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FIG. I .-Silicosis. Upper part of the lung of a South African gold miner showing silicotic nodules.

THE PATHOLOGY OF PNEUMOCONIOSISBy J. G;OUGH, M.D.

Professor of Pathology and Bacteriology, Welsh National School of Medicine, Cardiff

IntroductionTen years ago it appeared that pneumoconiosis

in general could be explained by the presence ofsilicon dioxide (free silica) in a noxious dust andthat the disease process was caused by this silicagoing into solution in the lung and in soluble formstimulating the formation of fibrous tissue. Thisinterpretation seemed to explain most of the knownfacts and was supported by the experimentalfinding that silicon dioxide, capable of producingsilicosis in animals, could be rendered inert bymaking the silica insoluble by coating it with iron(Kettle, 1932) or aluminium (Denny, Robson and

Irwin, I939). The solubility theory of silicosishas been challenged however on the grounds thatit does not give a straightforward explanation of allthe known forms of pneumoconiosis and there isno simple correlation between the silicon dioxidecontent of a given dust and its pathogenicity. Thisproblem will be discussed under the heading'Experimental Silicosis.'Another change in outlook has been the

recognition that wide varieties of dust are capableof causing pneumoconiosis. Whereas in I934,according to Kettle, the view was generally heldthat pneumoconiosis and silicosis were practically

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6I2 POSTGRADUATE MEDICAL JOURNAL December I949

synonymous terms, there is now considerableevidence that other elements including aluminiumand beryllium can produce pulmonary fibrosis.With respect to the incidence of pneumoconiosis

in Britain the most striking change in recent timeshas been the high certification rate of pneumo-coniosis in the coal miners of South Wales, andthe number of cases amongst them is numericallymany times greater than that occurring in all otherindustries put together. Earlier this century coalmining was regarded as a healthy industry apartfrom accidents, but now, in one coal field at least,there is found a serious incidence of pneumo-coniosis. This form of the disease will be con-sidered in detail. Other varieties of pneumo-coniosis will be dealt with more briefly, except thatasbestosis and siderosis will not be included as theywill be dealt with by other writers in this issue.

SilicosisThe basic lesion of classical silicosis is the

silicotic nodule in which collagenous fibrous tissueis laid down, usually in a concentric arrangement,to form spherical nodules in which the dustparticles can be identified. The anatomy andhistology of these lesions is very similar in a widevariety of industries in which there is exposure todust containing much free silica. Fig. i shows anexample from a South African gold miner. Thenodules in silicosis may be distributed fairlyuniformly throughout the lung but tend to bemore numerous in the upper and posterior parts.At first they are discrete but they may tend tocoalesce. The disease is frequently associatedwith tuberculosis and it is often difficult to decidehow much of the fibrotic process is due to thedust and how much to the associated infection. Ithas been suggested by Fallon (I937) that thesimilarity of tuberculous and silicotic nodules isdue to the fact that both are caused by the actionof lipoids from damaged endothelial cells. Thetuberculosis associated with silicosis may be of thecommon caseating variety with extensive cavita-tion (Fig. 2), but often leads to the formation oflarge masses of fibrosis several inches in diameter.In the silicosis of gold miners Irvine (I938) foundthat the conjunction of a tuberculous infection witha silicotic lesion does not in general lead to theformation of an active spreading tuberculosis, butto a modification of the silicotic process resultingin the production of large masses of fibrous tissueof mixed silicotic and tuberculous origin. Hepoints out that these mixed lesions are slowly pro-gressive but tend ultimately to break down andinitiate terminal active tuberculosis. The sameauthor, together with Simson and Strachan (I930),found that even where the lesions do not showobvious evidence of tuberculous infection the

latter can be demonstrated in a considerablenumber of instances by animal inoculation.

In man simple silicosis of the classical type mayproduce ill effects by the development of associatedemphysema but death is usually due to activetuberculosis although congestive cardiac failuremay also be the terminal event, consequent uponfibrosis of the massive type and emphysema. Themortality figures for South Africa show plainly,however, that the liability to death bears a directrelation to the relative prominence of thetuberculous factor.

Silicosis, in contradistinction to asbestosis, doesnot predispose to carcinoma of the lung. TheMiners' Phthisis Medical Bureau of South Africa(I944) showed from post mortem studies thatprimary cancer of the lung is not more common insilicotic miners than in either non-silicotic minersor in a similar body of males in the generalpopulation. Vorwald and Carr (1938) andGardner (I940) on the basis of radiologicalexaminations also found no evidence that silicosispredisposes to carcinoma of the lung.

Experimental SilicosisNodular silicosis of the classical type has been

produced in experimental animals both by theexposure to dust in the atmosphere and also byinjection of suspensions of dust into the airpassages of animals. There can be little doubtthat silica alone can produce a nodular fibroticlesion and this may occur with silicon dioxidedusts of a high degree of purity.

According to the classical work of Gye andPurdy (1922, I924) and Gye and Kettle (1922)the toxic action is to be explained by the silicagoing into solution and Kettle (I932) showed thatby coating the silica with iron and rendering itinsoluble the material can be made non-toxic.This view received strong confirmation from thefindings of Denny, Robson and Irwin (I939) whoshowed that the poisonous effects of silica can beneutralized by powdered metallic aluminium. Toproduce the neutralizing effect the two substancesmust be brought into direct contact and thisresults .in the formation of a layer of aluminiumhydroxide on the silica particles, rendering thelatter insoluble. They compared the effects of theinhalation of silica dust with those of inhaling thesame dust mixed with aluminium. The mixturedid not produce silicosis when breathed in highconcentration several hours a day for manymonths, while the disease developed in animalsreceiving the silica dust alone. Similar protectionwas obtained when silica and aluminium weregiven at separate times during the day, provingthat aluminium when inhaled could neutralizesilica already in the lungs. In recent work King,

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December I949 GOUGH: Pathology of Pneuinoconiosis 613

rii

A -

FIG. 2. Silicosis with active tuberculosis. Lung of a Cornish tin miner. There is a tuberculous cavityin the middle zone with adjacent silicotic nodules.

Wright and Ray (I949) have also shown byinhalation experiments that the toxicity of silicacan apparently be reduced by the action ofaluminium.

In a critical studv of the theories of silicosisKing (1947) points out that according to themodern ' chemical ' theory the toxic substance isthought to be silicic acid, and it might be supposedthat the pathogenicity of any stone dust wouldbear a direct relation to the rate at which it willrelease silicic acid into solution. He points outthat broadly speaking this is the case; quartz andflint which dissolve to the extent of io mg. ofsilica per IOO cc. of blood and plasma are the mostpathogenic, while shale and mica which are lesssoluble are also less pathogenic. There are,however, exceptions to this. Certain sandstoneswhich have a low silica solubility have a highpathogenicity and olivine, a magnesium silicate of

intermediate solubility, apparently causes no pul-monary disease in man and no fibrosis in the lungsof animals. King emphasizes that in mixed dustssome of the constituents may depress the solubilityof the free silica component, thus shale dustsmarkedly depress the solubility of quartz dusts.This interaction of different components wouldappear to explain many of the apparent dis-crepancies in the toxic action of a dust expectedfrom its total silica content. This, however, doesnot explain all the difficulties and King suggeststhat a possible explanation is that liberation of atoxic substance from silica in the body may bedifferent from that which occurs in a test tube.He speculates on the possibility that within cellssilicic acid may be released from quartz in aspecial toxic or ' nascent ' form.Some have attempted to interpret the patho-

logical reactions to silica in terms of surface

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614 POSTGRADUATE MEDICAL JOURNAL December' 1949

I..

FIG. 3. Coal zcorker's pneunloconiosis. Most of the lung shows focal emphysema in relation to coal nodules.There is massive fibrosis at the apex of the lobe. Such fibrosis is considered to be due to superaddedtuberculosis.

Photographs by Mr. 7. E. Wentworth

activity of the particles and have inferred thatrecently formed particles are more active in respectof being able to produce disease than are olderparticles. Policard (I947) has stated that olddust such as sand in its natural state has becomeless pathogenic due to weathering. He consideredthis was due to the loss of bases and the intake ofwater by the mineral particles and that particleswhich had been thoroughly weathered have losttheir effect on living tissues and are pathologicallyinert. King (I945) found that dust kept in alaboratory in a dry state for many years retains itspathogenicity. Nevertheless he has pointed outthat particles repeatedly leached with water losesolubility and this phenomenon may be concernedin the weathering of dust. Gardner (1938) foundthat ' quartz stored in a reasonably dry building,but subject to marked variations in atmospherichumidity, did not lose its pathogenicity over a

period of four years.' Likewise a sterile suspensionof silica particles in physiological salt solution keptin a refrigerator for many months neither in-creased nor decreased in capacity to excite re-action in the tissues.

Although there are objections to the solubilityhypothesis of silicosis it still seems to offer themost acceptable explanation. The problem is,however, by no means a simple one but apparentdiscrepancies, in some cases at least, may beexplained on the grounds that in mixed dusts someconstituents may depress and others heighten thesolubility of silica.The size of particles concerned in the production

of silicosis is important. The ones which enterthe lung are mostly below iot and the majorityare below 5,u. King (1947) has shown that inRinger's solution there is increased solubilitywith reduction of particle size below 5 microns

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Decemlber 1949 GOUGH: Paithology of Pneumoconiosis 615

and Gardner (I939) considers that the toxic actionof quartz in chronic lesions is limited to particlesof 3 pt or less.

Pneumoconiosis due to SilicatesThe question as to whether silicates are toxic

when inhaled has been very much debated sinceJones (1933) put forward the view that sericite, apotassium aluminium silicate, is the cause of muchindustrial silicosis, but of recent years this viewhas received very little support. Numerousinstances of pneumoconiosis due to talc (hydratedmagnesium silicate) have been described, however,in different parts of the world and the first case ofthis type in Britain proved by autopsy has beenreported by McLaughlin, Rogers and Dunham(I949). 'These authors suggest that talc pneumo-coniosis atnd asbestosis are similar diseases andthat the former is caused only by the fibrousvarieties of talc.Numerous examples of granuloma have been

described, caused by talc which has been depositedin the peritoneal cavity as a result of surgicaloperations.

Cases of pneumoconiosis have also beendescribecd in men exposed to a mica dust con-taining aJmost no free silica (Dreesen et al., I940).The signs and symptoms were said to resemblethose of silicosis.

King considers silicates less toxic than freesilica because of their lower solubility and thatsilicates may reduce the toxicity of a mixed dust bydepressing the solubility of quartz.

Coalworkers' Pneumoconiosis'T'his is described next because of its higlh numeri-

cal incidence and because it presents pathologicalfeatures distinct from those found in silicosis.Amongst coal miners there is a small percentage

who develop classical silicosis. These are menengaged in drilling rock, cutting through stratawhich separate the coal seams. Some workersmay engage entirely in this type of work and theirlungs, as for instance those working in the sand-stonie strata in the east of South WVales, may showsilicosis indistinguishable from that found ingold miners, tin miners and stone masons.On the other hand the men who work on the

coal seams, cutting the coal by hand picks or bymachinery, and those engaged in loading coal,present a pneumoconiosis distinguishable fromsilicosis of the classical type. As with classicalsilicosis there appear to be two forms of the disease-one, simple pneumoconiosis, due to action ofdust alone and the other, infected pneumo-coniosis, due to the combined action of dust andinfection.

In the simple form the dust is found in foci

throughout the lungs in the form of black spots upto about 5 mm. in diameter. The dust collectsaround the small bronchioles and their accom-panying arteries, having been brought there fromthe alveoli by phagocytes. For the most part thedust remains within these cells, the general shapeof which is preserved, although the nuclei areobscured. A delicate fibrosis consisting ofreticulin fibres develops in the foci of dust.Fibrosis may not proceed beyond this stage orthere may be the development of collagen. Thelatter does not develop to the same extent as insilicosis nor does it have the concentric dispositionbut runs irregularly or radially. The foci have acrenated edge with the processes extending intothe unaffected tissues. In and around the coalfoci the airspaces become dilated, giving a charac-teristic appearance described as focal emphysema(Fig. 3). This emphysema has also been describedin classical silicosis, but it is very much moresevere in the coal worker and the foci may enlargeand become confluent.The focal emphysema appears to be due to some

mechanical disturbance within the secondarylobules of the lung, as in these units it can beseen that the emphysema starts around thebronchioles leaving a rim of unaffected lung alongthe interlobular septa, except in the most advancedstages. In focal emphysema there are no bullaeprojecting from the surface of the lung so that wehave a condition unlike that of ordinary bullousemphysema.

Heppleston (I 947) considered that the em-physema is caused by a shrinkage of the fibroustissue in the coal foci, while Rogers (I944) con-sidered that there had been interference with thelumen of the terminal bronchioles leading topartial obstruction with trapping of air and con-sequent dilatation of the airspaces.The noxious element in coal dust is not known

with certainty. Coal always contains silica, in-cluding some quartz, so that although pneumo-coniosis is in a different anatomical form fromclassical silicosis it may be a very modified form ofthe latter disease. Trhe point to be emphasized,however, is that the dust formed from commercialcoal is a noxious dust. Pneumoconiosis identicalwith that in coal miners is seen in coal trimmers,who are men who load coal into ships. In the pastit has been argued that the respiratory disease inminers may be due to the fumes from the ex-plosives used in getting the coal or to the rapidchilling due to travelling against the incoming airin those mines entered by slants. The occurrenceof an identical form of the disease in men loadingcoal into ships shows that cold and fumes can be atmost only contributory factors and that theessential cause is the inhalation of dust.

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Infective Variety of Coalworkers'PneumoconiosisThe condition described above as simple

pneumoconiosis seems to be due to the action ofdust alone but superimposed upon it there isfrequently a massive fibrosis which appears to meto be due to the combined action of infection anddust (Fig. 3). The masses tend to occur mostfrequently in the upper and posterior parts of thelungs, sometimes unilateral, sometimes bilateral.They may be several inches in diameter and arefirm and rubbery in consistence. In the centresof the masses there are frequently spaces con-taining black inky fluid in which are crystals ofcholesterol. In some cases the fluid is expectorated,leaving a ragged cavity. These cavities appear tobe formed by necrosis of the tissue caused byobliterative endarteritis.

In about 40 per cent. of cases of massive fibrosistubercle bacilli can be demonstrated in the lesionspost mortem by culture or animal inoculation, andin those cases where no bacilli are found it isassumed that the infection has died out.

Cases are seen where there is superimposition ofactive tuberculosis on the simple pneumoconiosisfoci and stages from the earliest infective change upto the formation of large fibrotic masses can betraced. In the past tuberculosis has been re-garded as of low incidence in coal workers, butthe form of tuberculous reaction which I have beendescribing does not usually give rise to caseationor to the usual symptoms of open tuberculosis.There is greater formation of fibrous tissue, theprogress is very slow and the ill effects are prin-cipally on the pulmonary circulation, causing verymarked right heart hypertrophy and frequentlydeath is due to congestive cardiac failure. In asmaller percentage of cases the tuberculosisspreads more acutely and in these, in addition tothe pneumoconiotic lesions, there is caseation andbronchopneumonic spread of the infection.One other cause of death which occurs not in-

frequently is pulmonary arterial thrombosis. Thiscommences in a branch of the artery in relation toan area of massive fibrosis and the thrombus ispropagated towards the hilum of the lung.The outstanding differences between coal

workers' pneumoconiosis and classical silicosis arefirst, the former gives rise to more severe em-physema than the latter, and secondly the effectsof tuberculosis are somewhat different in the twoconditions; in classical silicosis the open type oftuberculosis is a common terminal event althoughheart failure from massive fibrosis also occurs; incoal workers, massive fibrosis leading to heartfailure is the uisual occurrence, whereas opentuberculosis is a less common complication.

GraphiteIn the past graphite, like coal, has been re-

garded as innocuous but two recent papers(Harding and Oliver, 1949), and Gloyne, Marshalland Hoyle, I949) have described graphite pneumo-coniosis in Britain. The disease is similar to thatmet with in coal workers and since naturalgraphite contains silica it may be that the diseasein graphite workers is also a modified silicosis.

AluminiumIt has been mentioned above that aluminium

has been found to reduce the toxic action ofsilica, but at the same time workers, particularly inGermany (Goralewski, I943), have described apneumoconiosis ascribed to dust of powderedmetallic aluminium. Among the clinical featur'eswas development of spontaneous pneumothoraxin several cases. At post mortem, collagenousfibrosis was found and dust particles were presentwhich could be distinguished from carbon by theirjagged outlines.

Hunter et al. (1944) found no pneumoconiosisin grinders of duralumin in Britain. It may bein the case of the German workers that the sub-stitution of other lubricants for stearin in thestamping process of making aluminium powdermay have been responsible and also the amount ofdust in the atmosphere was increased in con-sequence of unsatisfactory ventilation of work-rooms resulting from the war-time blackout.Examination of material from the German casesshows that it is undoubtedly a pneumoconiosis sothat aluminium dust must be regarded as a toxicsubstance under certain conditions of exposure.

In connection with aluminium another newly-recognized form of pneumoconiosis may be con-sidered. This has been described in Canada byShaver and Riddell (I947) and Shaver (I948),occurring in men exposed to the fumes arising inthe process of making the abrasive ' aloxite,' byheating bauxite (aluminium ore) with iron andcoal. These men developed diffuse fibrosi3 andemphysematous bullae, the latter tending to fusetogether forming larger cavities. Rupture of these,giving rise to pneumothorax was a prominentfeature. The precise aetiology is uncertain as theexposure involves high concentrations of bothaluminium and silica, both in a very fine state ofdivision. Very finely divided silica such as theso-called' 20 Angstrom silica' is known to have ageneral toxic action but does not cause pneumo-coniosis in experimental animals. Whatever bethe noxious element in the fumes causing diseasein aloxite workers the reaction in the lung is verydifferent anatomically from classical silicosis.

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December I949 GQUGH: Pathology of Pneumoconiosis 617

BerylliumSerious pulmonary disease has occurred in

workers exposed to beryllium and its alloys andcomflpounds (a summary has been given by theNew York State Department of Labour, I949).Cases have occurred principally in the U.S.A. inthe electric light industry in the use of berylliumphosphors in making fluorescent lighting. Thereare two main varieties of the disease-an acute onewhich in severe form leads to massive pulmonaryoedema and occurs principally in workers exposedto the soluble salts of beryllium in the refiningindustry, and usually within a few days of heavyexposure. The other is a chronic pulmonarygranulomatosis developing several months toyears after the commencement of exr osure,principally among workers handling berylliumphosphors but also in those exposed to the dust orfumes of the metal or oxide. The granulomashows round cells and giant cells resemblingsarcoidosis. No infection has been found toaccount for the condition and excess berylliumhas been found in the lungs. In the more chronicform fibrosis is present. A case has been describedby Agate (I949) in this country occurring in alaboratory worker exposed to beryllium.

Cotton DustCotton dust is known to produce a variety of

chest symptoms (byssinosis) but post mortemstudies have not yet revealed any distinctive under-lying lesions in the lung.

CqrborundumPerhaps the most surprising of all the recent

findings is that of Bruusgaard (I948) who hasfound pneumoconiosis by radiographic examina-tion of men exposed exclusively to carborundumdust (silicon carbide). Post mortem investigationswill be awaited with interest. In his classicalexperiments Gardner (1923) showed that car-borundum was not toxic to experimental animals.This was one of the most important facts indisposing of the theory that it was the hardnessor sharpness of particles that caused damage inthe lungs. It would be ironical if it were nowfound that carborundum produces pneumo-coniosis. However, Gardner (1938) found inexperimental animals that 6arborundum, togetherwith tuberculous infection, produced a fibroticreaction which may also explain the human cases.

BagasseOne of the more recently recognized forms of

pneumoconiosis is one ascribed to the dust ofsugar canes. Hunter and Perry (1946) havedescribed recent cases including one fatal one.

The men affected were engaged in breaking upbales of cane imported into this country.

Perry (I948) has described that' the bronchiolesbecome filled with vegetable dust which swellsunder the influence of bronchial secretions, blocksthe bronchioles and gives rise to small areas ofcollapse. When these areas become infectedtypical acute bronchiolitis and pneumonia result.In some cases the condition does not resolve andthere develops a fibrosis of the lung with coughand sputum and much shortness of breath, to-gether with radiographic changes showing thickbands of fibrous tissue traversing the lung field soas to simulate cavities. In one case necropsyrevealed chronic bronchiolitis and bronchiectasisof similar distribution to that associated with dustdiseases. No large cavities were found. Fungimay play an important role in breaking down thefibre into a very fine vegetable dust and maypossibly even render this toxic. Aspergillus ispresent in all specimens of bagasse dust, butprobably takes no part in causing the disease. Theappearances are certainly not those of silicosis. Thedisease resembles " Farmer's Lung," " BrokenWind " of horses, and in some ways byssinosis.These may all belong to a single group.'

SummaryThe theories of the nature of silicosis are

discussed.The changes found in coal workers' pneumo-

coniosis are contrasted with those of classicalsilicosis.

Reference is made to pneumoconiosis due tographite, talc, mica, aluminium, beryllium andbagasse.

I wish to thank Dr. L. W. Hale for the specimensfrom which the sections shown in Figs. I and 2were made.

BIBLIOGRAPHYAGATE, ;; N. (I948), Lancet, 2, 530.BRUUSGAARD, A. (1948), Proc. Ninth Intern. Cong. of Ind. Med.,

London (in the press).DENNY, J. J., ROBSON, W. D., and IRWIN, D. A. (I939),

Canadian Med. Ass. Y., 40, 213.DREESEN, W. C., et al. (I940), U.S.A. Public Health Bulletin,

No. 250. Washington Government Printing Office.FALLON, J. T. (I937), Canadian Med. Ass. J., 36, 223.GARDNER, L. U. (1923), Amer. Rev. Tuberc., 7, 344.GARDNER, L. U. (1938), Silicosis and Asbestosis, edited by

Lanza, A. J.,GARDNER, L. U. (I939), Report of the Director of the Saranac

Laboratories.GARDNER, L. U. (I940), J. Amer. Med. Ass., 14, 535.GLOYNE, S. R., MARSHALL, G., and HOYLE, C. (1949),

Thorax, 4, 31.GORALEWSKI, G. (I943), Dtsch. Tuber-bl., 17, 3.GYE, W. E., and KETTLE, E. H. (1922), Brit. 37. Exp. Path.,

3, 24I.GYE, W. E., and PURDY, W. J. (I922), Ibid., 39 75.GYE, W. E., and PURDY, W. J. (224), I., 5, 238.HARDING, H. E., and OLIVER, G. B. (I949), Brt. 9'. Ind. Med.,

6, 9I.HEPPLESTON, A. G. H. (s247), 3. Path. and Bact., 59, 453.HUNTER, D., et al. (I944) rit. J3. Ind. Med., x, I59.HUNTER, D., and PERRY, K. M. A. (1946), Id., 3, 64.IRVINE, L. G. (5938), Proc. Intern. Coni. on Siicosis in Geneva

I.L.O. Studies and Reports, Series F. (Industrid Hygiene), No.57, p. 1515

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IRVINE, L. G., SIMSON, F. W., and STRACHAN, A. S. (1930),Proc. Intern. Conf. on Silicosis in Johannesburg, I.L.O. Studiesand Reports, Series F. (Industrial Hygiene), No. I3, p. 259.

JONES, W. R. (I933), ,. of Hyg., 33, 307.KETTLE, E. H. (I932), Y. Path. and Bat., 35, 395.KETTLE, E. H. (I934), Ibid., 38, 20o.KING, E. J. (I945), M.R.C. Special Report Series, No. 250, p. 73.KING, E. J. (I947) Occ. Med., 4, 26.KING, E. J., WRI6HT, B. M., and RAY, S. C. (I949), Paper read

to the Path. Soc., Great Britain, January, 1949.McLAUGHLIN, A. I. G., ROGERS, E., and DUNHAM, K. C.

(I949), Brit. 3Y. Ind. Med., 6, I84.MINERS' PHTHISIS MEDICAL BUREAU OF SOUTH

AFRICA (1946), Report for the Three Years ending Jy 31,I944 (South African Government Printer).

NEW YORK STATE DEPARTMENT OF LABOUR (1949),Monthly Review, 28, No. 4, April.

PERRY, K. M. A. (1948), Proc. Ninth Intern. Cong. of Ind. Med.,London (in the press).

POLICARD, A. (1947), Proc. Conf. of the Institution of MiningEngineers and Institution of Mining and Metalurgy, London,P. 24.

ROGERS, E. (i944), Paper read to the British Tuberculosis Associa-tion.

SHAVER, C. G. (1948), Radiology, 50, 760.SHAVER, C. G., and RIDDELL, A. R. (I947), J. Id. Hyg. and

Tox., 29, 145.VORWALD, A. J., and CARR, J. W. (1938), Amer. J7. Path., 14,49.

PNEUMOCONIOSIS IN COAL MINERSBy J. C. MCVITTIE, M.B., CH.B., D.P.H.

Senior Medical Officer, Pneumoconiosis Medical Panel, Swansea

In his contribution Dr. Meiklejohn has tracedhistorically the recognition of a relationshipbetween disease and dusty occupation, and hasshown that the ancients were aware of the in-dustrial risk and that they, in fact, attributed thedamage in some degree to the dust they inhaled.Until I83I English medical literature had beendestitute of a single treatise on diseases of tradesand professions. In that year Gregory describedthe postmortem findings in a case of pneumo-coniosis 'with black infiltration of the wholelungs' in a Scottish coal miner. Subsequently-there appeared a number of references to pul-monary disease in coal miners, and valuable andcritical surveys of the literature appear in anexcellent paper on ' Coal Miner's Lung' by LyleCummins and Sladden, in the first report (medicalstudies) dealing with chronic pulmonary diseasein South Wales coal miners published by theMedical Research Council in 1942, and in thescholarly and comprehensive study of the diseaseby Fletcher. Although the reference to coal-miners' pneumoconiosis had priority in ourliterature, the later studies were concernedchiefly with miners' phthisis in metalliferousmines and with silicosis in other industries, and-there was considerable delay in bringing workersin the industries within the scope of the Work--men's Compensation Act. In 1907 the Committeeon Compensation for Industrial Diseases recom-mended that the question of scheduling silicosis(fibrosis due to the inhalation of free silica) shouldbe kept in abeyance for the time being. Later,owing to -successful measures adopted in the goldmining industry in South Africa under successiveMiners' Phthisis Acts, pressurE was brought tobear on the Home Office to deal with the subject.Pressure was brought not only by medical men

but by workers and their representatives who wereconcerned about the incidence of the disease, andwho were alert to the fact that increasing sicknessand disability were associated with changing con-ditions underground. In I925 Grenfell presentedthe evidence he had collected in South Wales. Inone year 22 cases (including 12 deaths) in drillersand ' hardheaders' had been collected from fivecollieries. It was emphasized that in one par-ticular pit the disabled men, whose ages rangedfrom 22 to 45 years, worked in the same place orheading. Four of the group had died and post-mortem evidence was available. In the follow-ing year Tattersall reported the tragic story of agroup of rock drillers in another area. As a resultof these and other representations a method wasdevised of dealing with the difficulties of thesituation in this country by a system of ' schemes 'each applicable to a particular industry or groupof industries. Thus the Various Industries(Silicosis) Scheme, 1928, applied to all workmenemployed at any time on or after January i, 1929,in ' the drilling and blasting in silica rock in orincidental to the mining or quarrying of otherminerals,' and by it silica rock was defined ascontaining not less than 50 per cent. free silica.This scheme identified the disease with particularoccupations and with particular working places,and the drillers, brushers and hardheaders wererequired to prove the analysis of rock. Therewas, too, a strange inconsistency between theabove scheme and the Refractories Industries(Silicosis) Scheme which came into force in I9I9.The latter embraced compensation for partialincapacity as well as death and total incapacity.Certification under the 1928 scheme was by acertifying surgeon who was not required to makean X-ray examination. These anomalies were

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