local miasmatists,from which the medical establishment could launch concerted preventive measures.

Continuity, Change, Molecules

It is likely that the concept of “continuous molecular changes” appeared immedi-ately relevant to Snow in the context of his anesthesia investigations. In his asphyxiastudy of 1841, he had commented on the continuity of respiration and its funda-mental chemical nature. Similarly, Justus von Liebig had expressed his own won-derment at the exhaustion and replenishment entailed in the chemistry of respira-

Common Ground: Continuous Molecular Changes 373

tion: In living organisms “an unfathomable wisdom has made the cause of a con-tinual decomposition or destruction, namely, the support of the process of respira-tion, . . . the means of renewing the organism.”3 Thereafter, the administration ofether and chloroform to living organisms had impressed upon Snow the ways inwhich the inhalation of nonliving molecules could create specific effects on the liv-ing system—both shutting it down in a definite sequence and reducing the rate ofrespiration, or the amount of CO2 exhaled. That is, the controlled duration of anes-thesia pointed to ways in which the continuity of molecular action could be regu-lated.

When Snow turned his attention to cholera in the fall of 1848, he was interestedin the action of the agent and its discrete impact on the human organism. In hisview cholera was a local affection of the intestinal tract, and in his first essay on thesubject he employed the concept of continuous molecular change to explain thepathological process involved:

Being led to the conclusion that the disease is communicated by something thatacts directly on the alimentary canal, the excretions of the sick at once suggestthemselves as containing some material which, being accidentally swallowed,might attach itself to the mucous membrane of the small intestines, and theremultiply itself by the appropriation of surrounding matter, in virtue of molec-ular changes going on within it, or capable of going on, as soon as it is placedin congenial circumstances. Such a mode of communication of disease is notwithout precedent. The ova of the intestinal worms are undoubtedly introducedin this way. . . . The writer, however, does not wish to be misunderstood asmaking this comparison so closely as to imply that cholera depends on verita-ble animals, or even animalcules, but rather to appeal to that general tendencyto the continuity of molecular changes, by which combustion, putrefaction, fer-mentation, and the various processes in organized beings, are kept up.

MCC, 8–9

Snow’s explanation does not seem straightforward to modern readers. He associatestwo processes—putrefaction and fermentation—with molecular change, but thenseems to exclude the microorganisms we now understand to cause these processes,bacteria and yeast. To grasp Snow’s meaning, therefore, requires us to imagine a timebefore germ theory, when it was still unclear whether fermentation was a vital or nonvital process. Putrefaction and decomposition in urine were considered self-propagating processes, but it was unclear what drove these changes. Contempo-rary medical researchers could accurately measure inputs and outputs and employlitmus tests to indicate acidity or alkalinity of the fluids and gases that living beingsregularly exchanged, but “we have no instrument, like the thermometer,” Snow re-minded his colleagues, “with which we can measure the force that communicates thechange to substances in contact with those in which it is taking place” (CMC, 150).


In 1849 Snow was uncertain whether the cholera agent was a microscopic organ-ism or some undetermined, specific animal poison. Parasitic worms, an establishedexample of an agent whose germinal cells (eggs) could be accidentally swallowed andeventually reproduce in the intestine, provided a useful analogy. He conjectured thatthe agent that caused cholera lodged in the mucus membrane of the intestine andthen proceeded to divert materials intended for the body’s sustenance to its own re-production. Cholera, like ether or chloroform, was a chemical agent that altered thebody’s metabolic processes, but unlike these anesthetics, cholera redirected those pro-cesses to make more of itself.4

Animal Chemistry

Snow structured CMC in three parts. In an opening theoretical section he addressedthe general questions of vital and nonvital processes and the chemical basis for bi-ology. Next, he presented a theory of the nature of epidemic diseases and defendedhis own views on cholera transmission. In the concluding section he substantiatedhis general theory of epidemic diseases and drew practical implications from it.

“Molecular changes,” for Snow, alluded to the forces that constantly act on all par-ticles of matter, whether they exist in life forms or in test tubes. For him molecularmeant “atoms of matter.”5 Flux occured on a molecular level in all matter, organicas well as inorganic. Matter in living and nonliving things is always changing—chang-ing state, forming new compounds, decaying, oxidizing, reproducing, combusting,and fermenting. It was also known that crystallization and “cohesion” were the re-sult of forces that occur at a molecular level. Snow knew his usage of the term con-tinuous molecular change would call to mind Liebig’s book on Animal Chemistry,which had been translated into English in 1850 and was repeatedly mentioned inmedical journals. Liebig frequently used the phrase continuous molecular action, andSnow adopted Liebig’s terminology for organic chemical processes.6 For Snow mo-lecular was the word that most effectively “express[ed] all that refers to the attrac-tion which exists amongst the particles of matter at insensible distances”—distancestoo minute to be perceived by the senses (CMC, 145).7

Besides the etymological link with anesthesia, “insensibility” was at the heart ofthe dispute over cholera transmission. In arguing for his fecal–oral theory and hishypothesis of water-borne spread, Snow regularly found himself opposed by thosewho believed that disease arose from sensible causes such as foul odors and visiblefilth. Some of Snow’s would-be allies, such as Frederick Brittan, Joseph Swayne, andWilliam Budd, were prepared to consider a cholera poison that acted the way Snowpredicted only if they could see the particle under the microscope. To the contrary,Snow wished such colleagues to embrace the idea that processes that occur at in-sensible levels of size and organization might explain the sensible phenomena all of them observed at the bedside.7a As Liebig put it, “The discovery of the laws of


vitality, cannot be resolved, nay, cannot even be imagined, without an accurateknowledge of chemical forces; of those forces which do not act at sensible distances.”8

By invoking this respected Continental authority, Snow hoped to establish consen-sus that an understanding of molecular structure developed in the laboratory wouldpermit medical men to make new predictions of how matter should behave at “sen-sible” orders of scale. Just as he had done with his investigations of ether and chlo-roform, Snow sought to create a scientific approach that melded laboratory medi-cine, bedside medicine, and a numerical, or quantitative method.

The Vital and Nonvital: Commonality and Difference

Snow also modeled his reasoning on Liebig’s to argue for a common ground betweenthe organic and inorganic. Molecular changes were characteristic of both realms: “Allchanges of composition whatever, whether occurring in a test-tube, or in a livingbrain, are properly included amongst chemical changes; and all that takes place inliving structures has a right to be called vital, whether it differs from what occurselsewhere or not. Thus, whilst the terms chemical and vital have each a separate sig-nification, they have a certain ground in common, since changes of composition inliving beings are at once both chemical and vital, and belong to both chemistry andphysiology; just as fossil animals belong to both the mineral and animal kingdoms,and to the sciences of geology and zoology at the same time” (CMC, 145–46).9

In other words, Snow’s common ground was the biochemical nexus; at the mo-lecular level vital changes entail chemical ones. He recast vital and morbid processesin biochemical terms, insisting that “the chief phenomena of living beings” could bethought of as “a number or collection of continuous molecular actions” (CMC,150–51). In his mind “there is no distinct line of demarcation between vital pro-cesses and those which are not vital” (CMC, 151). With respect to zymotic changes(fermentation), he acknowledged that “many persons would doubtless say that theformation of the [yeast] sporules is a vital process, and the production of alcoholand carbonic acid a chemical process inseparable from it. . . . [However,] it mustbe remembered that the decomposition of sugar into alcohol and carbonic acid isas closely connected with a process of organization as are the sensibility and con-tractility of animal tissues” (CMC, 152).9a Such statements warned his audience notto assume that vitality was something other than its processes nor that some pro-cesses were necessarily more vital (or fundamental to vitality) than others. Snow citedanother Continental researcher, Matthias Schleiden, in support of the view that “wemust regard the whole process of [vegetable] cell-formation as simply a chemicalact. The gathering together of granules of mucus to form a cytoblast we can as lit-tle explain as that, when we form a solution of two salts, if we throw into the mix-ture a crystal of one or other salt, that salt alone crystallizes around it” (CMC 152).10

Snow’s work on the degrees of narcotism induced by anesthetic agents had indicated


ways in which chemical agents affected nervous activity and suspended sensibility intissue, which confirmed for him the chemical nature of such complex vital func-tions.11 This interpretation of the biochemical nexus also offered an explanatorymechanism by which a cholera poison could rapidly reproduce in the mucous mem-brane of the alimentary canal.

Whereas “molecular changes” characterized both vital and nonvital processes,“continuous molecular changes” were characteristic of vital processes alone. ForSnow a continuous chemical process could not begin de novo and always requiredthe pre-existence of a similar vital process: “Combustion, putrefaction, and numer-ous other molecular actions, although capable of self-propagation, commence anew,under the requisite circumstances, without any contact with matter undergoing thesame change. There are, however, changes of a more complicated nature—those towhich plants and animals owe their development and continuance—that have nevercommenced anew within the experience of man. The most characteristic property,indeed, of vital actions probably is, that they are always caused by similar processeswhich have preceded them, whilst all other molecular changes may arise, occasion-ally at least, from other causes” (CMC, 150).12 He allowed one exception, combus-tion, which he considered a bridge between nonvital and vital processes. It could oc-cur spontaneously, but it was also the process by which animal life breaks downfoodstuffs.13

Oxidation

Oxidation was the common ground for Snow’s work on anesthesia and cholera. Inthe last installment of ON (1851), he had noted (following a train of thought sug-gested by Charles Philippe Robin in Paris) that a range of narcotic agents, from etherand chloroform to benzine and arsenic, possessed antiseptic properties. All appearedto preserve animal matter from putrefaction. He linked their various antiseptic pow-ers to a common capacity to inhibit oxidation, “probably in direct proportion totheir narcotic strength,” and he noted the bridging nature of combustion: “Substanceswhich have the property of limiting and preventing oxidation in the living body, havealso the property of limiting and preventing that kind of oxidation which consti-tutes ordinary [that is, nonvital] combustion” (ON, 18: 1091). Continuous molecu-lar changes that maintained biological functioning were oxidative processes, or partlyso. Consequently, narcotic anesthetics could interrupt those processes if adminis-tered in proper doses. Communicable diseases disrupted normal oxidative processesand, like anesthetics, became irreversible if not arrested in time, but whereas anes-thetics induced molecular changes, communicable diseases did their “mischief” viacontinuous molecular changes, commandeering the nutritional and maintenanceprocesses of the healthy body for the task of manufacturing more of the disease agent,infecting others, and starting the process anew.14


To explain why the interruption of oxidation in the case of anesthesia might bereadily reversible when the disruption produced by communicable diseases mightnot be, Snow introduced the idea of chemical counteraffinity. He described a seriesof experiments in which he found that the nitrogen that makes up eighty percent ofthe air is not inert in relation to atmospheric oxygen. Some of the experiments in-volved nonliving material, such as a red-hot iron wire and a burning candle, bothof which combined more readily with oxygen when the nitrogen was absent. He alsoexperimented on birds and other animals and noted that they died more quickly inoxygen-deprived atmospheres with high concentrations of nitrogen. He consideredit “evident, then, that the nitrogen of the air exerts an influence over the combina-tion of oxygen with other bodies. This depends chiefly on the affinity between thenitrogen and the oxygen—an affinity which is not great enough to cause their com-bination under ordinary circumstances, but is sufficient to counterbalance, to a cer-tain extent, the affinity between oxygen and other bodies. It is on this kind of counter-affinity, as it may be called, that the action of most narcotic and antiseptic agents onliving and dead animal substances depends” (CMC, 149).15 The key to effective nar-cosis was manipulation of this counteraffinity in such a manner that it was speed-ily induced and just as speedily reversed. Hence, Snow’s interest in continuous mo-lecular changes and chemical affinity had emerged from investigations of themechanism by which anesthetics inhibit oxidization.16 According to Richardson,Snow’s “greatest deduction . . . [was] that the action of volatile narcotics is that ofarresting or limiting those combinations between the oxygen of the arterial bloodand the tissues of the body, which are essential to sensation, volition, and all the an-imal functions.”17 The point of the “farthing candle” experiment (see Chapter 6) wasto demonstrate counteraffinity: The process of adding chloroform vapor to the bot-tle removed none of the oxygen from the air it contained, although the candle actedas if it were burning in an atmosphere that contained less oxygen than normal air.18

Along with his experiments on oxygen and nitrogen, the farthing candle experimentbridged the vital–nonvital divide by positing a biochemical nexus.

From Contagion to Communication

After his discussion of oxidation and counteraffinity, Snow gave examples of howhis general theory of continuous molecular changes explained the action of variousepidemic diseases. Such diseases resulted from the multiplication and spread of spe-cific agents—in short, they were “continuous.” By this reasoning disease agents couldnot arise spontaneously in the atmosphere or from the putrefaction of vegetable mat-ter, because any molecular changes involved therein were not capable of reproduc-ing the same agent. The common ground Snow had in mind, therefore, did not ac-commodate hard-core anticontagionists. Instead, he directed his remarks tocontagionists and contingent contagionists and hoped to shape a new consensus with


a term that had fallen out of fashion in all the hubbub over Asiatic cholera: com-municable diseases.

Snow’s gambit began with a definition. The communicable diseases were “an ex-tensive group of maladies, each case of which is caused by some material that, as ageneral rule, has been produced in the system of another individual” (CMC, 155).His term included diseases such as “syphilis, small-pox, measles, scarlet-fever, typhus,typhoid and relapsing fevers, erysipelas, yellow-fever, plague, cholera, dysentery, in-fluenza, hooping-cough [sic], mumps, scabies, and the entozoa” (CMC, 156). He con-sidered the term communicable preferable to contagious or zymotic because commu-nicability can be direct as well as indirect, and it emphasized the process of change.19

Communicable was flexible and inclusive; it should be acceptable to contact conta-gionists, swallowing contagionists, and contingent contagionists (who accepted in-halation of infectious agents produced by the sick). It did not distinguish amongmodes of communication; he lumped syphilis, influenza, and entozoa (intestinalworms) into the same category.20 Plus, it had another advantage that made it seemappropriate for a generation of medical men trained to believe that medicine wasconnected to collateral sciences like chemistry: It brought to mind a set of patternsof molecular change peculiar to living beings.

The organized matter . . . which induces the symptoms of a communicateddisease . . . possesses one great characteristic of plants and animals—that ofincreasing and multiplying its own kind. . . . The molecular changes takingplace in the materies morbi of some diseases resemble the changes in many liv-ing beings in another respect also: they permit of being suspended, under cer-tain circumstances, and recommence at the point at which they ceased. . . .There is always a definite period . . . before the illness commences, which iscalled the period of incubation. As regards the materies morbi itself, this . . .is a period of reproduction. . . . [C]ommunicable diseases . . . are apt to beextremely prevalent at particular times and places . . . which arises strictly outof their communication from individual to individual.”

CMC, 156–57

Every communicable disease followed a particular pattern, often involving a periodduring which its characteristic molecular changes appeared discontinuous to the medical observer but when the disease agent actually was reproducing inside the host.

CMC represented a turning point in Snow’s thinking about the mathematics ofepidemics. Four years earlier, he had suggested that the mode of communication ofepidemic diseases might explain the shorter duration of outbreaks in villages, com-pared to cities, and had noted that an epidemic dies out “for want of fresh victims”(PMCC, 928). Snow expanded on these insights in CMC by arguing that the mathematics of an epidemic outbreak are explainable entirely by reference to the


transmission characteristics of the disease in a population. Referring to epidemic dis-eases, he asserted that their extreme prevalence at times “arise strictly out of theircommunication from individual to individual” (CMC, 157). While “various irrup-tive fevers” are constantly present in London, cholera “has been twice spread overthe world . . . and seems to be dying out a second time everywhere but in the Southof Asia. . . . It is so difficult to support that the world seems scarcely large enoughfor it, and, were it not for its pastures in India, it would be in danger of passing altogether out of existence, like the Dodo in Mauritius” (CMC, 158).

Snow may have been the first to recognize the complete dependence of the riseand fall of human epidemics on the need to sustain the chain of human transmis-sion, and that that chain in turn depends entirely upon the changing prevalence inthe population of susceptibles and immunes.21 He offered an example: “syphilis, forinstance, keeps a pretty even course in this metropolis, because there is a steadyamount of vice for its support; and a still greater amount of virtue to keep it incheck; but when it is introduced amongst a community of savages, indulging inpromiscuous intercourse, it rages as a fearful epidemic” (CMC, 157–58). His pointwas simultaneously social and pathophysiological. Social practices can encourage orprevent communicable diseases from becoming epidemic. The epidemiologicalthrust of the concept of communicability lay in its attention to discrete social path-ways as well as discrete pathogenic agents, but one did not need to identify the latter in order to posit socioecological equations of disease.22

It was sufficient to know that in a communicable disease the victim had to receivethe “materies morbi”specific to that disease from another person. Thereafter, the“suitable materials” (which some called the infectious “virus”) resumed the processof reproduction, incidentally causing the symptoms of disease in its new host, at thepoint where it had been suspended when the particles were excreted by the previ-ous individual. By virtue of the principle of continuous molecular change, the “virus”could replicate only itself; cases of syphilis would only produce more syphilis, andso on, regardless of the route or conduit by which the “virus” entered the body. Somecommunicable diseases seemed to be transmitted through the air: “It is not im-probable,” Snow speculated,“that the specific cause of influenza and measles is drawnin with the breath, as these diseases affect chiefly the respiratory organs, and spreadalmost equally amongst all classes of the community” (CMC, 168).23 The alimentarycanal offered another mode of communication.24 Cholera, in his view, was spreadby accidental “swallowing of the morbid excretions of the patients” carried by “drink-ing water, or other articles of diet” (CMC, 168–69).25 Poverty, filth, and overcrowd-ing often facilitated the transmission of morbid materials from person to person,but Snow believed that they could not, in the terminology of the day, be predispos-ing factors that actually caused someone to come down with a communicable dis-ease. The underlying process was still unknown, but “as we have analogy to guideus, we are warranted in concluding that when the morbid matter of any disease isreceived into the system, in the way required in that particular disease, it is almost


certain to produce its specific effects, except in the instances in which the patient hasgained an immunity by a former attack. . . . There is no reason to invoke a sup-posed predisposition, or predisposing causes, to account for its existence in the per-sons in whom we find it. To be of the human species, and to receive the morbid poi-son in a suitable manner, is most likely all that is required” (CMC, 161). It wasinconsistent with the notion of continuous molecular change to imagine that any“disease has taken on contagious properties which it did not previously possess”(CMC, 171). To suppose, for example, that yellow fever was caused by marsh mias-matas in some locations and elsewhere transmitted from person to person “amountsto nothing more or less than supposing that some material produced in marshyground, without any connection with the human body, can be reproduced and growin the system of the patient. I believe we know nothing in nature analogous to this,and it is therefore an opinion which should not be adopted till there is strong evi-dence in its support. It is most likely that yellow fever was always a communicabledisease” (CMC, 171–72).

Continuous Molecular Change as Social Theory

Snow insisted that the study of communicable diseases should consider sociologicaland cultural factors in addition to the physiological. For example, medical contro-versy about the question of contagion often turned contentious because of “the greatpecuniary interests involved . . . on account of its connection with quarantine”(CMC, 173–74). In his formulation the notion of continuous molecular change de-manded the addition of a sociocultural level to the systems thinking he was using toexplain the communication of cholera (see Table 8.2).26

Culture, education, literature, emotions, and, most strikingly, memory exhibit thecontinuity of suspended activity in vital organisms. Cultural transmission is a formof vital replication: “In the human species, enjoying the faculties of speech, [the]connection between succeeding generations is much more intimate. . . . In ourown profession it has been truly said to last to the end of life, and institutions likethis Society have the effect, not only of preserving and transmitting the knowledgeof one generation of medical men to the next, but of increasing the boundaries ofthe science they cultivate, and rendering it more perfect and useful.” Language, as amedium of communication, is also subject to the natural laws underlying continu-ous molecular change: “The communication of certain molecular changes takingplace in the brain . . . extends collaterally in all directions, by means of vibrationsin the air, or in the ethereal medium which pervades space. . . . The faculty ofspeech gives to man a power of communicating his complex feelings and ideas, farexceeding that of lower animals; and the invention of literature has greatly increasedthis power in civilized nations. By speech, not only can fresh sensations and ideas becommunicated, but also that continuation of them called remembrance, by which


they revive after, it may be, a long interval of suspended action” (CMC, 154–55). Inthis vision memory is analogous to the dormancy period characteristic of commu-nicable diseases.

There are other analogies as well. One person’s idea (“a particular state of molec-ular action” within the brain), conveyed by a suitable medium (oral speech or writ-ing) to another person, can set up the same process of molecular action in the re-cipient’s brain.27 For Snow the notion of continuous molecular change explainedanimal behavior as well as animal physiology and the communicability of epidemicdiseases.28 His speculative oration painted an intricate web of social, chemical, andbiological communication. Three years previously he had said that simply becauseinfluenza seems to break out somewhere in many people seemingly at the same time,this is not evidence for miasmatic causation. An illusion was at work, for influenzatravels no faster than bad news, which is clearly communicated by the breath.29 Thesociocultural vision in CMC shows that Snow’s earlier comment was no verbal by-play. Bad news was not bad because the breath was bad; the breath was the neutralmedium for the transmission of a specific sort of information, just as it could trans-mit the agent that caused influenza. Similarly, drinking water, as such, was not dis-ease inducing, but it could be a neutral medium by which the continuous molecu-lar action of the cholera agent was transmitted.

Snow concluded his remarks by urging all members of the Medical Society of Lon-don to increase their investigations into the “modes of propagation” and the “meansof prevention” of communicable diseases. He invoked the example of Edward Jen-ner, a former fellow of the society, and his smallpox vaccine as one of the surest pathsto the advancement of the society and the profession. Perhaps Snow considered thisexample apposite, because (like himself studying cholera) Jenner had not been de-terred by the “insensible” nature of the causative agent of cowpox or by the fact thatthe science of his day could not reveal the mechanism by which cowpox protectedagainst smallpox.

Two years after delivering this oration, Snow became president of the Medical So-ciety of London. In his inaugural address he gave an assessment of the state of themedical profession in England and his sense of how the society could promote itsadvancement:

We are all agreed that the medical profession does not hold that position inthe country that we should wish. . . . The chief reason, in my opinion, is thatthe science of medicine itself is not in the position in which we could wish tosee it. . . . There is a right time for the advancement of every science. Med-icine could not approach to perfection till the collateral sciences were first advanced; but the time has probably now arrived when medical science mayadvance in the same rapid manner that chemistry has advanced within the lastseventy or eighty years. . . . I do not mean that we shall find a cure for everydisease, but that we shall have a rational knowledge of it, and know what to


expect from treatment. . . . If the profession should then not have quite theposition in society that we could wish, it will, at all events, not be placed be-neath the other professions; and we shall not see the civil engineer and thechemist placed over the medical man, in matters that belong exclusively to hisown profession.30

This passage reveals Snow’s abiding conviction that medicine ought to derive itsvalue and power from its foundations in basic research undertaken in the “collat-eral sciences,” particularly chemistry.31 He called for professional consensus builtaround principles derived from chemistry and physics. This notion that profes-sional identity should be based on scientific knowledge echoed the reformist rhet-oric of other medical men in Snow’s intellectual generation, such as BenjaminBrodie, William Farr, Marshall Hall, Robert Liston, and James Johnson. Snow’s lan-guage was characteristic of the London institutions in which Snow received hismedical training.32 Each collateral scientific field, such as chemistry, could illumi-nate medical concerns, but medicine was constituted by the totality of the collat-eral sciences and practical bedside medicine. Scientific medical practitioners knewhow to employ the collateral sciences to enhance their therapeutic abilities. Snowalso expressed frustration at the lack of influence in public health matters exertedby the medical profession generally and perhaps himself in particular, but the pro-fession was certainly partly at fault. For a quarter century they had engaged in con-tentious debates over the fundamental nature of epidemic diseases such as cholera,with no resolution in sight. It was no wonder nonmedical reformers like EdwinChadwick found a clear path to power.33 CMC was Snow’s attempt to forge a med-ical consensus about epidemic diseases, but it had no discernible effect in his life-time. Although members of the Medical Society of London applauded his learnedoration that March evening in 1853, his colleagues proved unwilling to share thecommon ground he had offered them.34

Notes

1. “Medical Society of London,” Lancet 1 (1853): 253–54; MTG 6 (1853): 282–83; AMJ 1(1853): 218. On the Thatched House Tavern, see Cunningham, Hand-Book of London, 492.

2. Snow, On Continuous Molecular Changes (1853). We cite the published version paren-thetically in the text as CMC.

3. Liebig, Chemistry and its Application, 123.4. In the early 1850s Snow decided that the “morbid poison” causing cholera was probably

cellular. He was not alone in this shift in thinking. In 1852 Farr stated that cholerine was thelikely “zymotic cause of malignant cholera.” He redefined a term previously used for milderdiarrheal symptoms during outbreaks of summer cholera; see the OED.

5. CMC, 147. Although Liebig and other Continental researchers used molecular, it was notin common use among British scientists. It does not appear in the index to a 900-page text-book, Brande and Taylor’s Chemistry.


6. For a discussion of the scope and nature of Liebig’s influence, see Eyler, Victorian SocialMedicine, 27–33. Throughout the period of Snow’s development as a chemist and anesthetistin the 1840s, Liebig had advocated the chemical analyses of animal tissues, stressing the in-ferential power of what he called the “quantitative method.” He had spoken to the British As-sociation in Glasgow in 1840 and toured Great Britain in 1843 lecturing on the applicationof organic chemistry to agriculture. In 1845 he sent his student August Hofmann to headPrince Albert’s new Royal College of Chemistry. If one followed Liebig’s method, carefullymeasuring “what went in (food, water, oxygen) and what came out in excretions and exhala-tions (urea, various salts and acids, water, carbon dioxide), much could be inferred aboutchemical processes inside the animal (or human) organism”; Bynum, Science and the Practiceof Medicine, 96.

Snow could have accepted Liebig’s general approach without subscribing to his pathologi-cal theories, which had some currency in London in the 1840s and 1850s as seen from thefrequent references to Liebig’s work in the medical journals. Snow, for example, appears notto have accepted Liebig’s assertion that yeast was a nonliving particle; Liebig, Chemistry andits Application, 121–27.

7. The word “insensible” disturbed a reviewer of Snow’s published oration. This person be-lieved that an “insensible” distance was real and conceivable, even if the measuring apparatusof the day could not deal with it; “Bibliographical notices,” AMJ 1 (1853): 484.

7a. The miasmatic-oriented GBH was unconvinced that insensible micro-organismscould cause disease. When commenting on the many “living animal and vegetable forms”in London water detected by Hassall, the GBH emphasized in 1855 that “where . . . par-asites are the cause of disease, they exist as a palpable morbid product occupying someconsiderable share of the affected body.” In the muscardine of silkworm, for example, theentire insect is destroyed by the disease. Parasitic infestations in humans also indicated tothem that “the causative thing, remains as a material shaped body, susceptible of oculardemonstration, side by side with its effects, and having bulk proportionate to them”; UKGBH, Report of CSI, 46. Since such sizable and visible effects were manifestly not the casefor cholera, the GBH did not find Snow’s theory or his analogy to intestinal parasites per-suasive.

8. Liebig, Animal Chemistry, vi.9. Like Snow, Liebig was a multilevel scientific thinker: “My object in the present work has

been to direct attention to the points of intersection of chemistry with physiology, and topoint out those parts in which the sciences become, as it were, mixed up together”; Liebig,Animal Chemistry, viii.

9a. In this passage, Snow shares Liebig’s view of the chemical nature of all vital processes,rather than the one offered independently more than a decade earlier by Theodor Schwannand Charles Cagniard Latour that fermentation was caused by a living fungus-like organism.

10. Snow cited Schleiden, Principles of Scientific Botany, 35. The idea that the body is, in ef-fect, a chemical machine had been proposed nearly fifty years earlier by Jöns Jacob Berzelius(1779–1848): “Unreasonable as it may seem . . . our judgment, our memory, our reflections,as well as other functions of the brain, are organic chemical processes as well as, for instance,those of the abdomen, the intestines, the lungs, the glands, etc . . .”; quoted in Nordenskiöld,History of Biology, 372–73.

11. For a summary of this research, see OC, 34–48.12. Snow did not assume that his audience would agree with him that all complex vital pro-

cesses arose from preexisting, similar vital processes, and the reviewer for AMJ did not. Thisperson differed from Snow on one major issue, asserting that because at some point in theworld’s history the first vital process must have emerged from nonvital chemistry, analogy ofprocess required that each time a new living being was formed, it must arise by the same


chemical process by which the species first arose, that is, spontaneous generation; “Biblio-graphical notices,” AMJ 1 (1853): 486.

13. “[R]espiration has been compared to combustion, and the lungs to a furnace; but as wehave seen that the carbonic acid is really produced in the capillary circulation of the system,and only evolved in the lungs, the whole body ought to be compared to the furnace, and thelungs to the draught and chimney department . . .”; Snow, “On asphyxia, and on the resus-citation of still-born children” (1841), 223–24.

14. Toward the end of his life Snow appears to have been trying to extend this idea further.Richardson states that had Snow lived, he would probably have proceeded to the formal in-vestigation of cancer based on the concept that cancer represented a local disruption of thebody’s nutrition; L, xxxiii. Perhaps Snow thought of communicable diseases and cancer as twoways that continuous molecular changes might hijack the body’s normal metabolic processes.In the former case the result was the multiplication of the disease “poison,” which could causethe disease in others. In the latter case the result was the proliferation of an abnormal tissuethat could ultimately kill the person through the diversion of nutrition and substance butwhich could not be communicated to others. The nearest contemporary analogy may be acomputer virus, which seems to have been the modus operandi that Snow envisaged as thedisease agent in cholera.

15. See also Snow, ON, 18: 1092. Neither his theory of counter-affinity, nor his thesis thatanesthetics were anti-oxidative and antiseptic, appear to have a basis in modern science.

16. S. Snow recounts one of Snow’s contributions to the discussions of the WestminsterMedical Society that may help us date the origins of this concept. In the fall of 1838 he joinedthe debate over the death of a night watchman from the vapors of a new type of stove, claim-ing that the death was due not to carbon dioxide but to lack of oxygen, the absorption ofwhich by the lungs was prevented by the presence of carbon dioxide “owing to the affinitywhich one gas bore to another”; JS-EMP, 206, quoting Lancet 1 (1838–39): 419. Three monthslater, however, Snow recounted further animal experiments he had done that had changed hismind, and he now thought that carbon dioxide could kill via a mechanism different from theexclusion of oxygen. Thus, Snow seems to have been working on the precise mechanism ofcounteraffinity among gases as early as 1838.

17. Richardson, L, xvi.18. Ibid., xvii. It is likely that Snow actually said something very close to Richardson’s ac-

count. Snow referenced Graham’s experiments on phosphorus (cited below) and described asimilar experiment; ON, 18: 1092. Zuck thinks it possible that Graham’s demonstration trig-gered Snow’s experimental work on inhalation anesthetics in late 1846 to early 1847; Zuck,“Thomas Graham.” Shephard believes that Snow’s model anticipated some aspects of the mod-ern theory of anesthetic action, with the anesthetic molecule exerting its counteraffinity ef-fect at the level of the cell membrane; JS, 145.

19. Snow considered zymotic pathology one form of communication among a set of pos-sibilities. He disagreed with Farr’s inclusion of acute rheumatism and scurvy in the class ofzymotic diseases without evidence that they were, in fact, communicable, as well as for themore basic reason that zymosis accepted miasmatic origin and diffusion of disease. He won-dered what Farr meant by zymotic with respect to direct or indirect communication becausehe took fermentation to be, in and of itself, a communicable process; CMC, 156. For the con-trary view that Snow followed Liebig in accepting zymotic pathology, see Hamlin, Science ofImpurity, 127–51.

20. Also see Farley, “Parasites and the germ theory of disease.”21. A similar insight a century later eventuated in the eradication of smallpox. The princi-

ple that Snow here sets out is true, however, only of diseases like cholera and smallpox thathave no animal reservoir.


22. For a similar point, see Shephard, JS, 263–64. In the passage on syphilis, Snow refersimplicitly to the systems concepts of feedback loops and homeostasis.

23. Snow devoted a great deal of research, summarized in the early chapters of OC, to de-termining if there were any means by which the administration of chloroform might possi-bly be construed as pathogenic. This research allowed him to rule out air itself as a cause ofcommunicable disease. This would not by itself refute miasma theory but would give Snow agood grasp of how any airborne substance or particle might be expected to behave.

24. The type of medication that would arrest an attack of cholera if administered duringthe premonitory diarrheal stage was the sort of substance that would arrest putrefaction orfermentation, thus showing its property of “destroying low forms of organized beings.” Onesuch substance was chloroform, which “has gained some reputation as a remedy for cholera,when introduced into the stomach.” Because chloroform had no curative powers when in-haled, this confirmed for Snow his hypothesis that the poison of cholera was confined to thealimentary tract, was not inhaled, and did not invaded the bloodstream; “The principles onwhich the treatment of cholera should be based” (1854), 181.

25. On this mode Snow’s speculation proved a stretch. He said that there “is evidence tend-ing to show that typhoid fever, yellow fever, and plague, as well as cholera, are communicatedby accidentally swallowing the morbid excretions of the patients”; CMC, 168.

26. Earlier in the essay he had said that the reproduction and dissemination of species ofplants and animals were all examples of the process of continuous molecular change; CMC,150–51.

27. Snow’s thinking may be compared to that of the theologian and philosopher DavidHartley (1705–1757), who explained the mechanism of the mind by drawing on the New-tonian idea of the transmission of vision by atomic vibrations in the nerves. He suggested thatexperiences, sensations, and memories were stored in the brain as “vibrationuncles” that wereassociated with impressions of pleasure or pain. The “vibrationuncles” were subsequently ac-tivated by repetitions of the appropriate experiences, generating responses by association;Hartley, Observations on Man.

28. Once again the analysis suggests an analogy between Snow’s interdisciplinary, multilevelapproach and the biopsychosocial model; Engel, “Need for a new medical model”. It seems asafe assumption that Snow was able to make analogies between processes that occurred at themolecular and at the social levels of organization (i.e., continuous molecular changes withhuman language and speech). It also seems safe to say that Snow had at least a rudimentarynotion that some type of information transfer might be the common element at these dis-parate levels of organization—hence our willingness to employ a term like “molecular mem-ory” in elaborating Snow’s thought. However, one would not want to go beyond that andclaim that Snow had somehow anticipated the mid-twentieth-century sciences of cyberneticsand information theory, which formed part of the theoretical basis for the biopsychosocialmodel in the 1970s. Still, just as the biopsychosocial model was fundamentally an antireduc-tionist model, the social sweep of Snow’s thinking in CMC and elsewhere seems clearly to in-dicate that Snow was not a simple reductionist. By saying that human communication andculture were kinds of continuous molecular changes, he did not intend to say that these phe-nomena were nothing but chemical processes or that they could be appropriately studied inthe test tube. He showed in CMC that his multilevel, interdisciplinary mode of thinking soughtfunctional analogies at all levels of organization from the molecular to the social and viewedknowledge at any level of organization as potentially helpful in elucidating the problems ofdisease.

29. “Chemical researches on the nature and cause of cholera,” Lancet 1 (1850): 155. Hiscomment occurred at a meeting of the Royal Medical and Chirurgical Society. Compare Snow


on influenza and bad news with the first sentence in Daley and Gani, Epidemic Modelling:“This monograph is designed to introduce probabilists and statisticians to the diverse mod-els describing the spread of epidemics and rumours in a population.”

30.”Medical Society of London,” Lancet 1 (1855): 292.31. The phrase “collateral sciences” was an allusion to London Medical Gazette being a weekly

Journal of Medicine and the Collateral Sciences, which Snow had been reading since he was amedical student from 1836 to 1838 and contributing to regularly in more recent years. In1851, however, the subtitle was dropped when LMG merged with MT to become MTG.

32. Warner, “Idea of science in English medicine.”33. In the utilitarian civil engineering solutions of the sanitary reformers, who held great

sway with Parliament, medical investigators figured marginally as collectors of data. Chad-wick and his circle were relatively uncritical of the evidence on which they based their patho-logical and etiological assumptions. It was just these areas that Snow targeted as the founda-tion of a cultural authority based on, in Christopher Lawrence’s phrase, “a new medical scienceof disorder, the promotion of medically informed solutions and the advancement of the claimsof the medical expert”; C. Lawrence, Medicine in Modern Britain, 49–50. See also Bynum, Sci-ence and the Practice of Medicine, 74–75.

34. To judge from the reaction of the author of the only contemporary review of CMC wehave found, Snow accomplished his task as orator well. The reviewer praised him for the rich-ness and originality of his ideas; “Bibliographical notices,” AMJ 1 (1853): 484–89. That the re-viewer went on for five pages and dealt with Snow’s various points seriatim and in detail in-dicates his level of interest in the oration. For more recent interpretations of CMC, see Pelling,Cholera, 210, and Winkelstein, “New perspective on Snow.”


388

ON WEDNESDAY, 10 June 1858, John Snow had his mind onhis magnum opus, On Chloroform. He was working from his case

notes dating back to the summer of 1851, when he had tried out chlorated muri-atic ether (ethyl chloride) on patients at King’s College Hospital. The substancehad worked fairly well and might have proved safer than chloroform, but it wasunstable and difficult to obtain. Snow had procured only enough for operationson twenty patients, and that pint had to be brought specially from Paris. Althoughthe cases were old and small in number, it was important to give the substanceits own chapter. Perhaps some other chemist or anesthetist might find a betterway to synthesize this agent and bring it into common use. It was all part of Snow’slong search for a safer, better anesthetic. In a matter-of-fact way he was listingcases, describing all the types of surgery in which the drug had been used. He hadjust penned the name of Fergusson, a surgeon he had worked with from the be-ginning of inhaled anesthesia and a name he must have written in his casebooksa thousand times when he was stricken and fell off his chair.1 He told his house-keeper that he did not understand the nature of his complaint. He appeared tohave suffered a stroke and tried to treat himself, resting on a couch for a day, self-medicating with ether for the pain, and hoping that whatever was wrong wouldsoon right itself.

Chapter 16

Snow’s Multiple Legacies

It did not. Friday morning he began vomiting blood. Dr. George Budd and Dr.Charles Murchison were called in.2 Paralyzed on his left side and moving in and outof delirium, he expressed hope in his lucid moments that he would recover and re-sume his professional activities and expressed a wish to see a colleague, Dr. JamesTodd, who had expertise in epilepsy and neuralgia. He lingered for five more daysand died on 16 June. He was forty-five years old. An autopsy revealed his kidneys tobe shrunken, granular, and encysted. There was scar tissue from old bouts of tuber-culosis. He had died from a stroke. His excitability and somnolence may have beenthe result of some chronic illness, rather than vegetarianism, as his carnivorous med-ical school friend Joshua Parsons would have it. Regular exposure to a variety of tox-ins in his search for the perfect anesthetic may have hastened his end, but it is justas likely that his renal troubles had brought on the hypertension and stroke.

John Snow today is viewed as a pioneering figure in both anesthesia and epi-demiology. He has also been identified as a sort of patron saint within the subdisci-pline of medical cartography. In each of these fields, Snow’s legacy has assumed avery different form.

The Anesthesia Legacy

More controversy over the safety of chloroform occurred during the summer andfall after Snow’s death. Catastrophic accidents at Epsom and Dorking had re-ignitedcalls for abandoning the anesthetic agent. The Times printed several letters that madeuninformed claims about the dangers of chloroform; had Snow been alive he wouldsurely have responded with lucid rebuttals. Others had taken up his message, how-ever, and it was being heard. In articles published by the Lancet, Robert M. Gloverand Henry Potter, a long-time colleague of Snow’s at St. George’s Hospital, offeredcautions about the safe administration of chloroform that reflected Snow’s precepts.In fact, the Lancet had emerged as the self-styled champion of Snow’s anesthesialegacy. Its editorials seconded his long-standing concerns about the hanky methodand endorsed his inhaler: “Chloroform on a napkin is a dangerous and uncontrolledagent; administered through Snow’s inhaler, it is robbed of half its danger, by themore perfect manner in which we can control its inhalation.” The journal greetedwith enthusiasm the posthumous appearance of On Chloroform and Other Anæs-thetics (OC) in October 1858, and took a stand on its merits in advance of formalreviews: “We strongly recommend to thoughtful perusal the valuable monograph onthe subject of Anaesthesia which [Snow] has bequeathed to the profession. No onecan rise from reading this valuable digest of a wide experience and the observationof ten years of scientific and practical labour, without a feeling of regret that so muchcarelessness should still prevail in the administration of this most potent vapour, anda sense of necessity for a more extended instruction in the principles of anestheti-

Snow’s Multiple Legacies 389

zation.” In addition, the Lancet extracted a quotation from the departed-but-now-undisputed master chloroformist on the necessity of gradual induction and Snow’scrucial insight that the induction of anesthesia is “not caused so much by giving adose as by performing a process.”3

When the review of OC did appear in the Lancet the following month, it con-tained assessments of Snow and his work strikingly different from the vituperativead hominem remarks that the journal had carried just three years earlier after Snow’stestimony before the Parliamentary committee investigating the nuisance trades. “Wehave nothing but good to say of Dr. Snow, living or dead,” gushed the reviewer. Con-sequently it would have been “only graceful and becoming” if the memoir of Snow’slife that Richardson had prefixed to OC had “alluded to the active part taken by theLancet, in bringing Dr. Snow’s merits before the professional world at a time whensuch encouragement was all-important to him—when he was comparatively unno-ticed and unknown, and struggling at the painful commencement of what must al-ways be an arduous career.” Indeed, the Lancet had published Snow’s earliest lettersand articles periodically throughout his career. It seems that in rushing to embracea dead colleague, it forgot the scolding it had dished out when he gave Queen Vic-toria chloroform. Perhaps the pique directed at Richardson was a reaction to the factthat he had given prominence to the role MTG had played in Snow’s career. Or per-haps the Lancet’s changing attitudes betokened professional jealousy or unease thatthe very journal associated with medical radicalism had not been as consistently sup-portive during Snow’s improbable rise from a hard-scrabble GP to a pioneer in in-halation anesthesia as had its rivals, especially LMG (which amalgamated with MTto form MTG in 1852). When the Lancet reviewer turned to the substance of OC,his praise remained unalloyed as he focused on Snow’s methods for promoting safeinhalation and preventing fatalities. These methods were the key to Snow’s successas an anesthetist for more than a decade: “It was from his hands that the sufferer,whether alone in the curtained bedroom, or publicly on the hospital table, could bestobtain the full advantage of this greatest and most beneficent discovery of modernmedical science.”4 Across class lines, in public hospitals and in private rooms, Snowhad administered chloroform safely and effectively. None could match this record.

The review that appeared in the British Medical Journal in December 1858 wasmore interested in assessing OC ’s potential contributions to medical literature thanin lionizing its author. Nonetheless, the reviewer graciously suggested that an un-timely death prevented Snow from correcting drawbacks attributable to incompleterevising and unfinished argumentation. It ends abruptly during Snow’s discussionof ethyl chloride, an apparently deliberate choice by the editor, Richardson, to pre-serve the precise point at which Snow had suffered his fatal collapse (OC, 423). Therewas no better work on the subject, according to this reviewer, despite the fact thatSnow had neglected a growing body of knowledge on local anesthetics. In addition,he was unconvinced by Snow’s arguments for the absolute safety of chloroform andwondered why Snow had not used ether for patients, such as Major Evans, in whom


he suspected heart trouble. In fact, the reviewer suspected that the major had diedof chloroform, not fatty degeneration of the heart. Why, wondered the reviewer, hadSnow not entertained this possibility?5 Persistent doubts about the safety of chloro-form eventually led to its abandonment, but the principles Snow established guideinhalation anesthesia to the present day.

Snow left behind colleagues and advocates but no real disciples in anesthesia.Joseph Thomas Clover (1825–1882) inherited Snow’s mantle as the most influentialanesthetist in London practice.6 Clover followed his teaching in one important wayby developing the balloon method (started by Snow) by which one could give a con-stant concentration of chloroform without worrying about its evaporation into theroom air as it was being given. And Richardson, despite his role in editing OC forpublication, writing a biographical sketch, and retaining possession of all scientificpapers belonging to the deceased, never took up the inquiries Snow left dangling.Richardson’s primary contribu-tion to the field during his later life was to go on todiscover some seventy additional anesthetic agents, although none were major im-provements over ether or chloroform.7

For several decades after Snow’s death it seemed as if the field was moving in quitethe opposite direction from his research and practice. The commitment to scientificstudy of the physiological and pharmacological basis of narcotism and the relianceon controlled dosages by means of his apparatus, which defined Snow’s method, wasreplaced by lack of interest in laboratory work. He would have been chagrined tolearn that many anesthetists, who preferred the fast and easy handkerchief to an ap-paratus, had safety records as good as his own.8 The originality and creativity of hisexperimental work was not recognized again until the mid-twentieth century, whenthe journal British Anesthesia reprinted On the Inhalation of Ether (1847). The re-sponse was so positive that the journal proceeded to reprint OC in the same format.

Even if Snow’s scientific accomplishments could not be fully understood until themiddle of the twentieth century, his scientific deficiencies were revealed much ear-lier, although, even here, it was many decades after his death before the field was suf-ficiently advanced to take issue with any of his major findings. In 1911 A. GoodmanLevy demonstrated the mechanism of cardiac failure under chloroform.9 Using catshe showed that injecting a small amount of adrenaline could cause sudden ventric-ular fibrillation in an animal very lightly anesthetized with chloroform. Indeed, heshowed that lighter doses of chloroform might produce more cardiac irritability thandid heavier doses. In retrospect, those who suggested that fear or emotional excite-ment during the beginning stages of chloroform anesthesia might cause death hadsome justification; Snow, insisting that only an overdose could cause death, had beenwrong. Levy’s work did more than reveal how Snow, dazzled by his comprehensivetheory of the family of narcotic agents, ignored bits of data that might have revealedthe truth. Levy also showed, in retrospect, that Snow was no experimental physiol-ogist in the modern sense. Levy used the methods made famous by Claude Bernardabout a decade after Snow and was able to isolate the effects of chloroform in dif-


ferent doses on different organs in a living animal system.10 Snow could do no morethan observe the behavior of the intact animal during life and then try to look formore clues by dissecting the animal after death.

Later in the twentieth century more sophisticated machines for administeringanesthesia supplanted Snow’s primitive apparatus, even as they relied on similar prin-ciples. Both ether and chloroform were replaced by a variety of newer agents. (Be-sides its risk of cardiac toxicity, chloroform was later shown to be both a liver toxinand a cause of cancer.) Snow’s concept of the five degrees of narcotism is still valid,and today’s practice has not moved beyond it as a way to use bedside observationsto identify the depth of anesthesia, but his crude ideas of interference with oxidativeprocesses and counteraffinities were eventually replaced by theories of specific cellmembrane receptor sites for specific molecules—ironically, a model perhaps evenmore in keeping with Snow’s idea of continuous molecular changes and fully con-sistent with his notion of molecules as small, traveling packets of information, evenif he could not possibly have foreseen the chemical details of the modern theory. Inthe end, Snow’s place in the world of anesthesia is symbolized by the handsome stoneerected on his grave in 1951 by the Association of Anaesthetists of Great Britain andIreland to replace the original stone, which had been destroyed during the Blitz (Fig.16.1).10a Snow is revered as a pioneer and father figure, even if the modern practiceof anesthesia retains only traces of his science or techniques. Members of the His-tory of Anaesthesia Society have been especially keen researchers and guardians ofSnow’s significance in the development of this medical specialty.

The Epidemiological Legacy

At Snow’s death in 1858, few people working in public health and sanitation believedhis theory of the cause and transmission of cholera, yet today he may well be themost recognized figure in the history of public health. The American Public HealthAssociation joins the Royal College of Anaesthetists in supporting an annual JohnSnow lectureship to honor a distinguished member of its profession.11 A major pub-lic health consulting firm in Boston is named John Snow, Inc. At the U.S. Centersfor Disease Control in Atlanta, when an epidemiological problem requires a rapid,straightforward solution, staff have been heard to ask, “Where’s the handle to thisBroad Street pump?”12 It is virtually impossible to find a contemporary textbook ofepidemiology that fails to give Snow a prominent place.13

The transition to public health icon began with the fourth cholera epidemic tostrike England, in 1866. This epidemic affected mainly east London, claiming about4,000 victims in the late summer and early fall. Earlier the Rev. Henry Whitehead,Snow’s colleague in the investigations of the Broad Street outbreak of 1854, had re-acted to the news that cholera was again headed toward England by writing two


articles in a popular magazine that reminded the English reading public of Snow’scholera investigations and theories.14 A young epidemiologist, John Netten Radcliffe,read these articles and invited Whitehead to accompany him in an investigation ofthe outbreak in the east London districts.15 The two men traced the cause of the out-break to uncovered reservoirs at Old Ford that became contaminated with choleraevacuations during July 1866. The reservoirs belonged to the East London WaterCompany, which only tapped them during emergency water shortages. In an appendix


Figure 16.1. Snow’s gravestone, Brompton Cemetery, Westminster, London. The base reads,

“Inscription restored in 1938 by members of the Section of Anaesthetics of the Royal Society

of Medicine and Anaesthetists in the United States of America. The original memorial to John

Snow was destroyed by enemy action in April 1941. This replica was erected by the Associa-

tion of Anaesthetists of Great Britain and Ireland in September 1951” (photograph by Zuck).

to a report to Parliament by the Privy Council, Radcliffe cited Snow’s theory withapproval and mentioned the Broad Street investigation as a model for examining lo-calized outbreaks,16 but his superior, John Simon, made no mention of Snow’s the-ory or writings on the 1848–1849 and 1854 epidemics, neither in his introductionto the report nor in a postscript.17 He made amends seven years later in an annualreport to the Privy Council: “Indeed, with regard to the manner of the spread of theentero-zymotic diseases generally, it deserves notice that the whole pathological ar-gument which I am explaining grew among us in this country out of the very co-gent facts which our cholera-epidemics specially supplied, and to which the late Dr.John Snow, twenty-five years ago, had the great merit of forcing medical attention:an attention at first quite incredulous, but which, at least for the last fifteen years, asfacts have accumulated, has gradually been changing into conviction.”18 The Lancetwas quicker in making amends. Near the end of the 1866 cholera epidemic, it statedthat “the researches of Dr. Snow are among the most fruitful in modern medicine.He traced the history of cholera. We owe to him chiefly the severe induction by whichthe influence of the poisoning of water-supplies was proved. No greater service couldbe rendered to humanity than this; it has enabled us to meet and combat the disease, where alone it is to be vanquished, in its sources or channels of propaga-tion. . . . Dr. Snow was a great public benefactor, and the benefits which he conferred must be fresh in the minds of all.”18a

William Farr’s analysis of cholera mortality during the 1866 epidemic as well asRadcliffe’s report on east London did what MCC2 had not—it made Farr a nearlycomplete convert to Snow’s theory. In an interesting reinterpretation of the local mi-asmatic conclusions presented by the GBH in 1854, he wrote: “The final report ofthe scientific committee proved conclusively the extensive influence of water as amedium for the diffusion of the disease in its fatal forms. The zymotic theory wasestablished, and Dr. Snow’s view that the cholera-stuff was distributed in all its ac-tivity through water was confirmed. The special report of Dr. David Fraser, T. Hughes,and Mr. J. M. Ludlow inculpated the Broad-street pump to some extent in the ter-rible outbreak of the St. James’ district. But the subject was further and more con-clusively investigated by a committee, aided by Dr. Snow and by the Rev. HenryWhitehead.”19

Further evidence of acceptance and a subsequent enhancement of Snow’s reputa-tion as an epidemiologist appeared in an early work on the history of British sani-tary reform.19a Alexander Stewart and Edward Jenkins made some fun of the “eagerpertinacity” with which Snow put his views forward, “amusing to some and irksometo many.”20 While disagreeing with some aspects of Snow’s theory, Stewart and Jenk-ins nevertheless described the south London data as “startling” and the Broad Streetinvestigation by that “indefatigable inquirer” as “such as to compel the assent of themost incredulous to the proposition that [the outbreak] was mainly attributable tothe contamination of the water. . . . “21 Government acceptance followed some-what more slowly. The Local Government Board stated in its 1886 review of cholera,


“the remarkable and shrewd observations of Dr. Snow, demonstrat[ed] incontro-vertibly the connexion of cholera with a consumption of specifically polluted water,startl[ed] the profession with the novelty of his doctrine, and inaugurat[ed] a newepoch of etiological investigation.”22 Near the end of his life John Simon again ad-mitted that the 1856 government report on impure water had followed in the wakeof Snow’s pioneering investigation in south London.23 Well before the end of thecentury, British public health authorities were describing Snow’s work in mythicterms.23a

Snow’s theory was being discussed and approved in America at about the sametime that his reputation was being reinvigorated in England, but his theories receivedvirtually no attention on the Continent, where the “soil theory” of Max von Pet-tenkofer of Munich remained dominant in cholera thinking.24 While neither theUnited States nor Great Britain experienced a major cholera epidemic after 1866,10,000 lives were lost to cholera in Hamburg in 1893.25 Since that outbreak in Ham-burg, however, there has been no serious challenge to Snow’s explanation of the wa-ter-borne basis for metropolitan-level cholera epidemics.

Snow’s role as an exemplary figure in epidemiological research was first suggestedby the American public health expert William T. Sedgwick (1855–1920). He devotedthirteen pages of a 1902 textbook to Snow’s investigation of the Broad Street pump,which he considered “one of the most famous, and one of the most instructive casesof the conveyance of disease by polluted water.”26 Because his account was based onthe CIC Report, it was accurate, comprehensive, and credited Whitehead’s role in theinvestigation. Sometimes referred to as “the Father of Epidemiology in the UnitedStates,” Sedgwick guided his textbook through four reprints between 1902 and 1914.27

Subsequently, Snow was championed in the United States by Wade Hampton Frost(1880–1938), the first professor of epidemiology at the Johns Hopkins School of Hy-giene and Public Health, who did much to shape modern academic epidemiology inAmerica. In 1936 he prepared Snow on Cholera, a reprint of MCC2, CMC, and theabbreviated version of Richardson’s Life of Snow; this edition, itself reprinted, madea small part of Snow’s writings on cholera readily available to American readers.28

Frost characterized Snow’s reasoning in MCC2 as “a nearly perfect model” (ix) andadded, “His account should be read once as a story of exploration, many times as alesson in epidemiology” (xiv). When epidemiology education expanded in the 1950sand 1960s, the writers of the next generation of textbooks took Frost’s advice toheart, so that it is hard to find an epidemiologist educated between 1960 and 2000who was not introduced as a student to the Broad Street pump episode as an ex-emplary case study.29

To today’s epidemiologist Snow demonstrated the success of the epidemiologicalmethod—the search for confirmation of theories of disease origin in observationsmade at the population level—both as science and as the basis for public health pol-icy. Snow showed that seeking to understand the mode of transmission of disease, aphenomenon observable only in the field, could be more important than identify-


ing the specific agent that causes the disease under controlled conditions in the lab-oratory. Snow approached public health research in a hypotheticodeductive mannerthat permitted him to draw conclusions with a quantitative firmness typically asso-ciated with laboratory investigations. No stranger to the world of the laboratory,Snow was able to make the crucial imaginative leap to incorporate population andpublic health data into an experimental mind-set.

Snow’s contemporaries Ignaz Semmelweis, who showed the means by which puer-peral fever was communicated, and William Budd, who worked out the mode oftransmission of typhoid fever, were also members of the scientific fraternity thateventually led to modern epidemiology, but neither Semmelweis nor Budd per-formed the sorts of comprehensive analyses for which Snow is now known. Snow’sscientific followers include Sir Ronald Ross, who discovered in 1895 that the Anophe-les mosquito is the vector of malaria, and Charles Nicolle, who found in 1909 thattyphus was louse-borne. Walter Reed likewise uncovered in 1900 the way in whichyellow fever is transmitted. Snow had shown that not just the causes of disease, buttheir routes of transmission, are highly specific. In addition, he modeled public healthaction by inferring that the corollary of that specificity is to interrupt these routes.He pointed out that cholera can be controlled by nothing more complicated thanmaking sure that the discharges of cholera patients are not spread to others. AfterSnow, typhus proved controllable via the wearing of clean clothes, and yellow fevermortality was virtually eradicated by isolating patients and interfering with the breed-ing of mosquitos. As the first scientist to display the power of the epidemiologicalmethod, Snow helped to pave the way for the great sanitary triumphs that massivelyreduced infectious disease mortality during the twentieth century, and he did so us-ing tools of investigation and analysis that can be recognized as “modern” by today’sepidemiologists.

The Cartographic Legacy

Snow is a historical icon in anesthesia and a case study in modern epidemiology, buthis legacy in medical geography and medical cartography consists of a paradoxicalreplacement of his illustrative use of disease mapping by mythical caricatures of hismethods and actions. The first reappearance of a Snow map occurred in Sedgwick’s1902 textbook on public health. He redrew the map of cholera mortality in GoldenSquare that Snow had included in the CIC Report. Although the legend included thephrase “after the original,” the changes were significant. Sedgwick replaced the barsrepresenting each cholera death with dots. He retained Snow’s Voronoi-like diagramof equidistant walking access to two nearest pumps, but he did not comment on itssignificance.30 A half century later E. W. Gilbert redrew Snow’s map of the GoldenSquare outbreak from MCC2 and included it in a 1958 article on pioneer diseasemaps in Great Britain. Like Sedgwick, Gilbert replaced Snow’s bars with dots.


Unlike Sedgwick, Gilbert radically simplified the map by omitting many of the streets,and the caption misleadingly read “Dr. John Snow’s map (1855) of deaths fromcholera in the Broad Street area of London.”31 As a result Snow’s altered map be-came staples in articles and books about medical cartography, although readers wereprobably unaware that they were viewing modified recreations rather than reprintsof the original. Between 1952 and 2001 Snow’s map or some recreation of it wasreprinted in at least forty books and articles on medical cartography (Fig. 16.2). Itgradually made its way beyond technical publications into school textbooks, such asthe 1993 National Geographic Society resource guide for middle and high school ge-ography teachers.32

The capacity to misrepresent Snow’s map increased with the advent of geo-graphic information system (GIS) technology in the 1990s.33 GIS combines twocapacities of computers: graphic ability to draw highly detailed and elegant mapsand computational capacity to handle vast quantities of numerical data that canbe tied to geographic locations. One may, for example, feed in the home addressesof all new cases of cancer in one region over the last decade and then plot thecases to ascertain whether there is any geographical association between thesecases and the location of power lines. GIS is an extremely powerful tool in iden-tifying associations that may be important in the causation of disease, but it isjust as capable of being employed to reveal spurious associations that can seemextremely convincing when plotted on a highly detailed map. For example, GISwas behind claims for the existence of so-called cancer clusters, which eventuallyproved to be random occurrences.34

The GIS community has declared John Snow to be virtually its patron saint.35 Itis a simple matter to interpret Richardson’s account that Snow “had fixed his atten-tion on the Broad-street pump as the source and centre of the calamity” during the1854 cholera outbreak to make it seem that he used disease mapping as an induc-tive, analytical tool. It is also satisfying to accept Richardson’s heroic portrait ofSnow’s subsequent actions: “He advised the removal of the pump-handle as the grandprescription. The vestry were incredulous, but had the good sense to carry out theadvice. The pump-handle was removed, and the plague was stayed. There arose here-upon much discussion amongst the learned, much sneering and jeering even; for thepump-handle removal was a fact too great for the abstruse science men who wantedto discover the cause of a great natural phenomenon in some overwhelming scien-tific problem.”36 This mythical Snow seems an attractive figure to those GIS afi-cionados who see themselves as standing up for the public health in the face of thejeering throng and as rushing out into the real world to save real lives while thestodgy, plodding scientists fussily demand more evidence before they are willing toact. Maintenance of this Snow myth also has survival value for GIS. Advocates ofdisease mapping can point to no other incident in which the construction of a mapplayed a pivotal role in identifying the cause and cure of a disease. The desire for afoundational myth in medical cartography, particularly GIS, contributes to the


remarkable persistence of false versions of the Broad Street incident and Snow’s roleas an investigator and public health figure.

There is irony in the promulgation of this Snow myth. Modern GIS bearsgreater resemblance to the methods used by mid-nineteenth-century sanitariansthan to the real Snow. He implicated the Broad Street pump because he had acoherent, multilevel theory of the pathology and mode of transmission of cholera.The theory was essential; the map was an illustrative device to support his re-ports of the outbreak, added several months after he had completed his investi-gations. The sanitarians, by contrast, had no equally detailed and coherent the-ory of how effluvia caused disease. They relied on superficial observations andassociations. For example, Edmund Cooper pointed to a drainage map of GoldenSquare to show that cholera cases were not clustered near sewer vents, whereasinspectors from the GBH used a nearly identical map to determine that effluviaescaping from the sewers were the cause of the outbreak. Similar reliance onchance spatial associations by GIS advocates allies them with these sanitariansinstead of their purported hero.

* * *

Snow’s life in medical science proceeded like a series of continuous molecularchanges, one idea engendering the next. It was to his profession that he devotedhis life. Ironically, the professionalization and specialization that his career ad-vanced, as well as the reverence with which he is held by members of their re-spective epidemiological and anesthesiology societies, eventuated in a fracturingof the unity of his work. Richardson included his memoir of Snow’s life in OnChloroform, thereby linking that life to his contributions to anesthesia. The sound-ness of his epidemiological theory was eventually acknowledged, but it came withlittle recognition that his work in anesthesia was compatible and, in fact, criticalin its formulation and substantiation. Snow’s writing is often a model of lucidity,but his argument has often been taken out of context to make him appear “aheadof his time.” By modern standards some of his views were wrong, just as our suc-cessors will find errors in our thinking. Ultimately, however, the limits and stay-ing power of Snow’s thought seem less significant to us than its complex inte-gration of available knowledge in European medical sciences during the first halfof the nineteenth century.


Figure 16.2. Family tree of authors who have recreated Snow’s maps as published in MCC2

and the CIC Report. Four authors actually redrew Snow’s original MCC2 map, and two elec-

tronically digitized them for computer analysis purposes. All maps published since 1964 are

copies of these initial redrawings. The maps noted in four boxes with thick black borders were

used for teaching GIS.

Notes

1. This is our reconstruction of events based on OC, 420–23; CB, 185–93; and Richardson,L, xli–xliv. Richardson wrote that Snow had “written the last printed sentence” of the bookjust before he was struck down; L, xlii. “Fergusson” is the last word in the printed text of OC.

2. George Budd was the brother of William Budd of Bristol. Snow sent George Budd a com-plimentary copy of MCC2; see his letter of thanks, 3 January 1855, Clover/Snow, VIII.4.i.

3. The Lancet printed a short notice of Snow’s death, noting that he had made contribu-tions to inhalation anesthesia; Lancet 1 (26 June 1858): 635. On deaths from administrationof chloroform, see Times (4–11 September 1858). On Snow’s first advocates, see H. Potter,“Cautions in the administration of chloroform,” Lancet 2 (1858): 32, 34, 289; and R. M. Glover,“Report on anesthesia and anesthetic agents,” Lancet 2 (1858): 369–70, 393–95, 416–18. Forthe critique of the hanky method, see “Chloroform in surgery,” Lancet 2 (1858): 314. For theendorsement of OC, see “Chloroform and its administrators,” Lancet 2 (1858): 407.

4. “Review,” Lancet 2 (1858): 555–56.5. “Review,” British Medical Journal 2 (1858): 1047–49. OC begins with a history of anes-

thetics, focusing more on ancient medicine than on the recent past. Thereafter, Snow includeddiscussion of inhalation as a route for administering medications of all classes; a brief historyof chloroform and a description of its chemical and physical properties; the stages of narco-tism and related key experiments from the ON series; practical aspects of preparing the pa-tient, administering chloroform, and treating aftereffects; a long section on deaths from chlo-roform describing his theory of the mechanism of death and analyzing fifty case reports offatalities; and administration of chloroform in different types of operations. Shorter sectionsof the book addressed ether, amylene, and an agent similar to Dutch liquid.

6. Clover trained as a surgeon before deciding to become a specialist in anesthesia. He ex-erted his influence primarily by serving on various study commissions and speaking at soci-ety meetings. Like Snow, he was resourceful in designing and applying new apparatuses basedon scientific principles; unlike Snow, he did no research himself on the physiology and phar-macology of anesthesia. His death left a leadership vacuum in British anesthesia, and the fieldsuffered a brief period of decline; Duncum, Inhalation Anesthesia, 26, 241–46, 457–59.

7. Some are discussed in Ibid., 264, 385–86.8. There were anesthetists with equivalent safety records, despite use of the handkerchief,

such as Syme in Scotland; Duncum, Inhalation Anesthesia, 204.9. Levy, Chloroform Anæsthesia.10. In Snow’s own day only Pierre Jean-Marie Flourens (1794–1867) exemplified this ex-

perimental method and thus became one of the few contemporaries upon whom Snow ac-tually relied for experimental evidence. Snow cited with approval Flourens’s experiments earlyin 1847 to show the order in which the various portions of the central nervous system cameunder the influence of inhaled anesthetics and to show that chloroform was capable of act-ing directly on peripheral nerves. Flourens was an associate of Magendie, who had earlier ex-perimented on dogs to isolate the respiratory center within the medulla of the brain (1842).He was thus well poised upon the advent of ether anesthesia to perform the studies necessaryto isolate the effects of ether on specific centers within the brain; Duncum, Inhalation Anes-thesia, 159–61.

10a. In the spring of 1859, Richardson undertook an appeal for funds for “a plain, butdurable monument” to be placed over Snow’s grave in Brompton cemetery as a “simple trib-ute to the memory of our late estimable and distinguished brother in science”; “Monumentto the late Dr Snow,” Lancet 1 (1859): 548, and British Medical Journal 3 (1859): 411, 415.


11. In September 2001 the University of Durham opened a new residential college namedthe John Snow College, adapting a depiction of a water pump as the college’s distinctive badge.At the time of his death, a few contemporaries did praise Snow’s “immense labours in thecause of sanitary science”; SR&JPH 4 (1858): opposite table of contents. In a presidential ad-dress at the Royal Medical-Chirurgical Society in March 1859, Charles Locock noted that Snow“paid great attention to the investigation of cholera, and published some papers on his viewsof the effect of drinking impure water as propagating that disease”; Proceedings, RM-CS 3(1858–61), 47.

12. Dr. David Satcher, then director of the Centers for Disease Control and Prevention (latersurgeon general) allegedly would say, “Look for the ‘Broad Street pump’ for good publichealth”; FP Report 3 (1997): 7.

13. For examples see Brownson and Petitti, Applied Epidemiology, 5; Friis and Sellers, Epi-demiology for Public Health Practice, 15–22, 138, 324; Gordis, Epidemiology, 9–10, 257; Kelsey,Thompson, and Evans, Observational Epidemiology, 85, 213–14, 236; McMahon and Tri-chopoulos, Epidemiology, 8–10, 69, 72–73, 86, 327; J. N. Morris, Uses of Epidemiology, 3, 142,144; and G. Stewart, Trends in Epidemiology, 7–8.

14. Whitehead, “The Broad Street pump,” and “The influence of impure water on the spreadof cholera.”

15. Whitehead recalled these events in the farewell speech he made on leaving the Londonministry in 1874; Rawnsley, Henry Whitehead, 226–27. John Netten Radcliffe (1830?–1884)was a Yorkshireman like Snow and received his medical education at Leeds. He was employedby the Privy Council between 1865 and 1869 to investigate and write reports on sanitationand worked under the supervision of its medical officer, John Simon. Later Radcliffe servedas medical inspector to the Local Government Board and wrote on plague and enteric fever.He was an officer of the Epidemiological Society of London and was eulogized by the soci-ety; Transactions of the Epidemiological Society of London 4 (1884–85): 1. See also Brocking-ton, Public Health in the Nineteenth Century, 262–64. When Thomas Snow defended his latebrother’s reputation in a letter to the Times, he claimed that MCC2 had been as full of spe-cific facts, of an equally decisive character, as Netten Radcliffe’s observations were in 1866; T.Snow, “Propagation of cholera,” Times (20 November 1885). See also T. Snow, “Dr. Snow onthe communication of cholera,” Times (26 September 1885).

16. UK Parliament, Ninth Report of the Medical Officer of the Privy Council, appendix 7.f.“Mr. J. Netten Radcliffe on cholera in London, and especially the eastern districts,” 264–367.

17. Ibid., see particularly 22 and 295–96.18. Simon, “Supplementary report,” Annual Report of 1874 to the Local Government Board,

in Public Health Reports, 460.18a. Lancet 2 (1866): 363–64. The editorial also endorsed an application, prepared by Ben-

jamin Richardson and Thomas Snow, to have “the sisters of the late Dr Snow . . . [who] are,in fact, almost if not entirely without means,” added to the civil list for a state pension. “Wecannot conceive a more fitting case for the exercise of Royal and national bounty,” stated theeditors at the Lancet. The Medical Society of London and the British Medical Association fol-lowed suit, and the pension was approved.

19. Farr, “Report on the cholera epidemic of 1866 in England,” xi. Later in the introductionhe wrote: “It is well known that the Broad-street explosion was traced to a pump, which drewits water from a well into which the dejections of a child found their way in a circuitous route”;xxxiii.

19a. Eyler argues that by the 1860s, increasing reliance on biological rather than chemicalevidence in medical research provided the theoretical context which led Farr to be increas-ingly receptive to Snow’s line of thinking; “Changing assessments of cholera studies.”


20. Stewart and Jenkins, Sanitary Reform, 9–10. According to Finn, this book was “a keydocument in the whole process of sanitary reform which unfolded from 1866 to 1875”; “In-troduction” (to reprint edition), 24.

21. Ibid., 11. They did not accept, however, that cholera was spread exclusively via the oralroute.

22. “General report of the results of the sanitary survey made in anticipation of cholera,1885–86,” UK Local Government Board, 15th Annual Report, 110.

23. Simon, English Sanitary Institutions, 241, 261, 263.23a. Richard Thorne Thorne, principal medical officer of the Local Government Board and

president of the Epidemiological Society of London wrote, “it was during this epidemic [of1854] that the circumstances occurred which have made the pump in Broad Street, GoldenSquare, historic in the annals of English cholera”; Thorne Thorne, Progress of Preventive Med-icine, 56. Rollo Russell claimed that “the large part taken by infected water in the propagationof cholera is established beyond all question by the inquiries of Dr. Snow”; Russell, Epidemics,Plagues and Fevers, 77. An early textbook on public health describes the Golden Square out-break as “the celebrated instance of the Broad Street pump”; Notter and Horrocks, Theory andPractice of Hygiene, 31. For the view that Snow was essentially unrecognized as a significantcontributor to public health until 1936, see Vandenbroucke, “Changing images of John Snowin the history of epidemiology,” and Vandenbroucke, et al., “Who made John Snow a hero?”

24. Among the cholera investigators in the U. S. who praised Snow’s work, see Peters, Noteson Cholera, 47–50; Peters agreed that cholera was caused by a specific poison found particu-larly in cholera discharges and largely conveyed by water supplies. McClellan wrote that “theinvestigations of Dr. Snow in London during the epidemics of 1849, 1853, and 1854 provethat cholera may be actively distributed through the medium of drinking water”; History ofthe Cholera Epidemic, 58. See E. Goodeve’s chapter on epidemic cholera in Reynolds andHartshorne, A System of Medicine, 389, and Wendt, Treatise on Asiatic Cholera, 120. Billingslists fourteen of Snow’s writings on cholera in Bibliography of Cholera.

25. R. Evans, Death in Hamburg.26. Sedgwick, Principles of Sanitary Science, 170–82.27. Jordan, Whipple, and Winslow, A Pioneer in Public Health, 62. Sedgwick founded a pro-

gram in public health at MIT in 1883 and then developed the first joint program for train-ing public health officials at Harvard in 1912.

28. Frost, Snow on Cholera.29. In the 1960s Milton Terris, professor of preventive medicine at New York Medical Col-

lege, developed a set of epidemiological exercises based on historical readings that were widelyused in programs in epidemiology, public health, and medicine. The exercise based on MCC2,initially drafted by Clark and Gelman, revised by Terris, covered both the south London studyand the Broad Street investigation; E. Clark and Gelman, “Epidemiology exercise: Snow oncholera.”

30. Sedgwick, Principles of Sanitary Science, ix. For more on the Voronoi concept and itsformulation, see Okabe et al., Spatial Tessellations, 6–12.

31. Gilbert, “Pioneer maps of health and disease in England.” See also Rosenberg, Explain-ing Epidemics, 119.

32. National Geographic Society, “Fighting cholera with maps,” in TC Tool Kit.33. Geographic information systems are “automated systems for the capture, storage, re-

trieval, analysis, and display of spatial data”; Clarke, Analytical and Computer Cartography, 11.GIS can be thought of as software that is used to organize and manage georeferenced dataand then to display this information on areawide maps. GIS therefore comprises two closelyintegrated databases, one statistical, the other geographical. The latter contains coordinate data


usually obtained from maps, fieldwork, and/or from airborne or satellite remote-sensing im-agery. The data can be in the form of points (such as cholera deaths, houses, clinics), lines(roads, rivers), and polygons (residential suburbs, health districts). The attribute database con-tains data about the characteristics of the geographical features, such as demographic data onage and sex distribution, socioeconomic profiles, immunization coverage, and type of roadaccess; see Maguire, “An overview and definition of GIS,” 9–20; Richards et al., “Geographicinformation systems and public health: Mapping the future”; Clarke et al., “On epidemiologyand geographic information systems: A review and discussion of future directions”; andLoslier, “Geographical information systems (GIS) from a health perspective.” In 1995 GIS wasidentified as one of the top-ten most notable new developments in epidemiology; Waller, “Epi-demiologic uses of geographic information systems (GIS)”; and Naphtali, “GIS in healthcare:When geography matters.”

34. S. Sachs, “Families are gathering clout in study of cancer clusters,” Dallas Morning News(27 September 1998); R. Perez-Pena, “Critics question overdue plan to track cancer and pol-lution,” New York Times (18 January 1998).

35. Snow’s Broad Street map has been called “one of the first uses of a rudimentary GIS . . .”; P. Forster, “Come the next pandemic . . . will we be prepared?” The Daily Telegraph (25 March 1999). Currently, the Broad Street pump incident features prominentlyin training exercises and programs for GIS; see, for instance, an internet exercise:http://www.esri.com/news/arcuser/0499/umbrella.html (accessed January 2001).

36. Richardson, L, xxi.


http://www.esri.com/news/arcuser/0499/umbrella.html

404

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420 Bibliography

Abbey-row, 350Abstinence pledge, 47, 53n43Acetone, 164n40Ackerknecht, Erwin H., 193nn59–60Acomb, 17, 18fAddison, Thomas, 244Addison, William, 86, 107n66Ague, 9, 167, 248, 396Albion Terrace, 208–10, 208f, 209f, 212–13,

225n22, 226n31, 257–58Albumin, 85–86Alcohol (C2H5OH)

chloroform, ether and, 157–58, 164n40narcotism and, 158–59physiological action of, 157–58

Aldersgate Street School, 64, 100–01, 146, 165,185, 238

Alison, William, 3, 12n5, 351, 353–54, 358n52All Saints North Street

baptismal records of, 33n10, 33n12, 34nn14–15Church of, 14–16, 15f , 21–23Parish of, 17–18, 22–23, 33n4

Alum, 353, 358n50American Public Health Association, 392Ampthill Square, 251n11Amyl alcohol (C5H12O), 366Amylene (C5H10), 365–70, 370n12

deaths from, 369–70, 371n25in midwifery, 368

“Anasarca Which Follows Scarlatina,” 104n30Anatomy Act of 1832, 30, 37n54, 77n17Andrew, John, Jr., 47–48, 54n45Anesthesia. See Ether; ChloroformAnglesey, Lord, 233–34Angus, Alexander, 82Animal(s)

chemistry, 375–76experiments on, 1, 3–5, 71–72, 90, 94, 98,

123–24, 126–27, 137n56, 141, 146, 148–50,150t, 151, 161, 366, 391

Animal Chemistry (Liebig), 157, 375Animalculae, 176, 290Anticontagionists. See also Miasma

maps and, 320, 337n2

and quarantine, 191n38, 192n44, 212, 226n30theories of, 167, 172–75, 175f, 178t, 192n44,

210, 223n8, 274, 378–79Antivitalism, 5Apothecaries, 4, 24–28

Act of 1815, 25, 77n13Hall (AH), 58t, 60fhospital, 68Licentiates of the Society of (LSA), 28, 68pre-1815 medical men, 36n44surgeon-apothecaries, 4, 6, 28(Worshipful) Society of, 24–25, 56–59, 58t,

77n14Archbishop Holgate’s Grammar School, 34n21Arnott, Neal, 341, 356n18Ash & Sons (manufacturer of dentists’

materials), 297Ashley, Lord, 238Askham, Mary, 17–18, 33n6Askham Bryan, 18fAskham-Empson genealogy, 19fAskham-Snow genealogy, 20fAsphyxia, 1–3

causes of, 93–94, 123definition of, 94in infants, 2–4, 90–95oxidation theory, 160–62Snow’s research on, 2–4, 12n7, 93–98

Association Medical Journal (AMJ), 243–44,351

Association of Anaesthetists of Great Britainand Ireland, 392, 393f

Asthenia, 45Astrakhan, 169Atkinson, Anne, 130Attree, William Hooper, 363Aubing, 328Autoexperiments, 124, 141, 159–60, 164n43,

178, 193n60, 201, 211, 232, 251n3

Babington, Benjamin Guy, 239, 252n19, 341Bacon, Francis, 74–75, 260Baldwin, Peter, 172,192n44Bancroft, Edward N., 13n29

Index

421

Barber-surgeons, 24–28, 26tBarker, Thomas Jones, 251n11Barrett, Frank, 338n27Bateman’s Buildings, 75, 77n12Bath, 56Battersea, 210, 244, 264Bavaria, 328Bayle, Gaspard L., 79n57Bazalgette, Joseph, 342Beauchamp, Mrs. Proctor, 253n29Bell, G.H., 170, 187–88, 189n17, 190n18, 191n41Bell, Jacob, 118, 142, 163n3, 226n25, 227n39Bennet, William, 233Bentham, Jeremy, 171–72, 190n26Benthamite, 171–72, 174, 181Benzin (benzene, C6H6), 151–52Bermondsey, 249Bernard, Claude, 105n45, 132, 391–92Berners Street, 283, 318Berwick Street, 285Berzelius, J.J., 384n10Bibliocholera, 189n4Bichat, Marie Francois Xavier, 3, 12nn5–6,

79n55, 93Bigelow, Henry, 134n1Bigelow, Jacob, 134n1Binghamton, 369Biopsychosocial model, 229n46, 386n28Bird, Golding, 71–72, 79n47, 86, 90, 105n34,

107n66, 109n87Birmingham, 349Bisulphuret of carbon (carbon disulphide, CS2),

151–52Blackall, John, 104n30Blackfriars, 245Blenkinsopp, 203Blisters, 43–44, 51n16, 52nn18–19Blood-letting, 86, 188Blue Coat Charity School, 22, 34n21Board of Governors and Directors of the Poor,

292–93, 296pump handle removal by, 294–95, 313n31,

313n37, 331Snow’s meeting with, 294, 313n31

Board of Health. See Central Board of Health;General Board of Health

Boards of Guardians, 171Boden theory, 328Böhm, Ludvik, 181, 185Bonaparte, Napoleon, 79n57Bootham School (Friends’), 35n24Bootham Ward, 32n2Boott, Francis, 110Borough Road, 155, 276Boston, 110

Botany, 63Brande, William, 144–45Bread, rickets and, 353, 358n50Breath

Breathalyzer, 158detection experiments for, 158–60

Brentford, 255Brera, V.L., 206Bridge Street, 245, 288Bright, John, 66Bright, Richard, 85–86, 98Brighton, 298Bristol, 215, 231, 400n2Bristol Microscopical Society, 227n38British Anesthesia, 391British Association in Glasgow, 384n6British and Foreign Medical Review, 104n29,

138nn66–67British Medical Association, 349–50,

357nn33–34, 401n18aBritish Medical Journal, 350, 390–91Brittan, Frederick, 216–17, 227n39, 231, 375Broad Street, 284f, 293f, 297, 309f, 311n3,

314n44. See also Golden SquareBenjamin Hall on, 290, 30940 Broad Street, 283–84, 290, 293f, 294–96,

306, 307f, 307, 309f, 310, 311n4, 314n40,336f, 394

General Board of Health (GBH) and, 308f,309–10, 337f, 346

Grand Junction Water Company and, 288New River Water Company and, 288, 298pump handle myths about, 397, 315n54, 320,

402n23aSnow’s maps of, 302–03, 309f, 316n75, 320,

331–37, 332f, 333f, 334–35, 336fwater pump at, 284–85, 289f, 290, 294,

301–03, 310, 313n31, 316n78, 336f,339n34, 397, 401n19, 402n23a

Brodie, Benjamin C., 70, 93–94, 128, 229n49,244, 383

Bromoform (HCBr3), 142, 151–53Brompton, 234

Cemetery, 400n10aBroussais, J.V., 216, 196n82Brown, John (Brunonian system), 45, 49, 85,

188Brown, P.E., 223n9, 224n12, 228n43Bryson, Alexander, 239, 246Buchanan, Andrew, 148Buckingham Palace, 242, 369Budd, George, 389, 400n2Budd, William, 192n46, 216, 228n42, 341, 354,

396, 400n2effluvial transmission of cholera, 216, 316n72

422 Index

fungus theory of, 215–19, 217f, 228n42parasites and, 227n36Snow’s hypothesis and, 218, 349, 351, 355n5,

375typhoid fever and, 216, 227n35as village epidemiologist, 226n24

Burling Slip, 321Burne, John, 66Burnop Field, 42–45, 51n15Burnopfield Colliery, 43Burnopfield Hall, 42Busk, George, 216

Cabanis, Pierre, 79n55Cairo, 196n87Camberwell, 233Cambridge Street, 283–85Cambridge University, 76, 77n13, 99, 237Campbell, Lord, 156–57, 235Campleshon, 22Canterbury, Archbishop of, 243Cantharides, 51n16Carbonic acid gas, 88, 90Cardiopulmonary resuscitation (CPR), 1–2Carlisle, Anthony, Sir, 66Cartography, medical, 321–23, 397. See also

MapsCase Books (CB) (Snow), 43, 78n27, 83, 252n28,

270, 360, 363. See also Snow, JohnCaspian Sea, 169Census

of 1841, 81of 1851, 310n1

Centers for Disease Control, 392Central Board of Health, 42Chadwick, Edwin, 171–72, 175, 255–56, 290,

294, 342, 354n1, 355n9, 383, 387n33Chambers, W.F., 190n19, 190n23Charing Cross Hospital, 99, 108n78, 362Chartist Movement, 170Chelsea Water Company, 247, 273, 277n4,

281n33Chemistry, 64t, 97, 223n8Chester Street, Belgravia, 40Children. See also Infants

chloroform and, 363–64rickets and, 352–53

Chloric ether, 142Chloroform, 4–5, 109n85, 133, 140, 143, 236,

366alcohol, ether and, 157–58, 164n40chemical properties of, 142children and, 363–64as cholera treatment, 165–66, 188n1, 250criminal use of, 155–57, 235–36

deaths while under, 145–47, 165, 364–65,368, 370n4, 400n5

early experiments with, 150tHannah Greener and, 143–47inhalers, 154, 154fmodus operandi of, 157–60as new letheon agent, 141in midwifery, 8, 240–44ON experiments with, 149–50, 150t, 153pharmacology of, 141–43, 153physiological effects of, 153–55, 234quantity of, 141trespiration and, 148–49Simpson and, 142, 240–41Snow on, 141–43, 141t, 146–47, 153–55,

360–62, 400n5various responses to, 361–62

Chlorophobia, 155–57, 235–36Choler, 189n16Cholera

Albion Terrace outbreak of, 208–10, 208f,209f, 212–13, 225n22, 226n31

anticontagionist theory of, 167, 172–75, 175f,176f , 178t, 192n44

Asiatic, 41–42, 169, 173, 178–79, 190nn18–19asphyxia, 200, 223n5, 250atmosphere and, 191n32, 191n38biblio, 189n4Broad Street/Golden Square outbreak of

1854, 8, 283–310, 293f, 309f, 310, 328–37,394, 402n23a, 403n35

chloroform and, 165–66, 188n1, 200,386nn23–24

CMC and, 374–75contagionist theory of, 166, 175–77, 176f,

178tcontingent contagionist theory of, 167deaths from, 191n42, 207, 209, 269–77, 276t,

308fat Edinburgh, 169, 174English, 168, 195n76epidemic of 1831–1832, 7, 33n4, 48, 70, 166,

169–70, 176, 178, 185, 187, 194n71,196n86, 198n104, 201, 215, 248, 321–23

epidemic of 1848–1849, 7, 11, 166, 171, 175,187, 199–200, 206–10, 215, 229n50, 248,256, 260, 288, 319f , 320

epidemic of 1853–1854, 7, 166, 175, 187,259–77, 263f, 276t

epidemic of 1866 and, 12, 316n78, 394etymology of, 190n18excessive drinking and, 211fomites and, 166fungus theory and, 215–19, 217f, 227n39,

228n40, 231–33

Index 423

Cholera (continued)Garrod on, 185, 205, 224nn14–15, 232, 244Horsleydown outbreak of, 207, 213immorality and, 174influenza and, 173, 232, 379–80mapping, 318–39. See also Cartography;

Maps; Snow, Johnmorbus, 169t, 189n16, 323mortality rates for, 189n17in Newcastle, 169, 248, 273, 277n7in North Street, 45oxidation and, 377–78pathology of, 40, 185–88and population size, 215prevention of, 203, 211–12, 248–49, 296published works on, 166saline treatments for, 186–87, 198n102,

198n104, 224n15, 250Snow’s theory of, 148, 202–10, 203f, 224n13,

226nn28–29Snow’s treatments for, 200, 249–51spasmodic, 168f, 169, 189n13, 322fstages of, 168, 185, 186, 386n24stomach acid and, 211symptoms, 168, 186terminology, 168, 169ttransmission of, 175–77, 176f, 192n54,

193n60, 201, 204–05, 379–80treatments for, 166, 185–88, 197nn94–95,

197n97, 199–200vibrio cholerae, 303, 193n60, 228n40water treatment for, 186–87

“Cholera and the London Water Supply” (Farr),259

Cholera Inquiry Committee (CIC), 301–10. Seealso Snow, John; Whitehead, Henry

Chorlton-Upon-Medlock district, 327Chowne, William D., 93Christchurch, 272, 275, 347Church of England (National Society), 22–23,

34n21Churchill, John (publisher), 137n64, 281n35,

302–03“Circulation in the Capillary Blood-Vessels,” 97,

107nn69–70Clapham, 6, 270, 280n29, 281n39aClark, E. Gurney, 402n29Clark, James, 242, 252n27, 341, 361, 363Clark, William Stephenson, 24, 36n36Clarke, Mansfield, 70Clover, Joseph Thomas, 135n13, 370, 391,

400n6Clutterbuck, Henry, 108n84, 165–66, 188n1, 238College of Physicians, 25, 26t. See also Royal

College of Physicians

Combustion, 377, 385n13Commissioners Inquiring into the State of

Large Towns and Populous Districts, 33n4,171, 340. See also Health of Towns

Committee on Scientific Inquiries. See GeneralBoard of Health

Company of Grocers, 26t“Condition of Surrey Court, Horsleydown,”

207–08Contagionists, 166

theories of, 166–67, 175–77, 176f, 178t, 201,223n9

Contingent contagionists, 181, 194n63, 210GBH and, 180, 194n63Johnson’s theory and, 178–79, 180fsanitary reforms and, 179–80theory comparisons and, 176t

Continuous molecular changes. See OnContinuous Molecular Changes; Snow, John

Cooper, Astley, 65, 68, 106n57Cooper, Edmund, 295, 300, 314n52,

315nn53–54, 328–31, 330f , 336, 399Copland, James, 177, 223n5, 232–33Corbyn, Frederick, 195n74Cornwall, 353Corvisart, Jean N., 79n57Court of Queen’s Bench, 156Cow yards, 284, 311n5Cowdell, Charles, 196n82, 198n104Cowen, William, 130Cowpox, 341, 382Cronstadt, 278n15Cullen, William, 44–49, 52nn25–26, 54n50, 85,

107n70, 136n30, 188, 194n69, 232Curling, T.B., 225n19Cutler, William, 138n71

Dalton, John, 116, 136n30Danish, 15Darwin, Charles, 80n58, 193n60Darwin, Erasmus, 193n60Davey Smith, George, 280n26b, 281n39aDavid Copperfield, 140Davidson, Dr., 96Davies, David, 145Davison, Robert, 213Davy, Humphrey, 367de Martine, Collard, 90de Martingny, Collard, 12n5“Death from Chloroform in a Case of Fatty

Degeneration of the Heart,” 365Demarquay, Jean Nicholas, 151Dentistry, 6–7, 110, 129–30Diamond, Hugh W., 82Diapnetics, 97, 113

424 Index

Dictionary of Practical Medicine (Copland), 232Dilettanti, 372Dilution, 150Disease mapping. See MapsDiseases

classification of, 79n56febrile, 11, 44, 173, 188, 200mental, 98

Distillation of water, 40Diuretics, 97Dodsworth, John, 23Dodsworth Schools, 23, 35n25, 36n28Donovan, Catherine, 155Dorking, 389Dosimetric technique, 138n81Dropsy, 104n30Drummond, J.L., 225n19Dulwich, 262Dumeril, Auguste, 151Dumfries, 257Duncum, Barbara M., 135n21Dunglison, Robley, 190n18Durham, 28, 41–42Dutch liquid (1,2-dichloroethane C2H4Cl2),

151–53, 400n5Dysentery, 173, 379

Easson, Kay, 38n57East India Company, 168East London Water Company, 209, 255, 393Edgware Road, 292Edinburgh, 5–6, 30, 140, 169, 174, 367Edinburgh Medical Journal, 351Edwards, William Frédéric, 3, 12n5Effluvia, 9–10, 173–74, 177, 216, 223n8, 232,

313n39. See also Miasma;Anticontagionists; ContingentContagionists

Elementary schooling in England, 22,34nn20–21, 35nn22–23, 35n25

Eley, Susannah (the Hampstead widow),285–87, 297–98, 315n62, 333

niece of, 297–98servant of, 298sons of, 285, 290

Eley’s Percussion Cap Factory, 285, 287, 297,311n7

Ellis, Richard, 35n23Embleton, Dennis, 213Emigrant Refuge Hospital, 190n19Emmet, Thomas Addis, 190n19Empson, Charles, 24, 31–32, 32f, 38nn59–60,

51n14, 56, 251n11Empson, John, 17–18, 33n6, 34n13Empson-Askham genealogy, 19f

Engel, George, 229n46English Poor Law of 1601, 42, 52n20Enlightenment, 74, 88Entozoa, 224n17, 225n19, 227n36, 379. See also

WormsEpidemic constitution, theory of, 44, 167Epidemic curve, 222Epidemiological Society of London, 229n50,

238–40, 246–48, 302, 316n73, 318–20, 332,337nn3–4, 341–42, 346–48, 356n22,401n15, 402n23a

Epidemiologist, village, 208, 212–13, 226n24Epidemiology, 6

clinical, 138n68shoe-leather, 266, 285–310

Epps, John, 61, 63, 70, 76n10, 78n41Epsom, 389Erysipelas, 44–45, 379Ether, 110–39

administration of, 113, 131, 134n11, 138n81alcohol, chloroform and, 157–59, 164n40as anesthesia, 110, 134n2, 366animals and, 124, 126–27, 137n56, 150–51cerebral functions and, 124chloric, 142inhalers, 112–14, 117–22, 119f, 120f, 121f,

131, 136n39, 137n54midwifery and, 135n17modus operandi of, 157–60respiration and, 113, 148–49sponge, 131, 138n81sulphuric, 143vicissitudes of, 131–34volatility of, 116

Etherizationfour degrees (stages) of, 124–27, 135n13,

363–64Ethyl bromide (C2H5Br), 151–53Ethylene (C2H4), 366Evans, Major, 364–65, 390–91Everett, Edward, 134n1Everitt, David, 71, 79n45Eyler, John M., 355n5, 401n19aExeter, 187, 215, 258, 323, 324f, 339n29

Farley, John, 206, 225n18Farr, William, 181–85, 182f, 191n42, 196n82,

265, 291, 383contingent contagionist theory of, 183fon crucial experiments, 259–60elevation theory of, 184f , 259–60, 274,

278n18, 327and Henle, 195n79on Snow’s theory, 259–60, 278n18, 394,

401n19

Index 425

Farr, William (continued)theories of, 356n18water supply inquiry of 1854 and, 261f, 262,

267, 270, 273, 279n23, 282n41, 285, 348on zymotic diseases, 181–85, 195nn78–79,

259–60, 278n18, 354, 383n4, 385n19, 394Farrell, Mr., 301Farringdon Street, 288Febrile diseases, 44, 52n26, 173, 200Ferguson, Daniel, 118, 121, 128Fergusson, William, 138n71, 242, 359, 368–69,

388Fermentation, 374–76, 384n9aFevers, 44–45, 52n26Fife, George, 30Fife, John, 30, 144Finn, M.W., 402n20First Reform Bill of 1831–1832, 5, 45First Report of the Metropolitan Sanitary

Commission, 280n32Flourens, Pierre Jean-Marie, 126–27, 132, 161,

165, 400n10Flourens’s theory, 147Fog Close House, 46Fox, W.D., 80n58Fracastorius, 176, 192nn49–50Fraser, Alexander, 30Fraser, David, 294–95, 297–301, 334–35, 346,

394Frazer, William M., 354n3French, John G., 251n6, 310Frerichs, Ralph R., 225nn21–22Friendly Societies, 82Frith Street, 75, 81–82, 102n2, 234, 251n8Frost, Wade Hampton, 395

Galbraith, N. Spence, 33n6, 33n10, 51nn14–15,76n1

Garrod, Alfred Baring, 100–01, 185, 205,224nn14–15, 232, 244, 250

Gateshead, 41, 248Gay-Lussac, Joseph-Louis, 116Gazetta Medica Italiana Toscana, 303Gelman, Anna, 402n29Genealogy

Askham-Empson, 19fAskham-Snow, 20f

General Board of Health (GBH), 166, 171, 175,192n46, 244, 268, 279n25, 280n31,312n24

anticontagionism of, 294–95, 384n7aBroad Street/Golden Square outbreak of

1854 and, 289–91, 301, 308f , 309–10,310n1, 312n17, 314n40, 315n53, 316n75,337f

Committee on Scientific Inquiries of (CSI),294–95, 297–305, 309, 311n5, 313n35,314n48, 314n52, 334, 316n76, 356n18, 394

contingent contagionism and, 180, 194n63disagreements with Snow, 346, 349precautions against cholera by, 296, 298Snow’s critique of, 275–77, 345–47

General practitioners (GP), 6, 80n64, 82–83,103n12

General Register Office (GRO), 171, 181, 259,265, 270, 291–92, 319f, 327, 331. See alsoFarr, William; Registrar-General; WeeklyReturns of Births and Deaths in London

Geographic Information Systems (GIS),397–99, 402n33, 403n35

George Street, 238Germ theory, 11, 196n82Gilbert, E.W., 396–97Gilbert, Pamela, 312n17, 312n26Glasgow, 244, 257, 352Gloucester Road, 251n11Glover, Robert M., 142–44, 389Golden Square, 8, 82, 277, 283–85, 287–88, 292,

297, 330f . See also Broad Streetdisease mapping of, 300, 302, 309, 328–37,

332f, 333f, 336fGoodeve, Professor, 87Goodman, John, 87Gould, John, 291Gotfredsen, Edvard, 135n14, 138n65, 138n67Graham, Thomas, 385n18Grainger, Richard D., 318, 319f, 337n2, 338n18Grand Allies, 41Grand experiment, 264–67. See also Natural

experiments; Snow, John, experimentacrucis of and grand experiment of

Grand Junction Water Company, 255, 288,298

Grant, John, 207–08, 225nn21–22, 226n31, 247,257

Grant, Robert, 77n14Great Exhibition of 1851, 156Great Stink, 354, 358n54Greek Street, 297Greener, Hannah, 143–47, 155Greenhow, Thomas Michael, 30, 41, 37n56,

50n8, 191n38, 198n108, 198n110Greenwich, 254Grocers’ Company, 25Gurthrie, George, 66Guy’s Hospital Medical School, 60f, 71, 159Guyton-Morveau, L.B., 195n79

Hackney, 345Hague, Howard, 108n78

426 Index

Hall, Benjamin, 9–10, 13n29, 290, 294, 309,312n23

Hall, Marshall, 145, 383Hamburg, 395Hamlin, Christopher, 80n63, 224n10, 228n44,

278n19, 353–54, 354n2, 355n5, 355n9,356n22, 358n54

Hampstead, 285, 287Water Company, 254Hampstead widow. See Eley, Susannah

Hampton, 351Hanover Square, 6, 238, 292Hardcastle, William, 24–31, 38n60, 42, 67, 75,

104n28Harnold, John, 203Hartley, David, 386n27Harvard University, 402n27Harvean Prize Essay, 142Hassall, Arthur Hill, 195n72, 247, 281n33, 290,

303, 341, 358n50, 384n7aHatton, John, 327–28Haughton’s School, 34n21Hawkins, Caesar, 128, 138n71, 364Health of Towns

Bill, 191n28Report, 318, 337n4

Henle, Jacob, 195n79, 204Henry VIII, King, 25Herefordshire, 364Herschel, John, 74–75, 78n38, 80n58, 222Higgins, Margaret, 155Hill, James, 188n1Hird, Francis, 199–200History of Anaesthesia Society, 392Hoffman, August, 384n6Holland, Henry, 134n1Holmes, Oliver Wendell, 135n25Hooke, Robert, 136n30Hooping-cough, 379Hôpital Necker, 79n57Horsleydown, 207–10, 213, 257Hospital for Clinical Midwifery, 63Hospital for Consumption and Diseases of the

Chest, 234Household Words, 140Huggins, Edward, 298Huggins, John, 298Hughes, Thomas, 294–95, 299–301, 334–35,

346, 394Hull, 30, 215, 258Humber estuary, 14, 258, 273Humidifier, 119, 136n36, 136n42Humors, 51n17, 172, 321Hungerford, 279n24Hunter, John, 73–74, 94

Hunter, William, 73–74Hunterian

School of Medicine, 4–6, 60f, 61–64, 69,73–74, 79n54, 84, 99, 100

Theatre of Anatomy (Lower WindmillSchool), 60f, 63

Huntington, 18Hutchinson, Mr., 245, 288 Hyde Park, 94Hydrocyanic acid, 152Hypothetico-deductive reasoning, 75, 229n49,

396

Ideologues, 74, 79n55Illustrated London News, 112Indentures, 28–30, 36n35Index case, 303, 316n73, 327, 335, 350, 401n19India, 167–69, 189n12

cholera in, 167, 170, 178, 201physicians in, 191n41, 193n59, 196n89

Industrial Revolution, 15, 32n2Infants

artificial respirator and, 2–3asphyxiation and, 2–4, 90–95

Influenza, 44, 177, 199, 232, 379–80cholera and, 173, 379–80Snow on, 173, 229n47, 379–80

Inhalersamylene, 367, 370n12chloroform, 154, 154f, 243, 253n29ether, 5, 117–22, 119f, 120f, 121f, 135n21

Inoculations, 177Inquiry into the Sanitary Condition of the

Labouring Population of Great Britain(Chadwick), 171, 340, 342, 354

Iodoform, 142

Jackson, James, 323Jackson, Robert, 193n60Jackson, Samuel, 189n14, 198n104Jacob’s Island, 347James I, King, 25James, James H., 195n74Jeffreys, Julius, 118–19, 136n36, 136n42Jenkins, Edward, 394, 402n20Jenner, Edward, 238, 382Jewell, Dr., 63, 77n14, 84Jewett, Frederick Hardy, 155J.L. Curtis and Co., surgeons, 82John Snow College, 401n11John Snow, Inc., 392Johns Hopkins School of Hygiene and Public

Health, 395Johnson, George, 186–87, 198n104, 198n109Johnson, Henry C., 138n71

Index 427

Johnson, James, 178–79, 190n20, 383Jones, G., 65Jones, Harry, 311n13Jones, N. Howard, 197n96Jopling, Charles, 155Journal de Chemie Medicale, 159Journal of Public Health and Sanitary Review

(JPH&SR), 239, 275, 348

Kay-Shuttleworth, James Phillips, 170–71, 351Kennington, 266–67, 266t, 280n30Kent Water Company, 254Killingworth, 31, 41–42, 166, 169King, Dr., 304King’s College Hospital, 59, 60f, 186, 388King’s Ling, 280n27Kircher, Athanasius, 176Knight, Henry, 7–8Knott, Samuel, 30Koch, Robert, 195n79, 228n40, 316n66Kouwenhoven, William, 1

Laboratory Investigation Division (PrivyCouncil), 103n13

Laennec, René T.H., 79n57Lamarckian evolutionary biology, 5Lambe, William, 39Lambeth Church, 275Lambeth Palace, 243Lambeth Water Company, 247, 254, 260, 348,

351districts supplied by, 262–64Snow’s subdistricts’ investigation and,

262–73, 266t, 278nn16a-17, 348, 357n32Lancet, 10–11, 13n29, 166, 169, 344–45, 356n20,

394on anesthesia and midwifery, 243, 253n35on arsenical candles, 72on bedside medicine, 197n94on chloroform, 140, 144–45on ether, 118, 128, 131on the hospital apothecary, 68–69on hospital medicine, 66–67, 78n27on medical schools, 61medical schools, requirement listings of, 57,

58tPetermann’s cholera map and, 327Shapter’s map and, 338n17on Snow’s legacy, 389–90, 394, 401n18aSnow’s Parliamentary testimony and, 10–11,

355n11on treatments for cholera, 186, 197n94on zymotic theory of diseases, 195n78

Lane, John Hunter, 63, 69, 77n13

Lankester, Edwin, 79n57, 180n72, 195n72, 216,227n39, 233, 311n5, 315n60, 316n72,316n78, 349

on Cholera Inquiry Committee (CIC),301–03, 307–10

Laryngoscope, 252n19Lassaigne, Jean-Louis, 148Latour, Charles Cagniard, 384n9aLatta, Thomas, 187, 198n102Laudanum, 156Lavoisier, Antoine Laurent, 2, 105n42Laycock, Thomas, 33n5Laycock, William, 48Layerthorpe, 48Lawrence, Christopher, 387n33Leather Market, 275“Lectures on the Entozoa or Internal Parasites

of the Human Body,” 225n19Lee, Henry, 250Leeds, 248, 401n15

General Infirmary, 53n35Leopold, Prince, 8, 242Letheon. See EtherLetter to the Right Honorable Sir Benjamin Hall,

13n29Lettsom, John, 84–85Levy, A. Goodman, 391Lewis, Sarah, 295, 305, 310n1, 314n40

daughter of (Lewis infant), 283–87, 307,314n40

Lewis, Thomas, 284, 294, 296, 310n1Licentiates of the Royal College of Physicians

(LRCP), 237Licentiates of the Society of Apothecaries

(LSA), 28, 54n44, 58t, 59, 68, 76n3Liebig, Justus, 157–58, 181–85, 223n9, 229n48,

249, 373–74on continuous molecular action, 375, 383n5

Lincoln College, 286Lincoln’s Inn Fields, 68Lind, James, 193n60Lindsay, W. Lauder, 174, 186–88Linnaean tradition, 107n70Lion Brewery, 298–99Liquor ammoniae, 200Liston, Robert, 65, 110–11, 128–30, 134n3,

134n7, 135n13, 138n71, 383Literacy, 33n9Lithotripsy (lithotrity), 6–7, 364Liverpool, 56Liverpool-Manchester Railway, 31Lloyd, Dr., 247Lloyd, Mr., 144Local Government Board, 394–95, 401n15,

402n23a

428 Index

Locock, Charles, 242–43, 252n27, 401n11Loimometer, 194n63London, 14, 25

Bridge, 155Fever Hospital, 173, 358n52Hospital, 46medical schools in, 59–63, 60f, 62t, 100–01sewage disposal in, 255–56Snow’s comparative mortality analysis of, 7,

271–73, 281n39awater quality in, 255–56

London Corporation of Surgeons. See RoyalCollege of Surgeons

London Epidemiological Society. SeeEpidemiological Society of London

London Medical and Surgical Journal, 76n10,77n13

London Medical Directory, 105n36London Medical Gazette (LMG), 68, 72–73,

87–89, 140, 191n28amalgation with MT, 148, 350, 387n31on ether, 111–12, 133, 134n11, 135n17Snow and, 139n91, 233, 390

Longet, François-Achille, 126, 138n66Lonsdale, Miss, 110Loughborough Dispensary, 145Louis, Pierre, 74, 79n57, 220t, 227n35Lucas, P. Bennet, 63, 77n13Lucretius, 194n70Ludlow, J.M., 294–95, 299–301, 334–35, 346,

394Ludwig, Karl, 105n45Lumleian Lectures, 149–50Lying-in Hospital, 4Lyon, B., 66

Maddox Street, 368Magendie, François, 12n5, 86–88, 105n42,

105n45, 196n82, 373, 400n10Magnus, Heinrich, 2Malaria, 9, 167, 248, 396Manchester, 280n30, 288, 327

Medical Society, 105n38Map(s)

cholera, 50n8, 318–37, 325f–26fCholera Inquiry Committee and, 316n75,

333f , 337fCommittee on Scientific Inquiries/GBH and,

309–10, 316n75, 337f , 399Cooper and, 300, 316n75, 329, 330f, 334,

339n29, 399Golden Square disease and, 320, 328–37,

330f, 333f, 336fGrainger/Board of Health’s, 318, 319f, 320London metropolitan, 225n21, 255f, 318, 319f

progress, 322–23, 322f, 326tshaded/cross-hatched, 319f, 324, 325t,

327–28, 337n2, 338n18Snow and, 302, 309f, 316n75, 318–20, 332f ,

339n29, 396–99, 403n35spot/dot, 302, 320–23, 325t, 328–29, 332Voronoi network diagram and, 333f

Marshall, Peter, 82–84, 98, 104n21, 108n75, 246,297

Marshall Street, 299–300Marylebone, 155Massachusetts

General Hospital, 134n1, 138n81, 367Institute of Technology, 402n27Medical Society, 323

Materia medica, 58t, 59, 63–64Mauritius, 233McClellan, Ely, 402n24McIntyre, James, 29–30Measles, 10, 379–80Medical Act of 1815, 27tMedical assistants, 42, 51n13Medical corporations (orders), 5, 26t–27tMedical Officers of Health, 171–72Medical radicals, 5, 70, 77n14, 170, 172Medical Society of London (MSL), 8, 84–85,

163, 240, 401n18aamalgamation with WMS, 85, 238chloroform, cholera discussed at, 165–66, 186Snow and, 238, 249, 372, 383, 387n34

Medical Times (MT), 148, 166, 350, 387n31Medical Times and Gazette (MTG), 13n29, 148,

248, 273, 297, 303–04, 312n15, 350,357n29, 368, 387n31

Medicineacademic posts in, 98–99apprentices in, 28–30, 37n49Bachelor of (MB), 99, 99tcollateral sciences of, 74–75, 97, 222, 383bedside, 44, 97, 113depersonalization of, 139n82forensic, 63, 100, 109n85, 146, 159hospital, 66–69, 73–75, 78n24Hunterian School of, 5–6, 60f, 61–63and hypotheticodeductive method, 229n49,

396as an inductive science, 229n49laboratory, 113military, 125, 131–32

Medico-Botanical Society of London, 71Medico-Chirurgical Review (M-CR), 178Medico-Chirurgical Society of Edinburgh, 140Meggison, Thomas, 144–46Merchants’ Hall, 48Merriman, Mr., 246

Index 429

Mesmerism, 111, 134n6Metropolitan Commission of Sewers (MCS),

207, 295, 342, 355n6Cooper and, 300, 314n52, 328–31

Metropolitan Free Hospital, 77n13Miasma, 41. See also Anticongationists; Effluvia;

Sanitarians; Sanitary reform movementanticontagionists and, 167, 174–75, 210in contingent contagionist theory, 167, 232influenza and, 177local, 167, 173–75, 179, 347, 373theory of disease, 7–10, 323, 343, 345, 354

Micklegate Stray, 22Micklegate Street, 14Micklegate Ward, 14–17, 16f , 22, 32n2Microscopes, 107n71Microscopical Society of London, 216Middlesex Hospital, 60f, 187, 287, 311n14Midwifery, 58t, 63–64, 135n17, 240–41

Hospital for Clinical, 63Millbank Prison, 273Mills, Mary, 129Milroy, Gavin, 210, 240, 258, 260, 272, 274,

347Moderation pledge, 47Monk Ward, 17, 32n2Monmouth House, 77n12Moor Street, 241Morens, David M., 196n86Morgagni, Giovanni, 79n55Morton, William Thomas G., 89, 111–13, 131,

134n1, 136n26Müller, Johannes, 88, 105n45Mumps, 379Munich, 395Murchison, Charles, 389Murphy, E.W., 142

Naphtha, 366Napoleonic Wars, 178Narcotism, 126–27, 126t

alcohol and, 158–59antiseptics and, 377degrees (stages) of, 159–60, 363–64, 392 Flourens’ theory and, 147meaning of, 147modus operandi of, 157–60process of, 150Snow’s oxidation-asphyxia theory and,

160–62ON studies and, 148–60, 150t

National Gallery, 124National Geographic Society, 397Natural experiments, 207, 260–72, 278n14Naturphilosophie, 88

New Burlington Street, 303New Jersey, 31New Poor Law, 171, 294, 303New River Water Company, 254–55, 288, 298New Slip, 321New York City, 190n19New York Hospital, 321New York Medical College, 402n29Newburn, 41, 213Newcastle, 4, 14, 24, 28–29, 29f , 37n50, 41–42,

213, 196n89, 248, 277n7Infirmary, 30, 143, 226n27Literary and Philosophical Society, 31,

38n57Lying-in Hospital, 4, 24Medical School at, 30, 37n54

Newton, John Frank, 39–41, 49nn1–3, 50n4,50n7, 201, 212

Nicolle, Charles, 396Nidderdale, 46Nightingale, Florence, 187, 192n43, 198n107,

287, 311n14Nitric ether (ethyl nitrate, C2H5ONO2), 151–52,

164n28Noncontagion, 166–67. See also

anticontagionistsNooth’s apparatus, 110–11, 134n8Norfolk, 280n27North London Hospital, 60f, 65, 77n21North Sea, 14, 279n24North Street, 14, 16–21, 23, 33n4, 33n11Northumberland, 41–42Norwood, 262Nottingham General Hospital, 122Nuisance trades. See Offensive tradesNuisances Removal and Diseases Prevention

Act, 343Nun Ings, 22Nysten, Pierre Hubert, 12nn5–6

Observations on the Management of the Poor inScotland, and Its Effect on the Health ofGreat Towns (Alison), 353–54

Offensive trades, 7–11, 13n29, 255, 284, 343,356n15

Olefiant gas, 366On Chloroform (OC) (Snow), 140, 143, 234,

359–60, 365, 370n3, 388–89, 386n23,400n5

On Continuous Molecular Changes (CMC)(Snow), 163, 227n34, 355n4, 372–83, 395

as concept, 373–75epidemic diseases and, 372, 378–81Liebig and, 375–76, 384n6, 384nn9–9a,

385n19

430 Index

oxidation and, 377–78, 385n15, 385nn16–18as social theory, 381–83, 386nn27–28vital vs. nonvital, 376–77, 384n12

“On Narcotism by the Inhalation of Vapours”(ON) (Snow)

chloroform experiments of, 149–50, 150tinstallments of, 148–60, 234

On the Alternation of Generations (Steenstrup),206

“On the Infectious Origin and Propagation ofCholera” (Bryson), 246

On the Inhalation of Ether. See On theInhalation of the Vapour of Ether inSurgical Operations

On the Inhalation of the Vapour of Ether inSurgical Operations (Snow), 114, 126, 128,133, 140, 391

On the Mode of Communication of Cholera(MCC) (Snow), 6–7, 200–23, 227n33,257–59, 304, 351

as Snow’s cholera hypothesis, 203f, 205–06,213, 219, 224n17, 224n14

supporting evidence in, 206–10, 208f, 209f,222, 225n18

On the Mode of Communication of Cholera,Second Edition (MCC2) (Snow), 259, 262,263f, 264–65, 273–75, 281n35, 301,312n15, 312n25, 315n63, 332, 332f,356n20, 394–95, 400n2, 401n15

contents of, 271t, 277, 277n8, 278n16,280n31

maps in, 320, 332f“On the Mode of Propagation of Cholera”

(Snow), 239, 246“On the Pathology and Mode of

Communication of Cholera” (PMCC)(Snow), 200–01, 212–23, 258–59

presentation at WMS, 212–13, 227n39,231–33

prevention of cholera in, 211–12as Snow’s cholera theory, 213, 224n15,

227n33supporting evidence in, 213–15, 214t,

222–23, 273Operating theaters, 110–13, 128–29Opium, 83Orton, John Gay, 369O’Shaughnessy, William Brooke, 185, 187,

196n89, 198n104, 224n15, 232Overy, Caroline, 104n25Owen, Richard, 341Oxford University, 76, 77n13, 99, 237Oxidation

anesthesia and, 377–78, 385n14, 385n18asphyxia theory and, 160–62

Pacini, Filippo, 228n40, 303, 316n66Paget, James, 64, 67–68, 100, 368, 370n16Pallister, W.A., 47, 54n45Paracentesis, 95–96, 106n65, 107n66Parish of Tanfield, 43Parasites. See Entozoa; WormsPark Road, 347Parkes, Edmund A., 186, 191n36, 193n60,

194n68, 197n97, 198n104, 224nn14–15,244, 250, 278n17, 280n26b, 315n62,339n33

Parkin, John, 227n36Parliament, 5, 7, 65, 256, 279n25, 290–91,

312n24first reform (1832), 22, 170

Parsons, Joshua, 63–65, 98, 344, 389Pathological Society of London, 238“Pathology and Treatment of Cholera” (Hird),

199Pelling, Margaret, 224n13, 225n18, 226n24,

228n40, 228n42, 355n5Pentonville, 298Perchloride of formyle. See ChloroformPeregrine, Thomas, 200Pericarditis, 86Pestgage, 194n63Petermann, Augustus, 321, 327, 336, 338n10,

338n19Peters, John C., 402n24Pharmaceutical Journal, 142, 156, 227n39Pharmaceutical Society, 118Pharmacology, 151, 135n20

of chloroform, 141–43, 153Philadelphia, 189n14, 198n104Phillips, Richard, 71, 79n46Philosopical Transactions of the Royal Society

(Hunter), 94Phosphorus, 123, 137n53Phrenological Society, 76n10Phrenology, 61Phthisis. See TuberculosisPhysicians. See Royal College of Physicians.Physiological Society, 238Physiology (Müller), 88“Physiology of the Mechanical Action of the

Heart” (Goodman), 87Piccadilly Circus, 234Pirogoff, Nikolai Ivanovitch, 135n13Plague, 177, 379

pits, 300, 313n35Plomley, Francis, 126Poland Street, 290, 298–99

Workhouse, 251n6, 298, 314n46Pollock, George, 365Porter, Roy, 104n25

Index 431

Potter, H.G., 30, 143–44, 389Preliminary Discourse on the Study of Natural

Philosophy, A, 70Preston Temperance Society, 53n43Prevention of Offences Act (An Act for the

Better Prevention of Offences), 156–57“Principles on Which the Treatment of Cholera

Should Be Based” (Snow), 197n96Privy Council, 103n13, 394, 401n15Prout, William, 98Provincial Medical and Surgical Association,

238, 357n33Provincial Medical and Surgical Journal (PMSJ),

77n13Prussic acid. See Hydrocyanic acidPublic health, 6, 49

rickets and, 352–53Snow and, 49, 69–72, 352–54

Public Health Actof 1848, 171–72of 1859, 82

Puerperal convulsions, 142Punch (magazine), 112Purgation, 86Putney, 268, 270, 276, 280n29, 281n39aPutrefaction, 161, 167, 374, 377Pyrexia, 44Pyroxilic spirit, 164n40

Quain, Richard, 138n71Quarantine, 172, 174, 192n44, 212, 226n30,

381Quarterly Journal of Microscopical Science,

227n39Queen Street, 21t, 22, 45Queen Victoria, 8, 242–44, 252n27, 253n29,

253n35, 361, 368–69, 390Quetelet, Adolf, 327Quick, Joseph, 279n24

Radcliffe, John Netten, 393–94, 401n15Random misclassification principle, 349,

357n32Rawcliffe, 21t, 22Read, John, 93–96, 106n57Reed, John, 213Reed, Walter, 396Rees, George Owen, 105n34Reform Bill of 1832, 170Regent Circus, 12n4, 93Regent Street, 300, 312n17, 368Registrar-General, 244–45, 302–03, 327. See also

General Register OfficeRegnault, M.G., 164n43Reid, Dr., 253n29

Reid, John, 3, 12n5“Report on the Last Two Cholera-Epidemics of

London as Affected by the Consumptionof Impure Water” (Simon), 275, 348,357n28

Report on the Sanitary Condition of theLabouring Population. See Inquiry into theSanitary Condition of the LabouringPopulation of Great Britain

Respiration, 1, 2artificial, 12n4, 93–94chloroform and, 148–49circulation and, 146–47combustion, 377, 385n13ether and, 113, 148–49Liebig on, 373–74oxygen and, 162physiology of, 89–90, 105n42, , 135n23,

137n53, 146rate, 150, 374Snow on, 89–96

Return to Nature: A Defence of the VegetableRegimen (Newton), 39

Rheumatism, 100, 385n19Richards, Samuel, 130Richardson, Benjamin Ward, 49n1, 53nn35–36,

83, 99, 104n21, 104n25, 107n72, 112, 240,349–50, 385n14, 390–91, 395, 397, 399,400n10a, 401n18a

on amylene, 371n25on chloroform, 143, 151farthing-candle metaphor, 161, 378

on multiple causation of cholera, 228n42Richardson, James, 292River

Clyde, 257, 273Lea, 209–10, 254–56, 255fNidd, 46Nith, 257, 273Ouse, 14–17, 258Swale, 14Thames, 7, 155, 207, 254, 255f, 255–57, 273,

277n4, 319fTrent, 273Tyne, 41, 248, 273, 277n7

Robin, Charles Philippe, 377Robinson, James, 110–13, 134n2, 134n9Roe, George, 66Rogers, William R., 283–85, 287, 307, 316n73Ross, Ronald, 396Rotherhithe, 247, 268, 272, 275, 343Royal Academy of Arts, 124Royal College of Anaesthetists, 392Royal College of Chemistry, 384n6Royal College of Physicians, 6, 25, 26t, 149

432 Index

Royal College of Surgeons of Edinburgh, 77n13Royal College of Surgeons of London (RCS),

24, 26t-27t , 60fexaminations for, 68, 78n33member of (MCRS), 28requirements of, 56–59, 58t, 76n3

Royal Humane Society, 3, 94Royal Lying-in Hospital, 5, 63Royal Medical and Chirurgical Society (RM-

CS), 85, 104n26, 116, 134n3, 318, 386n29,401n11

Snow and, 238, 244Russell, Rollo 402n23aRyan, Michael, 63, 77n13, 84

Sackville Street, 6, 234, 235f, 288Salpetrière, 79n57Salter, T. Bell, 349Sanitarians

anticontagionist theory of, 172–75, 175f,192n44, 399

and medical radicals, 172Milroy and, 258–59and quarantine, 172, 174, 191n38, 192n44and sanitationism (Baldwin), 172Snow and, 271–73, 340–43, 358n46, 387n33

Sanitary reform movement, 7, 17, 167, 170–75,271–73, 340–43, 354, 396

Sannier, August, 82Satcher, David, 401n12Savage, Mr., 65Scabies, 379Scarlatina, 199Scarlet fever, 85–86, 104n30, 379Schleiden, Matthias, 376, 384n10Schoolpence, 22, 34n21Schwann, Theodor, 384n9aScott, James, 70–71Scottish medical graduates practicing in

England, 77n13Scurvy, 385n19Seaman, Valentine, 321, 323Searle, Lucretia, 81Searle, William, 81Sedgwick, William T., 395–97, 402n27Select Committee on Public Health and on the

Nuisances Removal and DiseasesPrevention Act, 7–10

Semmelweis, Ignaz, 396Serpentine, the (Hyde Park), 94Sewers, 255, 300, 328–31, 342, 355n8. See also

Anticontagionists; Effluvia; Miasma;Metropolitan Commission of Sewers

Shapter, Thomas, 197n94, 323–24, 324f, 329,338n16, 339n29

Shephard, David A.E., 138n69, 224n13, 227n33,229n48, 370n6, 385n18

Sibley, Mr., 311n14Sibson, Francis, 122, 147, 232Simon, John, Sir, 103n13, 275, 278n14, 341,

401n15Snow and, 281n38a, 347–50, 357n28, 357n31,

394–95Simpson, James Young, 112, 140–43, 145,

163n1, 240–41, 367Skey, James, 100Slaughterhouses, 284Smallpox, 177, 179, 181, 341, 379, 382, 385n21Smith, Elizabeth, 155Smith, Protheroe, 223n9Snow, Charles, 45Snow, Frances (Askham), 17–21, 33nn5–6, 48Snow, George, 45Snow, Hannah, 18, 45Snow, John. See also Animal experiments;

Autoexperimentsacademic posts and, 98–101, 146on ague, 248alum in bread, 353, 358n50on amylene, 365–70, 400n5amylene inhaler by, 367, 370n12analgesia and, 139n83, 154–55, 250 as anesthesia specialist, 6, 122–31, 359–70,

385n18anesthesia legacy of, 389–92anesthesia practice of, 115t, 128–31, 165,

233–34antiseptics and, 377apothecary, qualifies as (LSA), 75, 80n62apparatus of, 90, 95–96, 138n75, 164n43apprenticeship of, 23–24, 28–30, 37n48,

51n14arsenic poisoning while dissecting and,

69–70, 73arsenical candle investigation of, 70–72asphyxiation research of, 2–4, 12n7, 93–98,

107n67birth of, 21blood solubility studies of, 146–53on brandy treatment for cholera, 48, 54n51,

223n6Bristol cholera fungus theory and, 218, 222,

228n43, 229n50, 231–33, 248Broad Street/Golden Square investigation

and, 285–310, 309f, 310, 314n43, 320,337n5, 402n23a

on Budd’s cholera theory, 228n41, 229n45at Burnop Field, 42–45calculated mortality during 1854 epidemic

and, 275–77, 281n40, 282n42

Index 433

Snow, John (continued)cartographic legacy of, 396–99, 398fCase Books (CB) of, 43, 78n27, 143, 237, 242,

252n28, 270, 314n51, 360, 363on chemical affinity, 162–63childhood/education of, 21–23, 35nn23–24,

36n28on chloroform, 141–43, 141t, 146–47,

153–55, 236, 400n5chloroform inhaler by, 154fand chlorophobia, 155–57, 235–36 cholera epidemic of 1831–32 and, 41–42,

50n8, 50n11, 201, 215, 226n27, 246cholera epidemic of 1848–49 and, 199–219,

226n31, 244, 260, 282n41cholera epidemic of 1853–54 and, 250,

259–77, 263f, 278n15, 347and Cholera Inquiry Committee (CIC),

301–05, 307–10, 311n14, 312n15, 312n25,315n60, 315n63, 334t, 335t, 395

cholera prevention and, 211–12, 248–49cholera theory elaborations of 1849–53,

244–49, 273cholera theory of, 148, 202–10, 203f, 220t–21t,

221–23, 226nn28–29, 233, 249–50, 341,383n4

cholera transmission, ecological levels in,256–57, 257t

on cholera treatment, 200, 223n6, 224n15,249–51, 257

and CMC, 372–83, 384n6on continuous molecular changes, 249,

385n14, 386n26dreams during anesthesia, 132–33dental operations and, 129–30early publications of, 86–89epidemic diseases, general theory of, 8, 10,

13n29, 188, 318, 379–81, 385n14epidemiological legacy of, 392–96, 401n11,

402n23aepidemiological perspective of, 130, 229n50,

265, 277, 281n40, 282n42, 396Epidemiological Society of London and,

238–40, 246–48, 302, 318–20ether, controlling dosage of, 114–17ether inhalers by, 5, 117–22, 119f, 120f, 121f,

137n54, 163n1ether research of, 112–17, 115t, 117f, 124,

131–34, 136n34, 138n66, 140, 400n5,400n10

etherisation, degrees (stages) of, 124–27, 126ton exercise, 47experimenta crucis of, 69–70, 260–65, 267,

271–72, 278n14fatal illness of, 388–89

GBH and, 247, 346–47as GP, 81–86, 234, 251n6, 251n11, 252n12grand experiment of, 264–65, 267, 280n26b,

278n14gravestone of, 393f, 400n10ahandkerchief in chloroform administration,

241on health of, 108n76home laboratory of, 135n24on homeopathy, 106n53hospital apothecary, application for, 68at Hospital for Consumption and Diseases of

the Chest, 234hypertension, suspected in, 108n77inhaled gases, chemistry and physics of, 102and Lancet, 13n29, 87, 138n80later cholera writings of, 350–52London medical training of, 56–69, 64t, 65t,

76n2, 100–02as LRCP, 237–38maps and, 226n23, 302, 309f , 312n25,

315n54, 316n75, 318–20, 331–33, 332f,333f, 334t, 335t, 336, 336f, 337n4, 396–99

medical mistakes of, 138n78Medical Society of London, orator of, 163,

238, 372, 387n34Medical Society of London, president of, 8,

106n62, 382metropolitan water supply/cholera thesis of,

256–60and midwifery, 240–41, 253n31on Milroy’s explanations, 210–11, 258, 260,

272, 274on mind-body interdependence, 98 as modified contagionist, 201as MRCS, 68, 252n12narcotism and, 134, 147–53, 165narcotism, degrees of, 126tnatural experiments and, 207at Newcastle medical school, 30and Newton’s Return to Nature, 49n1, 49n3and obstetrics, 100, 241–42OC and, 388–90, 400n5on occupations, 230n51, 344, 352, 356n15ON and, 148–60, 150t, 370n3, 400n2oxidation-asphyxia theory of, 160–62paracentesis, instrument of, 95–96, 106n65,

107n66Parliamentary testimony of 1855, 6–11,

13n29, 355n11at Pateley Bridge, 45–48, 53n34and the Pathological Society of London, 238pathophysiology of, 256pharmacokinetic model of, 142pharmacodynamics and, 157–58

434 Index

photograph of, 8fPhysiological Society, president of 238PMCC and, 200–01, 212–23, 214t, 227n33,

228n43, 231–33, 246, 273portrait of, 101f, 124practice of, 104n19, 104n21, 251n11, 252n12,

252n27preserving meat, experiments with, 161professional/social manner of, 83–86Provincial Medical and Surgical Association

and, 238public health and, 49, 69–72, 352–54, 358n50published research of, 91t–92tQueen Victoria and, 242–44, 368–69respiration and, 89–96residences of, 81–82, 234, 235f, 372resuscitator invention of, 2–3, 12n4on rickets, 108n78, 352–54Royal Medical and Chirurgical Society and,

85, 104n26, 238Royal Medico-Botanical Society and, 238sanitarians and, 271–73, 340–54,

358nn45–46, 387n33Simon and, 275–77, 281n38a, 347–50,

357n28, 357n31, 394–95on smallpox, 181, 341, 379and social class, 352–54south London analysis of, 214, 222, 244, 247,

263f, 265–77, 266t, 276f, 279nn21–24,279n26a, 281nn39–39a, 233, 336–37

as systems thinker, 219–23, 220t–21t,229nn46–47, 381, 386n22, 386n28

on temperance and teetotalism, 46–49,54nn48–49, 54n51, 98, 211, 344, 352

on therapeutic skepticism, 49, 55n52on toxins, 142on typhoid fever, 247as village epidemiologist, 208, 212–13as vegetarian, 40, 46–49, 83, 98and Wakley, 87Westminister Hospital and, 68–69Westminister Medical Society and, 84–86,

104n24Whiting and, 268–75

Snow, Mary, 34n15, 35n25, 45, 401n18aSnow, Stephanie, 228n44, 252n28Snow on Cholera (Frost), 395Snow, Robert, 35n25, 45, 248Snow, Sarah, 35n25, 45, 401n18aSnow, Thomas, 34n15, 35n25, 45, 356n22,

401n15, 401n18aSnow, William (John Snow’s father), 18–20,

33n10, 45occupational history of, 21–22, 21t, 23–24,

76n2

Snow, William, (John Snow’s brother), 35n25,36n28, 45, 48

Snow-Askham genealogy, 20fSociety of Apothecaries, 24, 65t, 77n14Soho Square, 12, 81, 286Somerset, 65Somerset House, 259South London Water Works, 254Southwark and Vauxhall Water Company

(S&V), 260, 262, 348–49, 351–52districts supplied by, 262–64, 278n17Snow’s subdistricts’ investigation and,

262–73, 266t, 280nn28–29, 357n32Southwark Water Works, 244, 272Smith, Thomas Southwood, 171–75, 175f, 185,

190n26Spallanzani, Lorenzo, 93Spasmodic cholera, 168f, 169, 189n13, 322fSpitalfields, 155Spitta, Dr., 6–7Spooner, E.O., 170, 179–81, 179n68, 185, 194,

195n72Spontaneous generation, 206Squire, Peter, 110, 118Squire, William, 110St. Anne’s, Soho, 81, 291St. Bartholomew’s Hospital, 60f, 64

Medical School, 100–01, 108n84St. Edmund, 323, 338n16St. George’s Hospital, 60f, 83, 128–30, 141, 152,

163n1, 164n42, 285, 389St. Giles, 312n26St. James Palace, 312n26St. James, Parish of, 283, 292–94, 312n26, 329

Cholera Inquiry Committee (CIC) and,301–10, 311n14, 333, 333f, 335–36, 356n20

Paving Board (Commission) of, 301–02, 306St. James Park, 312n26St. James Street, 372St. John’s Church, 28, 42St. Luke’s Church, 290, 295St. Mary, Bishophill Junior

Church of, 23Parish of, 21

St. Peter’s Grammar School, 34n21, 35n24St. Petersburg, 135n13, 278n15St. Saviour’s, 272Stafford, 215Stanhope, 42Steenstrup, J.J.S., 206, 225n20Stephenson, George, 31, 38n59Stephenson, Robert, 31, 38nn59–60Stewart, Alexander, 394, 402n20Sthenia, 45Streatham, 262, 268

Index 435

Sulphuric ether, 143Sunderland, 169Surgeons, 5

surgeon-apothecary, 6, 24, 56, 58tSurgeon’s Square Cholera Hospital, 174Surgery (the premises), 58tSurrey, 351–52Surrey Court, 207, 257Sutherland, John, 346–47, 356n22Swayne, Joseph G., 195n72, 216–17, 227n39,

231–33, 375Sydenham, 278n16aSydenham, Thomas, 44, 52n24, 107n70

epidemic constitution, theory of, 167,172–74, 186, 191n38

Hippocratic regimen, 49, 55n55, 172Syphilis, 379–80

Tait, William, 354Taylor, Alfred, 109n85, 159Teddington Lock, 277n4Teetotalism, 47–49, 54n42, 83Temperance, 46–47, 53n36Terris, Milton, 402n29Thackery, Harriet, 46Thames Ditton, 267, 275, 279n21Thatched House Tavern, 372Thomson. Robert D., 244–45, 253n37Thorax, 96Thorne Thorne, Richard, 402n23aThrawl Street, 155Times, 112, 157, 289–90, 295–96, 348–49,

356n22, 389Todd, James, 363, 389Tomes, Charles, 138n81Toynbee, George, 82Toynbee, Joseph, 82Toynbee, Joshua, 72Treatise on Verminous Disease (Brera), 206Tripe, John W., 345, 356n17Tuberculosis, 79n57Tucker, J.H., 238Turner, Richard, 53n43Turpentine, 200Tweedie, Alexander, 354, 358n52Typhoid fever, 173, 177–79, 216, 227n35,

358n45, 379Typhus, 10, 227n35, 358n45, 379

United Service Institution, 125, 128, 137n58University College Hospital, 65–68, 77n21,

224n14ether use at, 110–11, 128–30, 138n72

University College London, 60f, 77nn13–14, 99,237

University of Durham, 37n54, 37n56, 401n11University of Edinburgh, 30University of London, 6, 77n21, 99t. See also

University College HospitalUpper Poppleton, 18, 21–22Ure, Andrew, 116, 136n30

Valentin, Gabriel, 150Vegetarianism, 39–41, 46–49, 54nn50–51, 83Venables, Robert, 65, 77n20Vibrio cholerae, 303, 316n66Victorian Values, 227n39Vitalism, 2, 88, 373von Helmholz, Hermann, 105n45von Pettenkofer, Max, 328, 395Voronoi network diagram, 333f, 339n32, 396

Wakley, Thomas, 87, 187, 138n81, 243on medical men, 190n27and Snow, 105n37, 344–45, 253n35

Waldie, David, 367Wales, 56Waller, A.D., 138n81Walmgate Ward, 17, 32n2Wandsworth, 6, 208, 270, 280n29, 281n39aWarburton, Joseph, 46, 53n35Warburton, Joseph, Jr., 46, 53n35, 75Wardrop, James, 77n14Wardour Street, 297Warsaw, 232Warwick Street, 312n17Water

companies, private, 7, 208–10, 254–56, 259,261f, 277n4, 279n25, 318, 351

filtering/settling of, 247–48, 256, 273metropolitan supply of, 254–73quality of Thames water, 255–56, 260, 269,

271–73, 277n4, 351sewage contamination of, 207–15, 208f, 269,

271–73, 355n9Water pump

at Bridle Lane, 288at Broad Street, 7, 284–85, 288, 289f, 290,

300–03, 310, 313n31, 316n78, 330f,332–34, 336f

at Marlborough Street, 288St. Bride’s, 245, 288at Vigo Street, 288at Warwick Street, 288

Waterloo, 266t, 272, 280n30Watkin, Marion, 251n8Watson, Jane Toward, 42Watson, John, 42–44Watson, Thomas, 13n29, 190n19, 193n58,

194n65, 194n69

436 Index

Wetherburn (Weatherburn), Jane, 82, 234, 251n8Webster, John, 199–200, 232Weekly Journal of Medicine and Collateral

Sciences, A, 73, 387n31. See London MedicalGazette

Weekly Returns of Births and Deaths in London,209, 247, 250, 292, 329, 344

from November 1853, 259–62, 261fSnow’s grand experiment and, 261f, 264–65,

267–68Snow’s subdistricts’ investigation and, 265–73

Wellington, Mr., 368–69Wellington Row, 21, 34n15Wells, Horace, 112, 134n1, 367Wells, William Charles, 104n30West Ham, 350Western Literary Institution, 251n1Westminister Abbey, 7, 65Westminister Hospital, 60f, 65–69, 78n23Westminister Medical Society (WMS), 5–6,

315n60amalgamation with MSL, 85, 238arsenical candle investigation of, 70–72chloroform and, 141cholera epidemic of 1832 and, 70ether and, 114, 118–24membership, 84–85October 1849 meetings of, 212, 216, 227n39,

231–33, 251n3PMCC and, 227n39, 231–33Snow and, 2–4, 90–94, 173

West Moor colliery, 31White, Anthony, 66, 68Whitechapel Road, 155Whitehall Yard, 137n58Whitehead, Henry, 285–92, 295, 311n13,

314n43on Broad Street water pump, 299, 314n49Cholera in Berwick Street, 299, 314nn47–48and cholera epidemic of 1866, 392–93, 401n15

and Cholera Inquiry Committee (CIC),301–06, 307–10, 310n1, 315n60, 316n76,335, 339nn37–38, 394–95

on pump handle removal, 313n37, 350on Snow’s theory, 304, 314n49, 316n74, 335

Whiting, John Joseph, 268, 280n27Snow and, 268–75, 285

Widder, Agnes H., 103n3Williamson, Eleanor, 251n8Williamson, Sarah, 82, 251n8Wilson, Charlotte, 155Wilson, James Arthur, 149–50Wilson’s Green Coat Boy’s Charity School,

34n21Winlaton, 144Winslow, Forbes, 93Worboys, Michael, 193n61, 227n34Workhouses, 171Worms, parasitic, 204, 206, 223n9, 224n17,

225n18, 225n20, 374–75Worshipful Society of Apothecaries, 24–25,

56–59, 58t, 77n14Wright, Thomas Giordani, 29–30, 37n51,

37n54, 38n57

Yellow fever, 177, 232, 321York, 14–23, 17f, 45, 277n7

grazing privileges in, 22, 34n18public sanitation in, 17, 33n4schools in, 22–23wards of, 32n2Water Lanes of, 258Waterworks, 16–17

York, Jehoshaphat, 299, 306, 307, 307f, 309, 335York Minster, 15York Moderation Society, 48Yorkshire, 47

Zymotic diseases, 181–85, 195n78, 323, 353,376, 379. See also Farr, William

Index 437

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