639 OTHER LUNG DISEASES DUE TO DUST By A. Tr. DOIG, M.D., D.P.H. H.M. Medical Inspector of Factories Respiratory dust disease until comparatively recently was commonly thought of as comprising little more than silicosis and asbestosis. In the last decade, however, there has been general appreciation of the fact that the field is con- siderably wider. Silicosis, asbestosis and pneumo- coniosis of coal miners and coal trimmers have been described in this issue and the author has been invited to deal with the remaining dust diseases of the lungs. To do so in detail in this article is impossible. His object will be to indicate something of the scope of the subject dealing only briefly with the individual dusts and the conditions they cause. The references which are given have been chosen with a view to forming a starting point for further reading about the effects of individual dusts. Mineral Dust Pneumoconiosis with Fibrosis Although silica, asbestos and coal are the most important dusts which cause pulmonary fibrosis, there are others wvhich have a similar effect. Many of these are mixed dusts, containing several constituents, and in the case of naturally occurring minerals some proportion of free silica is generally present. In such cases it has to be considered whether the condition produced is due to the action of silica modified by other dusts present. It is often impossible to state definitely whether this is so or whether the other constituents of the dust also exert a toxic efect, but there is certainly a growing amount of evidence that some materials which were formerly considered innocuous are either by their own property or by virtue of admixed silica, capable of causing lung disease on inhalation. SILICATES: For long asbestos was considered the only harmful variety of silicate, and other silicates such as talc were regarded as inert. Merewether (1933) examined ii workers exposed to the inhalation of talc dust for periods ranging from II to 32 years, and in I934 he examined a further 13 workers with exposures of from 41 months to 40 years. He found abnormal appear- ances in the X-ray films of the chests but that these were associated with little or no clinical disability. Although this was the first in this country there had been earlier reports from the Continent suggesting the existence of a talc pneumoconiosis. Since 1933 also there have been many reports from America of cases of injury to the lungs from talc, based not only on X-ray appearances but on the existence of symptoms, of abnormal signs on clinical examination of the chest, of disability and, in some cases, on post mortem findings. In this connection it is interesting to note that talc has been implicated in the causation of peritoneal adhesions after abdominal operations. An editorial with references to ten articles dealing with this subject appeared in the British Medical Journal in 1948. McLaughlin, Rogers and Dunham (I 949) have recently described in great detail a fatal case of talc pneumoconiosis occurring in this country. Thev also review the literature on this interesting and important subject. Although admixture with quartz up to 20 per cent. has been reported in some American talcs, ordinary commercial talc as used in this country is silica-free as was the talc used by the patient of McLaughlin, Rogers and Dunhain. Under the microscope talc is seen to exist both as flakes of material and tiny fibres. McLaughlin and his colleagues suggest that the fibrosis is produced mainly or only by the fibres. Not only was the fibrosis similar to that of asbestosis but an in- teresting feature was the presence of curious bodies similar to asbestos bodies. It seems there- fore that we must accept talc as a fibrosis-producing agent and institute means of dust suppression where there is considerable exposure to it. A disabling type of pneumoconiosis due to Fuller's earth has also been reported (Middleton, I940; McNally and Trostler, 194I). Tonning (1949) recently described the post mortem appear- ances of a man aged 79 who had worked with Fuller's earth in his youth. The exact length of his employment was unknown but it had ceased about the age of 29, and so probably did not exceed IS years. Thereafter he had no dust ex- posure at work. The lungs were moderately em- physematous and contained numerous black firm nod-ules. Microscopically the dust was seen to be held in a loose mesh of fine reticular fibres and the lesions were invariably surrounded by emphysema. The histological picture differed from typical Protected by copyright. on October 16, 2020 by guest. http://pmj.bmj.com/ Postgrad Med J: first published as 10.1136/pgmj.25.290.639 on 1 December 1949. Downloaded from
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639
OTHER LUNG DISEASES DUE TO DUSTBy A. Tr. DOIG, M.D., D.P.H.H.M. Medical Inspector of Factories
Respiratory dust disease until comparativelyrecently was commonly thought of as comprisinglittle more than silicosis and asbestosis. In thelast decade, however, there has been generalappreciation of the fact that the field is con-siderably wider. Silicosis, asbestosis and pneumo-coniosis of coal miners and coal trimmers havebeen described in this issue and the author hasbeen invited to deal with the remaining dustdiseases of the lungs. To do so in detail in thisarticle is impossible. His object will be to indicatesomething of the scope of the subject dealing onlybriefly with the individual dusts and the conditionsthey cause. The references which are given havebeen chosen with a view to forming a starting pointfor further reading about the effects of individualdusts.
Mineral DustPneumoconiosis with Fibrosis
Although silica, asbestos and coal are the mostimportant dusts which cause pulmonary fibrosis,there are others wvhich have a similar effect.Many of these are mixed dusts, containing severalconstituents, and in the case of naturally occurringminerals some proportion of free silica is generallypresent. In such cases it has to be consideredwhether the condition produced is due to theaction of silica modified by other dusts present. Itis often impossible to state definitely whether thisis so or whether the other constituents of the dustalso exert a toxic efect, but there is certainly agrowing amount of evidence that some materialswhich were formerly considered innocuous areeither by their own property or by virtue ofadmixed silica, capable of causing lung disease oninhalation.
SILICATES: For long asbestos was consideredthe only harmful variety of silicate, and othersilicates such as talc were regarded as inert.Merewether (1933) examined ii workers exposedto the inhalation of talc dust for periods rangingfrom II to 32 years, and in I934 he examined afurther 13 workers with exposures of from 41months to 40 years. He found abnormal appear-ances in the X-ray films of the chests but that thesewere associated with little or no clinical disability.Although this was the first in this country there
had been earlier reports from the Continentsuggesting the existence of a talc pneumoconiosis.Since 1933 also there have been many reports fromAmerica of cases of injury to the lungs from talc,based not only on X-ray appearances but on theexistence of symptoms, of abnormal signs onclinical examination of the chest, of disability and,in some cases, on post mortem findings. In thisconnection it is interesting to note that talc hasbeen implicated in the causation of peritonealadhesions after abdominal operations. An editorialwith references to ten articles dealing with thissubject appeared in the British Medical Journal in1948. McLaughlin, Rogers and Dunham (I 949)have recently described in great detail a fatal caseof talc pneumoconiosis occurring in this country.Thev also review the literature on this interestingand important subject.
Although admixture with quartz up to 20 percent. has been reported in some American talcs,ordinary commercial talc as used in this country issilica-free as was the talc used by the patient ofMcLaughlin, Rogers and Dunhain. Under themicroscope talc is seen to exist both as flakes ofmaterial and tiny fibres. McLaughlin and hiscolleagues suggest that the fibrosis is producedmainly or only by the fibres. Not only was thefibrosis similar to that of asbestosis but an in-teresting feature was the presence of curiousbodies similar to asbestos bodies. It seems there-fore that we must accept talc as a fibrosis-producingagent and institute means of dust suppressionwhere there is considerable exposure to it.A disabling type of pneumoconiosis due to
Fuller's earth has also been reported (Middleton,I940; McNally and Trostler, 194I). Tonning(1949) recently described the post mortem appear-ances of a man aged 79 who had worked withFuller's earth in his youth. The exact length ofhis employment was unknown but it had ceasedabout the age of 29, and so probably did notexceed IS years. Thereafter he had no dust ex-posure at work. The lungs were moderately em-physematous and contained numerous black firmnod-ules. Microscopically the dust was seen to beheld in a loose mesh of fine reticular fibres and thelesions were invariably surrounded by emphysema.The histological picture differed from typical
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silicosis in an absence of the whorled collagenousnodules and closely simulated that of pneumo-coniosis of coal miners with focal emphysemaround the dust aggregations.The position in regard to other silicates is less
definite. Lung injury has been described follow-ing inhalation of mica, china clay, sillimanite,sericite, etc. For some years following I933, agreat controversy raged about sericite following theassertion by W. R. Jones (I933) that silicosis wasdue not to free silica (quartz) but to sericite whichis a silicate of aluminium and sodium. Thistheory has now been proved to be without founda-tion and has been abandoned. Nevertheless thereis some experimental evidence that sericite is byitself harmful.The use of grinding wheels made of natural
sandstone was attended with a very high incidenceof silicosis, but now they have practically dis-.appeared their place being taken by manufacturedwheels made of carborundum, emery or someforms of aluminium oxide. This has been accom-panied by -a marked decline in the number ofcases of silicosis in the grinding industry. It ispossible, however, that under certain circum-stances, carborundum, which is silicon carbide,may not be entirely harmless. Some surveys ofworkers employed grinding metals with artificialabrasive wheels have shown the presence ofnodular shadows on the X-ray film, and whilethese may have been due to particles of the metalbeing grbund, particles of the abrasive wheelcould not be excluded. Recently at a factoryhandling powdered silicon carbide and aluminiumoxide in such a way that considerable quantities ofdust were created, 53 employees were examinedradiologically. Fifteen films were stated to showsome pulmonary fibrosis which in seven was of anodular type resembling silicosis, but three ofthese cases had substantial previous exposures tomineral dusts (Smith and Perina, 1948).ALUMINIUM: Considerable interest has arisen in
the possible action of aluminium and its oxides onpulmonary tissue, and reports in the literature areconflicting. On the one hand we have very strongevidence that finely powdered aluminium oraluminium oxide even when present in a con-centration of only i per cent. has a powerfulinhibitory action on quartz, protecting experi-mental animals from silicosis. This work firstreported from Canada (Denny, Robson and Irwin,1937) has since been widely confirmed not only formetallic aluminium, but also for aluminiumhydrate (Gardner et al., I944). On the other handwe have reports that workers exposed to finely-divided metallic aluminium or its compounds maysuffer chronic respiratory disease. Such reportsappeared in the Continental literature about 1940
(Goralewski, 1940, I941; Goralewski and Jager,I941; Jager and Jager, I94'; Jottert and Eickhoff,1942, etc.). A type of pneumoconiosis has beenreported in furnace work ers exposed to thevolatilized fumes of alumina (Shaver and Riddell,I947). Several cases were found to have aspontaneous pneumothorax, a feature which hadalready been noted by the German workers.Experiments in animals have suggested thataluminium may favour the development oftuberculosis in the lungs. The whole question isbeing thoroughly investigated in this country andabroad, and until definite results are obtained itwould seem reasonable to consider that prolongedexposure to finely-divided particles of aluminiumor aluminium oxide dust may be harmful.
GRAPHITE: Graphite is a naturally occurringcrystalline form of carbon, although a pulverizedform of coke is also called graphite. Naturalgraphite consists of carbon mixed with otherminerals and after incineration may leave as muchas 33 per cent. ash. According to Harding andOliver (I949) various graphites contain 8 to'i8.6per cent. of total silica, and 3 to io per cent. offree silica. In this country there have in recentyears been several reports of serious lung diseasecaused by graphite dust. Dunner (I945), Dunnerand Bagnall (1946), and Dunner (1948) recordfive cases of graphite pneumoconiosis. Two fatalcases with detailed post mortem findings were re-ported by Gloyne and others (I949) and a mostinteresting observation in one of their cases wasthe finding of golden yellow 'graphite bodies'similar to the ' asbestosis bodies ' of asbestosworkers and ' anthracosis bodies' of coal miners.Harding and Oliver (1949) record three fatalcases and give brief notes of six workers whoshowed X-ray changes. They point out thatgraphite pneumoconiosis is not the benign con-dition it has in the past been assumed to be; itcan on the contrary lead to complete incapacityand death. Histologically the lesions they describeare similar to'those of coal miners, with pigmentaggregates, linear or radial fibrosis and focalemphysema. In advanced cases massive fibrosisoccurs without definite nodule formation.
Pneumoconiosis without FibrosisCertain dusts, among them iron and tin, seem
to be inert when inhaled. The particles, providedthey are small enough to enter the alveoli areengulfed in phagocytes, some of which are coughedup, while others are deposited in the aggregationsof lymphoid tissue at the bifurcations of thebronchioles. They are capable of lying there foryears without inducing any deposition of fibroustissue or other reaction, but because they arerelatively opaque to the X-rays they may produce
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December I949 DOIG: Other Lung Diseases Due to Dust 641
ai.9 ..... . .. ........
FIG. i.-A.T.T., worker with Fuller's earth for 35years (Dr. Middleton's case).
changes in the X-ray film which may be indis-tinguishable from those of silicosis. Opportunitiesfor inhaling iron oxide dust occur in manyoccupations and it is most important that thecondition produced should be correctly assessed.Reticulation or nodulationi on an X-ray film of thechest does not mean fibrosis or disease, and manya worker has passed through a very unhappy periodafter being told he was suffering from silicosiswhen, in fact, he was merely exhibiting a dustingor tattooing of his lungs with iron oxide.
Such X-ray films are frequently met with inwelders who are constantly exposed to fumes fromthe work. The heat of the electric arc or the oxyacetylene torch melts and boils the metal beingwelded, iron coming off as a vapour and oxidizingalmost immediately to iron oxide in minuteparticles. Welders who have spent years at thiswork, particularly if they have performed sub-stantial amounts of weldingiaside boilers tanksand other ill-ventilated spaces may be found onX-ray examination to show reticulation ornodulation.The conpdition was first described by
Doig and McLaughlin in I936, and at that timewe were not sure what was the cause or the outlookfor the patient. We did, however, emphasizethat the X-ray changes we described occurred in
.UN
FIG. 2AMi aged 40. Dyspnoea after exposure tofireclay dust during 1 3 years cutting and grindingbricks
men who were apparently in good health. Furtherexperience by clinical examinations of somehundreds of welders has made us certain that the.condition is benign and not accompanied bysymptoms, abnormal physical signs or diminishedcapacity for wo-rk.Some welders with dust reticulation have been
re-examined at intervals up to 14 years and foundtto remain quite fit and continue at work withoutany difficulty. The X-ray changes are notassociated with dyspnoea or clinical evidence offibrosis. Chest expansion is good and tolerance forexercise is normal. These findings have been amplyconfirmed by numerous investigators not only asregards welders (Britton and Walsh, 1940; Groh,i944; Sander, 1944; Lanza, I945, etc.) but alsoas regards other workers exposed to iron oxidesuch as silver finishers (McLaughlin et al., I945;Barrie and Harding, I947).As has been stated the X-ray picture in this
condition is identical with silicosis and examinationof a single X-ray film' does not supply evidence ofthe inert nature of the condition. Serial X-rays.taken over a period of years, particularly afterexposure to welding has ceased -may, however, givesupporting evidence. X-ray changes in silicosisare permanent; if they change it is for the worse,indicating a progression of the process, and such a
Hi
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FIG. 3.-J M. aged 65. Exposure to 'carbon' dustconsisting mainly of ground coke for 30 years.Moderate dyspnoea.
change is unfortunately commonly met with.Improvement inthe X-ray appearances has notbeen described nor is it to be expected in a diseasecharacterized by the laying down of a considerableamount of fibrous tissue. On the other handDoig and McLaughlin (I948) have described two*of our original welders whose X-ray appearanceschanged for the better, and indeed in one case thepicture returned to normal some years after giving.up welding. Such an observation is only com-patible, to our minds, with a condition in whichthe dust lies amongst normal tissue and is not shutin by fibrous tissue or associated with otherchanges of a permanent nature.There is only one report in the literature of a
post mortem examination of a welder who showedX-ray changes of the dust inhalation type duringlife (Enzer and Sander, 1938). This is illustratedby excellent photomicrographs showing no fibrosisround the collections of dust which were found togive the Prussian blue reaction. The man's deathwas not related to his occupation or his lung con-dition but was the result of an accident. Insuccessive papers McLaughlin and his colleagues(i945), Barrie and Harding (1947), and Harding(1948) describe the post mortem findings in five
FIG. 4.-F.G., aged 52. Electric welder 30 years, oxy-acetylene welder three years. X-ray appearancesunchanged over nine years. Remains symptomlessand at work.
silver finishers who showed during life the typicalX-ray changes of dust-deposition in the lungs. Inthe first four cases there was absolutely no fibrosisround the deposits of iron oxide. In the fifth casethere was a minimal amount of fibrosis of the'reticulation type '-not at all like that producedby silica. Harding thinks that in this case in-dividual susceptibility may have been of im-portance, but there is always the possibility that theiron dust at some period of the man's workinglife-over 40 years-may have contained silica orother fibrosis-producing-constituent. Indeed it isnot without the bounds of possibility that he mayhave used sand as the polishing medium at onetime. The author has himself seen sand used forthis purpose in a Sheffield polishing shop in 1939.
Further evidence of the inert behaviour of ironoxide has been obtained from animal experimentswhich have been carried out by numerous ob-servers, for example, Harding, Grout and LloydDavies (1947) who produced X-ray changes in thelungs of rats exposed to iron oxide dust butexamination of the tissues showed no fibrotic orother reaction. Finally there is statistical evidence.The Registrar General's Supplementary Reporton Occupational Mortality, I 93 1, shows that of
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December 1949 DOIG: Other Lung Diseases Due to Dust 643
FIG. 5. J.W.I., aged 53. Bronchial carcinomaassociated with early asbestosis (confirmed atautopsy) in an asbestos weaver (Dr. F. N. R.Price's case).
the ii,542 welders in England and Wales in thatyear there were only I23 deaths compared withi6i expected on the basis of age-rates for all males.The author has collected from various factories in-formation about sickness absence in welders andfind that they are favourably placed as regardsother groups, not only for total sickness but also forsickness due to respiratory disease. Collen and hiscolleagues (I944) and Collen (1947) give reliableevidence about the incidence of pneumonia in wel-ders, showing that the incidence, death rates andcase fatality rates for welders in the Kaiser-Oregonshipyards were similar to all other shipyardworkers and that there was no difference inseverity, number of days required for treatment orthe incidence of complications.
Taking all the evidence then there seems to beproof that iron oxide, inhaled into the lungs inamounts sufficient to give rise to changes on theX-ray film, lies inertly in the tissues for yearswithout giving rise to pulmonary fibrosis or otherpermanent change.* Other dusts which are considered on presentevidence to be inert in the lungs include barium,calcium and tin. In 1933 Arrigoni carried out anenquiry amongst the barium workers at Valsassinain Italy. He found that many men, particularly
FIG. 6.-Hayworker's lung (Dr. J. M. Campbell's case).Extreme dyspnoea, eventual recovery.
grinders and packers, showed marked changes inthe X-ray films but that symptoms and abnormalclinical signs were slight or absent. Tin, likebarium, is much more radio-opaque than ironand therefore deposits in the lungs cause par-ticularly dense shadows. Pendergrass and Pryde(1948) reproduce an excellent X-ray of this type,the subject being a man aged 45 years who hadbagged tin oxide for 15 years. He had no dis-ability, the X-ray abnormality being discoveredduring a routine survey of all the workpeople.Workers exposed to lime, gypsum or marble dustsdo not appear to suffer any harmful effects andwhile X-ray abnormalities indicating dust de-position have been met with, these are generallycomparatively slight in degree (I.L.O., I938).The manufacture of cement, which is a complexcompound of lime, is usually attended with ex-posure to considerable quantities of dust. Cementis irritating to the skin and mildly to the upperrespiratory passages. It cannot be regarded as aninert dust yet there is a considerable body ofevidence which suggests that workers manu-facturing or handling cement do not get pneumo-coniosis. For instance, Gardner and others ex-amined and X-rayed 2,278 workers in I939. Over55 per cent. of the group had been exposed for
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FIG. 7.-A.L., aged 57. Byssinosis. Stripper andgrinder in a cotton mill for 40 years (Dr. F. N. R.Price's case).
more than ten years, but no cases of disability weremet with and X-ray abnormalities were of theslightest. The authors consider the dust risk inthe cement industry as trivial compared with rockmining and other silica industries.
PneumonitisThe dust or fume from some metallic com-
pounds is directly irritating to the lung parenchymaand leads to atypical forms of pneumonia usuallyspoken of as pneumonitis.
Manganese, as is well-known, may cause achronic disease of the nervous system. Since 1921there has also been suspected a relation betweenmanganese and pneumonia. At Sauda, in Norway,the installation of a manganese smelting factorywas followed by a tenfold increase in the mortalityrate for pneumonia. Similar reports have beenmade in regard to workers in German factories, andminers of the ore. In this country Lloyd Davies(I946) showed that a group of men exposed tooxides of manganese existing as fine particles inthe air had, between 1938 and I945, a pneumoniarate of 20 to 90 times that of other workers in thefactory. The cases usually resolved withoutleaving any disability, but compared with non-industrial pneumonia resolution was slower and
*ISe
FIG. 8.-Pulmonary fibrosis and dyspnoea in a managed 46, engaged in tea blending for five years withno other dust exposure (Dr. Douglas Bell's case).
less influenced by sulphonamides. In a later re-port Lloyd Davies and Harding (1949) makefurther observations including the results of animalexperiments. The changes in the bronchial andalveolar epithelium are well illustrated with photo-micrographs. It has been stated that some otherfactor is necessary in addition to manganese beforepneumonitis results, but these authors concludethat manganese dust in suitable particle size, intro-duced into the respiratory system, will withoutthe presence of other factors, cause pneumonitis.
Beryllium is a metal which has become of con-siderable importance in recent years. Inhalationof its compounds in a fine state of division is knownto cause pneumonitis. First reports of this con-dition came from Russia in 1936, relating toworkers exposed to beryllium oxyfluoride, and theirritant action was at first thought to be due to thefluorine. The literature on the toxic action ofberyllium is now extensive and it is recognized thatnon-fluorine containing compounds are generallyjust as toxic. The production and use of berylliumand its compounds in Britain lags behind theUnited States, where numerous reports of pneu-monitis from beryllium have appeared. Whatseems to be the first record of such a case in thiscountry is that of Royston (I949).
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December I949 DOIG: Other Lung Diseases Due to Dust 645
Cadmium fumes are particularly irritating andmay cause a severe pulmonary reaction. Pneu-monitis may also follow exposure to the fumes ofosmium and vanadium.
Delayed Pneumonitis (Granulomatosis)Another type of pulmonary reaction has been
observed in persons exposed to beryllium. Thiscomes on after a more prolonged period of contact,and sometimes months or years after contact hasceased. It has been particularly associated withthe manufacture of fluorescent lamps in which azinc beryllium silicate was often used. The firstreport (Hardy and Tabershaw, 1946) concerned17 cases in workers in the fluorescent lamp industryamong whom there were six deaths. The symp-toms were loss of appetite, loss of weight, markeddyspnoea, cough and weakness, and a feature wasa tendency to progression after removal of contact,unlike the acute pneumonitis which was usuallyameliorated by removal from the industrial ex-posure. X-ray changes are variable but usuallyconsist of granularity, reticulation or nodulation.The illness shows a marked similarity to sar-coidosis; indeed the late Leroy Gardner reportedin 1946 that he had in his files some ioo cases ofsarcoidosis of which 6o were known to have ex-posure to beryllium. This particular lesion causedby beryllium is neither a true pneumonitis nor apneumoconiosis; the lung changes are only part ofa general pathological condition characterized bygranulomata in various organs including the liver,spleen and sometimes the lymph glands. In thiscountry only one case has so far been described(Agate, I948).Lung Cancer
It is now known that the incidence of cancer ofthe lung in certain occupations is sufficiently highto suggest a significant etiological relationship be-tween the disease and the occupation. The bestexample is probably that of the Schneeberg minersin Saxony who for four centuries have been knownto die at a comparatively early age from lungdisease which Harting and Hesse in I879 showedwas pulmonary carcinoma. They attributed 75per cent. of all deaths of the miners to this cause.later a high incidence of lung cancer was also dis-covered in mines of Joachimstal in Bohemia on theother side of the mountains. The actual cause ofthe condition is not certain as the ore containsseveral suspected substances. At first cobalt wasmined in the form of its arsenide, later bismuthand nickel and, finally, uranium. Arsenic orradio-activity are both considered likely causes.We also have evidence in this country that
arsenic may lead to lung tumours although no ex-cess of this disease has been noted in miners of tin
ore which contains arsenic. Several cases infactory workers exposed to arsenic dust have beennoted by the Factory Inspectorate who, in 1945,referred the question of the etiological relation-ship of arsenic and cancer to the Medical ResearchCouncil. A detailed investigation was carried outand it was found that workers exposed to arsenicshowed a significant excess of deaths from cancerover other occupational groups and that there wasan especial predilection for cancer of the skin andlungs (Bradford, Hill and Fanning, I948). Therole of arsenic in carcinogenesis has been dealtwith by Currie (I947).Amor (I938) has reported a high incidence of
cancer of the lung and upper respiratory tract innickel smelters. Here again there is exposure toarsenic which is present in the ore. In this countrychromium has not so far been found to have acarcinogenic effect and the report by Teleky in1937 that inhalation of chromate dust produced arelatively high incidence of lung cancer does notseem to have evoked much interest or comment atthe time. After the war however, reports of ahigh incidence of lung cancer in bichromate manu-facture were received from Germany (Gross andKoelsch, 1943); and confirmation has now beenforthcoming by the researches of Machle andGregorius (I948) in America who showed thatworkers in the chromate industry had a crudedeath rate 25 times the normal and that 25 percent. of all deaths were due to this cause. In thegroup of workers under 50 years of age, the ratesfor lung cancer va&ied in the different factoriesfrom 20 to 70 times that of the general populationin the same age-group.Some ten years ago a number of cases of lung
cancer occurring in men suffering from silicosiswere reported and an impression arose that silicamight play an etiological part in producingmalignant lung disease. This has not been borneout by further enquiry but evidence is accumu-lating that cancer of the lung is unduly frequent inasbestos workers usually associated with asbestosis.Merewether (I949) has reported that cancer of thelung or pleura occurred in 31 (13.2 per cent.) of235 cases of asbestosis, in which post-mortemexaminations were made, whereas in 6,884 cases ofsilicosis proved at autopsy there were only 9I cases(1.32 per cent.).AsthmaAsthma due to purely inorganic dusts is not
common. Hunter, Milton and Perry (I945) ex-amined workers in all the platinum refineries inBritain and found that of 9I who had contact withcertain complex platinum salts, 52 suffered from apeculiar asthma-like syndrome. Repeated sneez-ing was followed by profuse watery discharge from
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the nose, tightness of the chest, shortness of breathand wheezing. These symptoms persisted duringwork and for about an hour after when they wouldsubside. Commonly, however, a bout of coughingwas experienced in the early hours of the morning.
Vegetable DustsVegetable dusts are of less importance than
mineral dusts but their ability to produce respira-tory disease is by no means small. The study oftheir effects has been largely neglected and theirimportance probably underrated. This is partly,at least, due to the fact that the condition of chronicbronchitis which sometimes results from theirprolonged inhalation is not accompanied by anycharacteristic X-ray picture indicative of dustinhalation, as in the case with the pneumoconiosisdue to mineral dusts. The chronic effects ofvegetable dusts are thus less easily distinguishedfrom non-occupational bronchitis.
Vegetable dusts lead to acute, sub-acute andchronic pulmonary conditions. Their mode ofaction is obscure and in many cases it is not knownwhether the noxious agent lies in the vegetablematter itself, for instance some protein, alkaloidor other active principle which is irritating or toxic,or whether it lies in the impurities. In regard tochronic disease silica has been considered, for freesilica derived from soil is a universal contaminantof vegetable material. The amount present, how-ever, is small, generally about 2 per cent. or less,and most of it is present as relatively coarse grains,so that it is not generally thought likely that silicaplays any part in the production of lung diseasefrom vegetable dust. The biological contaminantsare more important. Vegetable matter almostalways contains a high content of bacteria, andspores and mycelia of fungi, some of which areknown to be pathogenic, and it is exceedinglylikely that some types of pulmonary disease resultfrom the bacteria or fungi in the dust. Anotherpossibility is that the biological contaminants mayact indirectly, not by themselves infecting therespiratory tract, but by their digestive action oncellulose or other constituent of the vegetablematter, altering it to form toxic substances. Againsome conditions produced by exposure to vegetabledusts are obviously allergic in character. Onemust also consider a mechanical action. McNairand Middleton (I924), for example, were im-pressed with the fact that dust from most kindsof grain contained a considerable quantity of sharpstiff hairs and they believed that these con-stituted the harmful part of the dust. Anotherpossible explanation is that dry vegetable matter oninhalation readily swells and this might result insmall areas of atelectasis prone to becomesecondarily infected.
It seems that vegetable dusts more than mineraldusts have a common type of action. In otherwords, whereas silica produces a nodular fibrosis,beryllium a granuloma and arsenic malignantdisease, most vegetable dusts, grain, hemp, flax,cotton, etc., may cause mill fever, or result,, afteryears of exposure, in a similar type of chronicbronchitis and emphysema.
Mill FeverThis is an acute, transient and slight illness
occurring only in new workers. It usually comeson after one or two days in the mill, lasts a dayor two and does not reappear; one attack confersimmunity. It usually takes the form of a chill,with fever, headache, lassitude and malaise, andoccasionally there may be respiratory symptomssuch as sneezing, cough and dryness of the throat.Often the symptoms are not sufficiently severe tonecessitate absence from work but if any time islost it is only a day or two. This curious littleillness has several names according to the dustproducing it-' combers' fever' in hemp mills,' hackling fever' and ' flax fever' in flax mills,'mill fever' and ' cotton cold' in cotton mills,' grain fever,' ' malt fever,' etc. It is uncertainwhether an attack caused by one dust confersimmunity to. some other vegetable dusts, but Ihave known several workers who had experiencedmill fever from jute and who suffered no illness ordiscomfort on later working in flax mills.The condition is of little importance, severe
cases and complications being apparently un-known. Probably between 25 and 50 per cent. ofnew workers in the flax industry suffer from ittoday. The cause is unknown. Various sug-gestions made include the action of a foreignprotein, histamine, a bacterial endotoxin andallergy.
Illness due to Fungi and BacteriaIn many respiratory diseases, particularly the
subacute or chronic types, saprophytic bacteria orfungi commonly exist in the sputum, and it isobviously no easy matter to decide whether aparticular organism is present as a primary orsecondary infecting agent. There is, however, agroup of respiratory diseases which we believe aredue to fungi or bacteria, not merely because theseare found in the sputum, but because the illnessesoccur in small outbreaks associated with exposureto dust from mouldy or infected vegetable matter.From time to time outbreaks of an acute illness
called ' weaver's cough' have occurred in cottonweaving sheds (Collis, 19I3; Bridge, 1928).These outbreaks have always been associated withthe handling of mildewed yarn, usually the warpwhich is more heavily si7ed tb2rl the weft. The
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December I949 DOIG: Other Lung Diseases Due to Dust 647
illness starts with irritation of the nose and throat,tightness in the chest, then follows paroxysmalcough, scanty tenacious sputum and generalmalaise. After removal from the weaving shedthe acute symptoms rapidly subside but frequentlya liability to bouts of coughing persists for someweeks. The association of the illness with thehandling of mildewed yarn and its absence inworkers even in the same factory who handlednon-mildewed yarn points very strongly to amildew as the cause. The air over the loomsusing the affected yarn was found to containmany fragments of mycelia and conidia, andexamination of the dust and of the yarn revealedthe presence of various fungi including penicillium,aspergillus, mucor and others.
Campbell (I932) described'cases of an acute butmore severe illness in farm workers who had beenhandling mouldy hay. After some noticeableshortness of breath for days or weeks the affectedworkers became incapacitated with extremedyspnoea and cyanosis. X-ray films showed a finegranular stippling and some ' fibrosis ' spreadingfrom the hilum. The symptoms lasted for weeksor months before slowly passing away in con-junction with a slow resolution of the X-raychanges. Fawcitt (1936) describes other cases in-cluding post mortem findings in one case in which'there was at first partial recovery, but dyspnoeapersisted and death took place two years afterthe acute illness. The lungs showed much em-physema, collapsed areas and marked patchyfibrosis. Potassium iodide is said to be useful intreatment.
Similar severe illness has occurred after thresh-ing mouldy grain (Tornell, 1946; Hoffmann,1946), and in the sawing of maple logs which hadlain for a year or two after felling and becomeheavily infected under the bark with a fungus(conosporium corticale) (Towey, I932).
It seems probable that bagassosis should alsobe placed in this group. Bagasse is dried sugarcane after extraction of the sugar and is importedfor use in the manufacture of fibre boards fordecorating and insulating purposes. It is an ex-cellent growth medium for a great variety ofbacteria and fungi. On leaving America it has aglucose content of 2 or even 4 per cent., but onreaching this country it is nearly sugar-free.Several cases of acute or subacute bronchiolitis orbronchopneumonia have occurred and have beenreported in this country and America. Hunterand Perry (I946) give an excellent review of theliterature and describe i i cases of their own, one ofwhich was fatal. The evidence that the disease isdue to fungi, though suggestive, is not conclusive;Schneiter, Reinhart and Caminita (1948) thinkit is due to the endotoxin of Aerobacter Cloacae.
Monday FeverThis term was introduced by Prausnitz (1936),
but numerous observers before him had describedan aggravation of respiratory symptoms onMondays. It is quite different from mill feverbecause it only occurs in workers with many years'experience and no acclimatization takes place;rather the condition tends to get progressivelyworse. The description by Prausnitz cannot beimproved:
'After working for years without any appreci-able trouble except a little cough, they noticeeither a sudden aggravation of their cough, whichbecomes dry and exceedingly irritating, or peculiarattacks of breathlessness. These attacks usuallyoccur on Mondays, whilst the rest of the weekfinds them in fairly good condition. For a longtime the trouble may be almost or entirely limitedto this " Monday fever," but gradually thesymptoms begin to spread over the ensuing daysof the week; in time the difference disappears andthey suffer continuously.'The same symptoms are experienced on return
to work after a holiday or sometimes with the re-suimption of seasonal work. Malt workers forinstance have told the author that they are affectedby the new grain which they handle in the autumnafter the summer break.
Chronic Respiratory DiseaseChronic bronchitis has been reported in workers
exposed to practically all kinds of vegetable dust,cotton, grain, flour, flax, hemp and even tobaccoand tea. The disease differs little from chronicbronchitis occurring in the general population inpersons not unduly exposed to dust and theproving of an etiological relationship between thedisease and the occupation is a matter of difficulty,almost impossible in individual cases. Unlike thepneumoconiosis caused by mineral dusts the con-dition has neither typical X-ray appearances norcharacteristic post mortem changes. Any re-lationship has usually to be proved by statisticalmethods, either on mortality or morbidity ratesfor chronic lung disease. This is not an easymatter and has been carried out adequately foronly a few dusts. It is not sufficient merely tocollect figures for all workers in a particular in-dustry as exposure to heavy dust- concentrations,and hence the particular liability to chest disease,may be confined to a relatively small section of theworkers. Sections which are favourably placed asregards dust risk may therefore mask the effectson those unfavourably placed. Cotton weaversfor example are shown in the Registrar General'sOccupational Mortality Supplement for I931-2and I921-2 to have standardized mortality ratesfor respiratory disease below the average for all
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males, but the rates for cotton card room andblow room workers are much above the average.
Chronic respiratory disease due to cotton dustis known as byssinosis, and is met with particularlyin card room and blow room workers. An ex-cellent review of the literature has been made byCaminita et al. (I947). Clinically the condition isone of chronic bronchitis and emphysema with atendency to asthma which has often supervenedafter a period of suffering from Monday fever.This condition, in conjunction with the clinicaland industrial history is, however, deemed to besufficiently characteristic to enable a properly con-stituted Medical Board to decide not only whetherdisability is present, but whether the disease isoccupational in origin. In the latter case com-pensation is payable to workers who have had morethan 20 years' experience and who are certifiedas being totally disabled*. Necropsies reveal nomore than the presence of chronic bronchitis andemphysema; there is no nodulation and no cottonfibres are found in the lung.
AsthmaAcute asthma, due to allergy to a particular dust
has been noted in workers exposed to very manyvegetable dusts. As a rule only isolated cases aremet with, those being in workers who are undulysensitive to a particular dust. Sometimes smalloutbreaks are met with. Much interest was shownabout 40 or more years ago in the occurrence ofasthmatic symptoms in workers using SouthAfrican boxwood (gonioma kamassi). Out of II2men seen, 34 experienced difficulty in breathing(Legge, 1905, 1907), but the condition does notseem to have been a true nocturnal asthma butrather a cardiac asthma. Many of the men hadother symptoms such as nausea and sickness,faintness, weakness and sleepiness, and injectionof an alkaloid extracted from the wood causedrapid death from syncope in animals. Similarsymptoms, probably more likely due to bronchialspasm were described by Bridge in 1935 and 1936from Mansonia wood (sterculiacea altissima).
In 1948 the present author investigated twosmall outbreaks of asthma due to Western redcedar (thuja plicata). In one factory there weresix cases of asthma and a seventh man was alsovisited who had suffered from asthma inter-mittently since I922 when this wood was first intro-duced into the factory. Like the others affectedhis attacks coincided with the use of the wood,and since his retirement two years previously hehad been free from further attacks. In the otherfactory my colleague, Dr. A. N. Currie, had found
*Compensation may now be obtained in respect ofpartial disabilitv (see page 656).
two cases of asthma in I937. At my visit ii yearslater one of these cases was still working and stillallergic to the wood, the other had died. I alsoexamined a third case and heard of three morecases in men who had left the factory but whosepresent whereabouts were unknown.
Animal DustsThere are very few reports in the literature on
the harmful effects of animal dusts and they mustbe accounted of minor importance in the pro-duction of respiratory disease. Occasionally theymay carry infections. Pulmonary anthrax for-merly not uncommon in the West Riding ofYorkshire where it was called 'wool-sorters'disease,' was due to breathing the dust arisingfrom infected wool; the crushing of bones frominfected animals to make bone meal may carry asimilar risk when sun-dried bones are used.Sensitization effects from animal dusts have alsobeen described, for example from feathers (Bridge,1934)-
SummaryDusts met with in industry may give rise to a
wide variety of reactions in the respiratory tract ofworkers exposed to them. The main types aretabulated below:
Mineral DustsI. Nose and throat irritation and ulceration:
December 1949 DOIG: Other Lung Diseases Due to Dust 649
It is suggested that the possible association ofrespiratory disease and occupation should be morefrequently borne in mind. In doubtful cases helpin investigating any such association could readilybe obtained from the Medical Inspectors of theFactory Department in the case of factory workers,or the Ministry of Fuel and Power in the case ofminers.
AcknowledgmentsI have pleasure in acknowledging my indebted-
ness to my colleagues for their co-operation. Dr.E. R. A. Merewether has also lent me the X-rayfilm reproduced as Fig. i, Dr. F. N. R. Price thosefor Figs. 5 and 7, Dr. J. M. Campbell that forFig. 6, and Dr. Douglas Bell that for Fig. 8, forwhich I wish to express my thanks.
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