Document RoB7ak1N0yemJerpR98RE1q7

;A^r .v iL- 1 ki THE JOURNAL OF INDUSTRIAL HYGIENE VoLCHE XV JULY, 1933 XuiIBER 4 PULMONARY ASBESTOSIS: ITS CLINICAL, RADIOLOGICAL, AND PATHOLOGICAL FEATURES, AND ASSOCIATED RISK ' OF TUBERCULOUS INFECTION* Philip Ellman, M.D., M.R.C.P. Physician in Charge of The Tuberculosis and Chest Clinic, Ccnirdy Borough of East Ham, London, etc. HE close study which has been ing the last few years, some of which Tdevoted to silicosis, resulting from exposure to silica dust, has I have already reported (2, 3). While these findings are in close agreement established fairly clearly the clinicwaitlh those of other observers they help and pathological results which follow, to establish the existence of asbestosis together with the greatly increased as a disease with definite characteristics predisposition to succumb to tubercu distinguishing it from silicosis. losis. Similar close study is to-day being given to the effects which follow Clinical Features u?on the inhalation of another dust, that arising when asbestos fibres are manipulated. A full description of the mineral asbestos, and of the in dustries in which it is employed, has been given by Merewether and Price (1). No further reference to this side 01 the question therefore is needed. Thus paper is restricted to presenting the clinical, radiological, and patho- ?ical findings in asbestosis, based uPon an experience of cases seen dur- 22,2^ecived for publication March 17, The slow development of a charac teristic type of fibrosis distinguishes pulmonary asbestosis; it produces in sidious lung changes; but the patient may be comparatively free from symp toms for several years, usually from 5' to 15; in some cases, before symptoms arise, years elapse after the worker has left the industry* and his exposure to asbestos dust. Nevertheless, in my experience, one or two exceptions have occurred wherein symptoms have fol lowed after exposure of 1 to 3 years or less. The onset of symptoms and 165 m tt lj j*;V 4 . 4r(: I ' .zri '?. Y i. { 1 " tL j *'. 1`I U ; 166 THE JOURNAL OF INDUSTRIAL HYGIENE [xv, no. 4 their severity depends to a large extent on the nature of the work, and on the amount of dust inhaled. Symptoms may even be absent despite the pres ence of clinical and radiological signs (4). Dyspnoea.--Dyspnoea is one of :he earliest symptoms, and at first occurs only on exertion. It is, however, pro gressive, and, ultimately, dyspnoea and even orthopnoea at rest may be come established, which may be out of all proportion to the physical signs present. Cough.--Cough sooner or later ac companies the dyspnoea; it is a harsh, non-productive cough, often associated with fleeting chest pains. Expectoration.--Expectoration is of ten absent; in ray cases it has varied a good deal. When present it is usually scanty in amount, and of a thick, tenacious, glairy, mucoid nature. Bur ton Wood has described it as resem bling "semi-coagulated albumen." In a few cases, where there has been little bronchial secretion, almost clear fluid has been coughed up. During the winter months, when these patients are peculiarly liable to acute respira tory affections, the sputum may be more abundant and often more puru lent, although pus cells have always been present. Haemoptysis has been strikingly absent, and even blood stained expectoration has been the exception. Anorexia.--Anorexia may occur eariy; it is usual in more advanced cases, but is by no means consistently present. Cyanosis.--Cyanosis may be pres ent, especially in. more advanced cases; according to Merewether it is no: necessarily dependent upon the degree of fibrosis. A dusky complexion is common to these patients, and Oliver speaks of a pronounced deadening of the skin, varying from mild bronzing to slight blueness. Emaciation.--Emaciation has been rather a striking and distinctive feature in my cases, with a loss of weight out of all proportion to the physical signs. Slumber sweats have occurred in sev eral cases. Finger clubbing.--Clubbing was found in the more advanced cases, in which bronchiectasis was usually present. Asbestos corns.--Corns form a char acteristic skin lesion complained of by most patients. An asbestos fibre pen etrates the skin, whereupon a hyper keratosis forms round it; but no asbes- tosis bodies are found in these corns. They form on the hands and arms, and even on the skin of the legs, owing to dust fibres penetrating the stockings. Seasonal incidence.--All symptoms become aggravated in the winter, when bronchial colds are experienced; hence during the winter months most of the cases are recognised. Patients may only discontinue their work because they are forced to do so on account of respiratory embarrassment on the least effort. ' Whilst most of the symptoms present are similar to those of silicosis, emacia tion and loss of weight out of ail propor tion to the physical signs, anorexia, the complexion and cyanosis are distin guishing features of asbestosis. Clinical examination.--Examination, of the chest shows limited expansion, even below 1 inch. The movement is especially limited at the bases, where, indeed, the fibrosis commences. The apices are frequently retracted. The 11 \t f1 * \ i 1 j ! 1 i l Ji pe at ap br ha ex up to SO' di ra be ra ba ca sp uf cc t: io se an tr< at st it tr th p: P t: J c h t wr . -J'5f i -y *-> -_-T 'V-iW. ", _ /u/y 7^55] PULMONARY ASBESTOSIS 167 percussion note is impaired, especially at tbe bases, diminishing as the apex is approached. Auscultation betrays diminution of breath sounds at the base, although was evidence of corns on her hands. The chest expansion was limited, specially at the bases, and both apices were retracted. There was dullness at both bases, where breath sounds were diminished, and fine, dry, crackling crepitations were heard, harsh breath sounds with prolonged chiefly over tbe left base. aspiration may be heard over the X-ray examination revealed restricted i upper zones, indicative of compensa diaphragmatic movements, especially on the left side. Linear striation at the bases i tory emphysema. The adventitious was increased, with a faint homogeneous rounds are almost characteristic of the opacity, especially on the right side, where {! disease, comprising fine, dry, crackling a fine punctate mottling could be observed. riles; they are usually heard over the A little glairy, tenacious, mucoid expec i''us Xs.?, % *ei t bases and in the axillary region. Pleu ral friction sounds, due to associated toration was obtained, in which were found a few asbestosis bodies and dust fibres, but no tubercle bacilli. basal pleurisy, are not uncommon. Diagnosis.--The case is one of an'early The physical signs in the average degree of pulmonary asbestosis (Stage 1). iar- 'by OU- jI* $ case are, in fact, those of basal fibrosis, spreading, in more advanced cases, upwards, although they are usually Radiological FE.vnraES Radioscopic examination of the K-r- confined to the lower and middle zones. chest, followed by a technically satis ms. an-1 ; to The apex is usually free; and the upper lobes are not infrequently emphy sematous. factory radiograph, affords in my view, the most reliable single piece of evidence in establishing a diagnosis of the stage and extent of the disease in OlT.i the may au?e it f.f oast Case 1.--Female, aged 22. She worked in ia asbestos factory for 4 years as an m&tiress maker. She had to sew asbestos cloth, and then stuff it with asbestos fibre. The stuffing bad to be shaken in order to spread it out, thus producing dust; then the mat tress required thumping to distribute the thickness of tbe packing, with the further production of dust. She bad always been healthy, and had no previous history of chest trouble, nor was there one of tuberculosis in her family. Present illness.--When first seen, on cases of pulmonary asbestosis. Mod em radiological technic should be em ployed, with apparatus for radiography at a distance of 2 metres, and facilities for exposures of 1/10 second or less; in this way the quality of radiograms can be standardized, which is very necessary in following the development of a pneumoconiosis by means of serial radiograms taken over a period of time. Radiography discloses the presence January 2, 2931, she stated that her illness of a fine diffuse fibrosis, which has been commenced 6 months previously with a dry, claimed to be characteristic of asbesto `.ia- hacking cough which was associated with a loss of weight from 147 lbs. to 130 lbs. Two sis; but other allied dusts capable of months ago she became conscious of short producing pulmonary fibrosis may pos :;on ness ol breath on e.veriioa, which became sibly lead to a condition indistinguish progressively worse. She complained of able from that c: asbestosis. Cer some pain at the base o: the left lung, which tainly Pancoast and Pendergrass (5)- was worse on inspiration. There were no sweats and no haemoptysis. doubt whether anyone viewing a num The Clinical examination.--The patient was ber of radiograms, indicative of pneu The this and pale, with cyanosed lips. There moconioses, sustained in several in- l y -:r f x.! 1 a -`-v-vi 1 !i. T-* 1 i) -; f f I I 163 THE JOURNAL OF INDUSTRIAL HYGIENE (aw, no. 4 July, iOSS) dustries could select those of asbestosis subjects; however radiograms of pulmonary asbestosis are certainly very characteristic. In the fourth and final stage, the fine punctate mottling can be observed to have spread beyond the limits of the lower zone to the middle and even ; ^ ' tosed- The che ;.hc apices WO signs were pro!, out diminished crackling, scutto Dr. Stanley Melville has cooperated upper zone, but the apices usually throughout hot: closely in the study of my cases from the radiological aspect. Roughly four stages in order of progression of the disease have been observed. In the remain free. This fine diffuse punc tate mottling stands out in definite contrast to the coarse nodular mottlin* seen in silicosis. 1 \ the left. The h left side. The < by Dr. Schuster eoDtair* asbesto* found ropearedl- first stage, the movement of the dia This diffuse mottling, so distinctive ' ! or.e occasion, in phragm on one, and sometimes on both, sides, is restricted; the root shadows are unusually heavy; and the basal linear striation on one or both of asbestosis, has been described as presenting a "ground glass" appearance by Burton Wood (6), and by Merewether as the veiled appearance ; j X-ray examir. gave evidence or acid mediastiau Both lungs show eraily distribute sides is Increased. The right chest has of the involved zone. Stanley Mel- { characteristic o not been observed to be specially in volved more than the left; indeed the left base on a film is normally some what obscured by the heart shadow, ville says the impression is that of a dirty, blurred smearing of the involved zones, as though a piece of india-rubber had been rubbed across the film. \ ; j j rated pulmonar 1932 there was resy, with the b< chea displaced ances were typ and is not so visible. The trachea is centrally placed; the heart is usually normal in shape, size, and position; but the costo-phrenic and even the cardio-phrenic angle may be ill defined. The radiological features thus confirm the clinical findings that the disease is characterised by a fine diffuse fibrosis, commencing at, and involving principally, the bases of the lung. 1 . - motttinsrzn the added infection cavity in the ut although the :u this can just b gram. Close examination of the film may de When tuberculous infiltration com- Diagnosis. -- tect some loss of translucency, and a fine homogeneous opacity or haze at one or both bases. In the second stage the homoge plicates asbestosis, it can usually be detected and distinguished from the underlying fibrosis, just as in cases of silicosis. ; ( j j advanced degree skiagrams hav tion regarding a suspicion c infection, thot neous opacity becomes more obvious, J found. and a fine punctate stippling may be Case 3.--A female, aged So.--This woman. ' detected at one or both bases, while the basal linear striation is more obvious, with very definite restriction worked in an asbestos factory from l9l6to 1921, had been quite healthy previous to working there, and had never had chest trouble. la 1919, cough and dyspnoea Case 5.--A worked as a t< from 1924 to leave the fact of diaphragmatic movements and some developed and became worse, but she con cough, and tig times blurring of the diaphragmatic tinued at work until 1921 when she was had persisted f angles. The inter-lobar pleura is us ually thickened, and in my experience frequently drawn down to the base by compelled to give it up. In 1921 she was notiSed as a case of pulmonary tuberculosis; her weight was then 119 lbs.; it is now 99*. She has twice been in a sanatorium; al- . j became progre: dated with ios The patient the end of 12 the fibrosis. though the sputum has been examined on emaciated, am In the third stage definite evidence numerous occasions, tubercle bacilli have pounds in wei of pleural involvement may be present, with or without mediastinal displace not been found. Clinical ez-!nir,.c.iion.--I Srst saw her in May. 19S9, when there was present cough, Her face was ChVcfl.' 2 sic-a was poor, ment, depending upon the inequality dyspnoea, acd occasional sweats. She was bases, especia of fibrosis in the two lurtss. thin and emaciated, .and her face was cyi* < --vyj-. T,> *o. 4 the --erved - the even 'dually ' punc. definite uottiiag 'Active ;bed as appear and by earanC8 -y Mel:at of a nvolved -rubber n. as eonhe dis' dii?i2:g volving *T5* n coma fly be the - --es of woman i 1916 to 'ions to i chest yspnoea he conne was ;he was ?"ios;s; :-.v99*. ;ra; alne-d on li hive ` . ! : j I | i ; i . | * ' usr ia vvagh. he was -i C~2- , Juhj, 1083} PULMONARY ASBESTOSIS 169 n0sed. The chest expansion was poor, and the apices were retracted. Expiratory sicns were prolonged in the upper zones, but diminished in the lower zones; dry, crackling, scattered crepitations were heard throughout 'noth lungs, but especially over the left. The heart was drawn over to the left side. The sputum, carefully examined tv Dr. Schuster in June. 193^. was found to contain ashestosis bodies, which have been found repeatedly since both singly and. on one occasion, in clumps. X-ray examination in November. 1930 gave evidence of basal pleurisy, with heart and mediastinum displaced to the left. Both lungs showed punctate mottling gen erally distributed. The appearances were characteristic of those found in uncompli cated pulmonary ashestosis. In January. 1932 there was evidence of bilateral pleurisv, with the heart, mediastinum, and tra chea displaced to the left. The appear ances were typical of ashestosis. but the mottling in the upper zones suggested superadded infection, with apparently a small cavity in the upper zone of the left lung, although the annular shadow suggestive of this can just be detected in the first skia gram. Diagnosis.--'This patient exhibits an advanced degree of ashestosis. Here serial skiagrams have given important informa tion regarding the progress of the case, with a suspicion of super-added tuberculous infection, though no bacilli have yet been found. appreciable impairment of percussion was detected. Breath sounds were diminished at both bases, where fine, dry, crackling rales were heard, extending well up into the axillae. The expiratory sounds were pro longed in the upper zone; and a few plsur-ji friction sounds were heard at the left base. X-ray examination in April, 1932. re vealed restricted movement of both sides of the diaphragm, with evidence pleura: thickening at both bases. The right lur.g showed basal fibrosis, with characteristic punctate mottling of the lower zones. The left iungshowed fibrosis and mottling of the lower and middle zones. The mottling was Fig. 1.--Case 2. Ashestosis bodies in clumps in the sputum. Case -5.--A female, aged 2$. This girl worked as a teaser and carder for 6 years, from 1924 to 1930, when she was obliged to leave the factory because of giddiness, cough, and tightness of the chest, which had persisted for 4 years. These symptoms became progressively worse, and were asso ciated with loss of weight. The patient came under observation ar the end of 1931. when she was thin and emaciated, and stated that she had lost $ pounds in weight during the last 6 months. Her face was somewhat cyanosed. Clinical Examination.--The chest expan sion was poor, with definite dullness on both '-ases. especially the left, which decreased a? the apices were approached, where no somewhat coarser than usual, and tended to conglomerate in the left middle zone, where there was a suggestion of tuberculous infil tration. Expectoration was extremely scanty, bur the trace present was tenacious and muco purulent. Tubercle bacilli were persist ently absent, but ashestosis bodies and fibres were present. At a subsequent X-ray examination in January. 1933. the mottling detected definitely indicated an increased spread of the nbretic condition in h lungs during comparatively short period: the middle zones of both lungs were new completely involved; but there was no definite evidence of infiltration. Diagnosis-.--This case sh-_.vs definite and b' ' ^-v>.'.C-^>v---v-!`- _:- II I j i i i i: Il ii Jubj, /'>*'] July, 19$3] PULMONARY ASBESTOS!: i trrm 171 53 So aa ^3 Zaa sO J = L aa *C-<a--T ''S =5 o S 3J0 iO .'ll r z;- - ij.V. -tsy--,./ . . . - ;. .. -A- -- ) *I 'f I 172 THE JOURNAL OF INDUSTRIAL HYGIENE [xvt no. 4 progressive spread of fibrosis in both lungs in less than 9 months. Pathological Features* Macroscopic appearances.--The vis ceral pleura is usually considerably thickened, while the pleural sacs may be partially or even completely ob literated by dense fibrous adhesions. The bases of the lungs are usually firmly adherent to the diaphragm. Bronchiectasis is fairly common: bronchiectatic cavities sometimes occur. Specimens often, show a honeycomb appearance of the lung. Usually the lungs are firm on palpa tion, tough, and airless; the areas of dense fibrosis show greyish-black mot tling owing to carbon immobilization. The upper lobes, by contrast, may be spongy, crepitant, and emphysema tous; this compensatory emphysema may often be detected clinically and radiologically. Microscopic appearances.--The in terstitial tissue of the lungs is every where increased, so much so that in some cases the alveolar structure can no longer be detected; it is completely obliterated; but in other areas there is evidence of compensatory emphysema. Indeed, although fibrosis may appear to the naked eye to have escaped the apices, much fibrosis may be seen in them on lung section. In and around the densely fibrous areas, ashestosis bodies are found in profusion: they tend to occur in radially arranged clumps. Carbon pigment is present in vary ing quantities. Advanced areas i-f fibrosis can be found, associated with dilated bronchioles and bronc-hiectaric * I sub indebted *0 Professor M. J. Stewart for his valuable beio in this section. change. In addirion to the dense fi brosis, inflammatory catarrhal changes may be observed, wit!) desquamation of alveolar and bronchiolar epithe lium, and thickening of the alveolar and bronchiolar walls. Here asbesio=ls bodies tend to be fewer in number. Foreign body giant cells, distinct from Tuberculosis giant ceils, may be present in the connective tissue. Giovne, (10) who has recorded these cells, and termed them "asbestosis giant cells," suggests that they present an attempt to destroy the asbestos fibres by phagocytosis. These giant cells are larger than tuberculosis giant cells: their cytoplasm has a stippled and pigmented appearance, in contrast with the structureless cheating ap pearance of tuberculosis giant cells. Case 4--A female, aged 31. This woman worked in an asbestos factory, making mat tresses. from 1919 to 1922. She had previ ously been healthy, and there was no tuberculosis in the family. After 2 years' work in the factory she began to feel lan guid. to lose her appetite, and to develop a cough. As the work did not seem to agree with her. she left the factory and went into domestic service; but she has never felt well. Every winter she has had a troublesome cough, with shortness of breath on exertion, and has been easily fatigued. Early in 1931 she consulted a doctor, who notified her as suffering from pulmonary tuberculosis. Clinical --When seen she va? obviously ill. thin and wasted, very iysp- noeic. while her face was somewhat cys- nosed. Sputum contained tubercle '-.tu-ili: and asbestosis bodies, which were h-uni :n clumps on one occasion. There were physical signs in the lungs of advanced phthisis, with cavitation :r. toe left upper lobe. and. some moctns later, definite physical signs appeared in the right upper lobe. At the bases phystc-:.. asbestosis. could be detected, v;;.:--iunuess. Jut. weal rnles upPover Ashovmo'-'* dors. the ' was clear evid: uppe the -:1 ?> ri f F: Note ..i o. invoi Tn- the thea Dr. yucs ion lie- cse osis 'Oru ' t as iant lant pied rust ap- 1 r.atrevi* DO July, toss] PULMONARY ASBESTOSIS 173 weak breath sounds, and dry, crackling rates. rcJfhor different from the rules in (he upper zones. The signs were, however, overwhelmingly those of tuberculosis. An X-ray examination in April. 10-31. .showed definitely restricted diaphragmatic movements on omK sides. There was some dorsal scoliosis, the heart tending to be in ;b? hollow of the concavity. The trachea w-.is drawn to the left. The right lung, was dear, whilst the left lung showed definite eridzr.ee of tuberculous infiltration of the upper and middle zones, with cavitation in the left upper zone. There was evidence patches of plastic lymph. In one place in the middle of a sac was a strand of adhe sions, which on separation showed lung immediately beneath the visceral pleural attachment, but there was no pneumothorax opening. The diaphragmatic pleura was thickened and completely adherent to the diaphragm. The right pleura showed tough adhesions at the extreme apex. Over the middle of the upper lobe was a dense linear scar of old pleurisy with tags of plastic lymph attached to it. Here and there the visceral pleura showed white plaques of thickened pleura, -1 tx \ i is . n 9 ?Ov . ' Nr| w..-m id a f-uth rued, who t i .::i ; in ! Fta.6.--Case 4. Foreign body giant cell Note asbestos body within the ceU. .if bilateral basal fibrosis, with pleural involvement of the left base. The patienthadiTtsTitutiona: treatment in hi-spital and at a sanatorium ford months. |r. June. IP32. sue discharged herself from .he sanatorium and went h-.-me: she "U.; then acutely ill. and had advanced physical signs of tuberculosis in both lungs, She di-vi .jc, August obth. Vliod. Post mortem examination was ma<ie bv Dr. .t. R. Gloyce whose findings were fcilvtv*: the left pleural sac was found : ' be compietely r diterraed by adhe*: -n*. except at the extreme base, where there w...* irnali free sac with, greatly thickened pleura conraining yellowish ru- Fig. 7.--Case 4. Section shoeing diffuse asbestos fibrosis with askestosis bodies in chimps, radially arranged. (Low power.) especially over the upper lobe. There was one thickened nodule in the diaphragmatic pleura with adhesions to the diaphragm. The left lung showed dense areas of ashestysis. almost confluent in the lov.er lobe. The upper lobe was completely involved in tuberculosis with several ragged cavities, and was practically destroyed by the cavi ties. The lower h-be showed a few caseous tubercles: in the upper part one <-.f these of asbestosis. In the upper h-be there were numerous '-c.seous deposits of tubercle from the size "f a pea to that of a walnut. Mi-iu,e and hover lobes also showed a few it ? i :. \ ~ A t I S v -- - - i t ./-< i- i * l ; ':* \. Ii \ I j ik i j tt. < | ( r T 1 \ 174 THE JOURNAL OF INDUSTRIAL HYGIENE !*<, 'to. 4 minute discreet nodules of tubercle. Xo iesions in any other system. Diagnosis.--Whilst the signs of tubercu losis tended to mask those of asbestosis, there \v:ts little doubt that this case was, in ail probability, originally a case of pure pulmonary a$V>estosis complicated bv an advanced degree of tuberculosis. Post mortem examination of the lungs showed advanced asbestosis in both lungs; clumped bodies of asbestosis had been observed in the alveoli and on one occasion in the sputum. Asbestosis Bodies Highly characteristic golden-yellow bodies are found in the sputum and fibrosed lungs of asbestos workers. They have been present in all autopsies upon, cases of pulmonary asbestosis. They vary in size and shape; but, characteristically, they have bulbous enlargements at the extremities, with a regularly or irregularly segmented body, resembling dumb-bells: when fractured they are club-shaped. The appearance of fully formed bodies has been aptly compared by Glovne to beads on a necklace: the beads vary in size, and represent the irregularly segmented body. These bodies have been found by various observers to vary in length from 20 to over 200 microns. An asbestos fibre forms the central core of each body, and can frequently be detected (10). The golden-yellow material covering each fibre contains an iron substance, which gives a Prussian blue reaction: prob ably it is a silicate, which protects the Sore from further change. When stained with ammonium sulfide, the central core of an asbestos fibre stains lightly against a weil stained body. Asbestosis bodies are probably as bestos fibres which have become coated with colloidal golden-yellow material --probably iron silicate--derived from bod}' tissues, oxyhaemoglobin being the chief source. In addition to being found in the sputum and lung juice, (11) they have been found in the feces (12), and even in the spleen, (13) which raises the question as to how they gained access to this organ. Pm. sumably they travelled cither by embolic spread in the blood stream, or by phagocytic cells. The bodies have also been found in the upper nbdorninal lymph glands (M. J. Stewart, personal communication). The presence of asbestosis bodies in the feces is as pointed out by Gloyne of practical value where no sputum is available, since, as in cases of phthisis, the sputum may have been swallowed, rather than coughed up. The bodies are best seen with an oil immersion lens, and show up clearly without staining as golclen-yellow structures. They can, however be stained by haemotoxylin, by potas sium ferrocyanide, and hydrochloric acid, giving prussian blue reaction, and by ammonium sulfide. Asbestosis bodies in clumps.--The bodies may be found in the lung tissue either singly or in clumps, and may occur similarly in the sputum, although they more usually are found in the sputum singly or in groups of two or three. The bodies tend to be scanty if there is little bronchial seeretion: and, given a pu'monary fibrosis, the profusion of bodies in the sputum appears to show a tendency to vary directly with the extent of the disease. When the bodies are mc-re abundant in the sputum, they may occur in radially arranged clumps: such an occurrence indicates disintegration of lung tissue by either simple suppurative broncho- j t : i * j 1 * 1 j j ; i ' t ! ? j j j j j j j \ j [ ' t j j ! \ ; : July- 1 OS- pneumon: jnfecnon bodies in parable rin pbthis: What I bestos borecorded : miner wo: who had : of a Lsn entiv oth. tos fibres lions with A recei: is interesconnectio "Ccystft iron (silic. 40.1 per ce appeared t itself. It prevented very adeq oxide. This oh? icz onpoU "The fair consist or become co ubie and r< quiescent; oli. They diately th< only after presumabl the result jpicuie be coating of Kettlesis bodie eous riss harmless silica. 1 colloid ? . erabie in' Ai'j-y. j. I juiih tom PULMONARY ASBESTOSIS 175 pneumonia, or secondary-tuberculous infection (U). This occurrence of bodies in clumps in the sputum is como:irable to the presence of elastic tissue in phthisis (M. J. Stewart). What have been called "pseudo-as bestos bodies" (15) have recently been .recorded as found in the lungs of a coal miner working in the mines of Alabama, tfho had never worked in asbestos, and 0f a Lancashire coal-miner. Appar ently other dusts may simulate asbest0s fibres, and lead to similar reac tions with the lung tissues. A recent observation by Kettle (16) is interesting and noteworthy in this connection: "Crystalline silica heavily coated with iron (silica, 59.9 per cent.; ferric oxide, 40.1 per cent.) and injected into the tissues appeared to be as inert as pure ferric oxide itself. It would appear that the silica is prevented from going into solution by its very adequate coating of insoluble ferric oxide. This observation has an important bear ing on pulmonary asbestosis. The familiar asbestosis bodies appear to consist of asbestos spicules which have become coated with iron. They are insol uble and remain for many years apparently quiescent in the pulmonary tissue and alve oli. They are not formed, however, imme diately the asbestos enters the body, but only after an interval of some weeks, and presumably damage to the lung occurs as ibe result of solution from the surface of the pivule before it is rendered inert by the coating ci iron/' Kettle record* the met that asbesto sis bodies injected into the subcutan eous tissues of mice are as inert and harmless as the iron coated crystals of silica. This protective action of the colloid substance is a point c-f consid erable interest. cities in spntuni.--The presence of asbestosis bodies in sputum indicates merely exposure to asbestos dust: it cannot alone justify'- a diagno sis of pulmonary asbestosis. A diag nosis of a diseased condition of the lungs depends upon the cumulative findings of: (a) exposure to asbestos dust: (b) clinical evidence of pulmon ary fibrosis: (c) radiological evidence of fine, diffuse, pulmonary fibrosis: anti (d) asbestosis bodies in sputum, feces, or lung tissue. It is astonishing how asbestosis bod ies persist in the sputum for years, even despite short periods of exposure. In one case a patient was exposed to as bestos dust for I year; yet the bodies were present in the sputum 14 years later. In another case, exposed to the dust for only 10 weeks, the bodies were present in the sputum 5 years later. Apparently, once the bodies are formed, unless they are carried away or ex creted in the sputum, they remain in the lungs more or less permanently without being dissolved. Case 5.--Female, aged Si. She was en gaged in an.asbestos factory from 1911 to 191". She was first seen in September, 1930 for a slight cough, which had persisted for some years. The cough had troubled her seriously during the previous 9 months, when she had recommenced work at the fac tory, after being away for some eighteen years. There had been dyspnoea with the cougii, which had become progressively worse, and was marked on exertion. Dur ing the next 4 months there was not much loss of weight; the cough persisted, with some tnuco-pur.ilent expectoration, half an ounce in 2i hours; it was never blood-stained. There were severe night sweats, and the appetite was poor. Lassitude was present. Asbestos corns were present, especially ca the hand and elbow. Clinical --Physical signs in the chest were mainly at the base, and typi- i i 5i t } t \ i i i ? 9 i l i 1i i , i i i i f r \ i ; \ 176 THE JOURNAL OF INDUSTRIAL HYGIENE [', no. 4 cal of those of a bilateral pulmonary fibrosis, with pleural thickening at the right base. X-ray examination disclosed some scolio sis, with dorsal convexity to the left; the heart tended to lie in the hollow of the curve. Movement of the right side of the dia phragm was restricted. On the right side there was evidence of pleural chickening at the V.ase. with lowering and thickening of the inter-lobar septum. The basal linear ytriaticn was exaggerated, and there was some ill defined mottling of all zones. On bodies in dumps. The condition suggested a rapid, complicating tuberculous process. X-ray examination now showed restricted movement of the right side of the diaphragm, and increased fibrosis at the right base. Oq the left side there was infiltration of the upper and middle zones, with excavation in the upper 2one, with pleural involvement, and basal fibrosis. Diagnosis.--The case was originally r>n$ of pure pulmonary asbestosis, complicated later by tuberculosis. Here the tuherculo- July, 1033\ -1 :o V'ivf r;-:: A. i ' ` f y A> Fig. S.--Case -5. Asbestosis bodies occurring in clumps in the sputum the left side some fibrosis was detected at the base. The tenacious mucc-puruient sputum was found to contain numerous and mixed organisms, mainly bacillus friedlander ,nd pneumococcus. No tubercle baciiii were fnund. Asbestos fibres and asbestosis bodies were present. All symptoms had become much aggra vated by July. 1932, and the weight had cropped from 113 lb. to >2 lb. The pulse was rapid, and there was evening pyrexia, bputum increased in amount, and tubercle bacilli were found in October. 1932. a;'Ter frenuen: examinations. Asbestods bodies o: great variety were preyen:, with A-fi...:; sis was implanted upon an asbestosis. The ciumping of the asbestosis bodies indicates disintegration of lung tissue. Case f.--A -rc.T. ay'td .1 3. This man worked as a card-room superintendent in an asbestos factory tor 0 years. 1920 to 1929. His work brought him into contact with a high concentration of dust. He remained free from chest trouble until 5924. when he became conscious of mild dyspnoea "it exer tion. with an irritating, dry cough. The symptom* grew gradually w..r>e. until 'in 1929 he was so breathless on the slightest exertion that he was compelled in October to cease wont; he was then confined to bed TTt*ai:;a  no, t'-.J c** 08 "J ih~ syaii'-a in 3 Hy y/y, PULMONARY ASBESTOSIS 2-- ^ 3= -- V9 ^ ft 5 X *5 $?.- > ? 7 .3,2 2*o C -r */t"S 15 ^ J2 p -3 y --x -- >> ^-s5 ,*C2* "5 " * s ^ z: *r ;a u 2 5|rr3 JS r 'r x *51*, ;^ J 4 J r3 s ^ 2 ;* : i x fc > J i} i irs THE JOURNAL OF INDUSTRIAL HYGIENE no. ^ (. July, l-'-U because of right-sided pleural effusion. He N-ray examination showed the right dia- deace of a ri now suffered from progressive anorexia and phrugm almost completely obscured, while i with advatv- palpitations: he was breathless even at rest; the movements of the left wcto very re tc'StS- Tub : the face was cyanosed, with an earthy com stricted. The trachea was slightly drawn { the pus. thi plexion; he was obviously wasted, and his over to the right There was a dense opacity > straw colyi: weight had fallen from 203 lb. to 131 lb. over the greater part of the right hemiMarked clubbing of the fingers was present. thorax, consistent with anenevsted effufi.,n. ; done by me D.'!!]>,O.?; Cfi'm'cal extunination.--The apices were Fine punctuate stippiing was seen over the I advanced r contracted. The right side was practically area not covered by the dense opacity at the : rated by :xu immobile and the chest was flat. Move- right base. The left lung showed character- t there was s : i .. ? i \ i > i i i i Fig. 11.--Case 6. Showing asbestos?* bodies in clumps. The central asbestos fibre is well shown in the long curled body. (I am indebted to Prof. Matthew J. Stewart for the microphotographs of asbestosis bodies La dumps in Cases 5 and 6.) ' since the a ment of the left base was very restricted. istic fine punctate mottling, involving the : clumps. There was dullness over the whole of the lower and middle zones. ' Ocsf right chest and the left base. Breath Numerous asbestosis bodies, both singly ' .. c.-j sounds were diminished over the whole of and in clumps, were found in the sputum; ! purposes :: the right chest, and some Sne rales were but repeated examinations for tubercle ba spent the - heard at the base. The breath sounds over cilli were negative. Nevertheless, exami `. rsp-vred to the left chest were coarse, and the expira nation of pleural Said showed it to be a clear ' time. He tion was definitely prolonged. Fine, charac tuberculous exudate. Ag dyspnc l teristic, crackling raies were heard over the This patient died or. February U. li-ZZ- left base and is the axilla. A a autopsy by Dr. S. P*. Gloj ne showed evi- r.eb. Tie ? > v l .* * > 'to. `ia -liile cry re. ' drawn Parity ' `ifnii. v<?r the :he "aeter- t t July, igs$\ PULMONARY ASBESTOSIS 179 I deoce of a right-sided tuberculous empyema that the dog was lethalled in its own inter I jth advanced bilateral pulmonary asbes- est. The thoracic organs, trachea, heart, toSjs. Tubcrcule bacilli were found in and lungs (through the courtesy of Dr. he Pl,s> which was clear and Kerr who obtained them for me) were tra"' coloured when a paracentesis was kindly examined by Dr. X. Schuster, whose done by me. _ findings have been reported elsewhere (S), Diagnosis.--The 'nase was clearly one of but may be briefly summarized here. i advanced pulmonary asbestosis. compli The macroscopic appearances showed cated by tuberculous pleurisy. Apparently that, whilst there was no sign of acute pleu i there was some disir.tegrationof lung tissue. risy. there was a general opacity of the vis- 4i X : re the Fig. 12.--Case 7. Macroscopic appearance of dr.g's lung since the asbestosis bodies were found in clumps. Case 7.--A rowjh-haire'l terrier '.vc. '0 yean -Ad. This terrier was kept for ratting purposes in an asbestos factory, where he spent the greater part of his life, and was exposed to asbestos dust during most of the time. He developed a cough. and increas ing dyspnoea for 2 years, during trie last b months of which he became thin and emaci ated. The dyspnoea became so distressing ceral pleura, with parches of 'localized pleural thickening. and hands of adhesion* between the b'hs-s. The lungs had lost their usual spcr.gy consistency: on section there .v.ti evidence of diffuse fibrosi* under the pleura. The bronchioles were dilated: i-ar- throughout the lung. Evidence of any Micr^ojf.ic examinatKiO revealed much i i t i \ t t 1 ISO THE JOURNAL OF INDUSTRIAL HYGIENE [xv, no. / the same conditions as found in the human subject. Chronic interstitial fibrosis of a fine diffuse nature with dilatation of the bronchioles was present. Fibres of asbes tos were seen in- large numbers, both in the alveoli and interstitial tissue of all parts of the lung. The fibres corre sponded exactly, under the microscope with the appearance of pure asbestos after it had been crushed. But no as'oestosis bodies were found; this important negative fact was confirmed by Professor M. J. Stewart and Dr. Glovne. The former, in deed. informs me that he has recently made of a grey rat caught on an asbestos factory premises. Although the lung changes in the case of this dog were closely allied to those of as. bestosis in the human lung, two noteworthy features were absent--asbestosis bodies and evidence of acute inflammation. \ possible relationship between the formation of asbestosis bodies and an acute inflamma tory exudate might suggest itself, had not asbestosis bodies been found experimentally in guinea pigs in. the absence of any appre ciable inflammation (9); apparently they are produced during normal metabolism. Fig. 13.--Case 7. Section of dog's lung showing asbestos fibres. (Microphotograph by Dr. Schuster.)' an examination of another dog, which stayed from 7 p.m. to 7 a.m. in an asbestos factory for over 9 years, and at death was 131 years old. Here also he was unable to find any asbestosis bodies, and only a few asbestos fibres were present. Apparently this second dog did not have the same oppor tunity as the first of inhaling asbestos dust, since it was only at the factory with the night watchman. This absence of asbestosis bodies was also observed by Stewart in 3 rats from an asbestos factory, aithoueb fibres were pres ent in the lungs. Glovne. however, after careful search, has found one small body, together with numerous fibres, in the lungs Fig. 14.--Case 7. Foreign body giant cell. Sote coarse stippled pigmented ap pearance. The presence of asbestos fibres, represented by fine lines can just be seen. (Microphotograph by Dr. W. Busman. Pathological Department, Manchester Uni versity.) The Tuberculosis Risk in Asbestosis Tuberculosis is generally recognised as the most serious risk to which silico tic patients are exposed; but the ques tion of tuberculosis complicating as bestosis has remained rather an open one. Until recently, the opinion was held that for tuberculosis to complicate asbestosis was comparatively rare, and this was regarded as a distinctive July, 1933] j - feature in co: \ costs, j Recently, he { (16) working e \ mate, finds that belong to a gr< which produce ; into the subt :' both produce s sis, and both a.cle bacilli. C seem to sup; work, as there increasing nun losis are being to asbestos dus be met with workers at wc they tend rat those who hat tending clinic: (17) in 1930, f< of tuberculosis 374 asbestos w and formed th was no outsts tuberculosis ; On the other h (IS) in 1931, w of tuberculosis, in a series of and among 3c referred to in Inspector of I 7 tuberculosis * i terminal fact< seventeen of r. asbestosis, the not at work, which four we A typical with an early bestosis, was cases who hae . tos dust for ; A 1' l of A ' :''r> not My rt- } i? -i * i .nt ? T. July, 19S3) PULMONARY ASBESTOSIS 181 ^ feature in contra-distinction to sili- which consisted in coating lead pipes, cosis. did not entail exposure to high dust " Recently, however, Professor Kettle, concentrations. Tubercle bacilli and j working experimentally with ani- asbestosis bodies have been found in r ^als, finds that silica and asbestos dusts sputum. This case has been watched j belong to a group of active substances for 3 years, during which the tubercu | which produce lesions when introduced losis has remained stationary. In this i . into the subcutaneous tissues; they connection Wood and Gloyne (IS) f both produce serious pulmonary nbro- have pointed out that oboiescent tu 1 gjs, and both assist the growth of tuber- berculosis may remain quiescent in t cle bacilli. Clinical evidence would spite of exposure to asbestos dust. 5 seem to support this experimental Another case, one of pure pulmonary I work, as there is little doubt that an asbestosis, (case 5) under my care has, * increasing number of cases of tubercu- during the last few months, developed | losis are being seen in subjects exposed pulmonary tuberculosis, which I can i to asbestos dust. Such cases may not say quite definitely, from clinical, j be met ^th in an examination of radiological, and sputum controls, has ? workers at work with no symptoms; been implanted upon the asbestosis | they tend rather to be seen among with decided aggravation of all symp , those who have left work and are at- toms. Among my series, serial skia | tending clinics. Hence Merewether, grams raise the suspicion of super- I (17) in 1930, found only 4 active cases added tuberculous infiltration in 2 ^ of tuberculosis in an examination of cases. I am further informed by Pro | 374 asbestos workers actually at work, fessor Stewart that at autopsy, when - and formed the impression that there no microscopic evidence of lung tuber } was no outstanding susceptibility to culosis has been observed, tuberculosis | tuberculosis among these workers. may be found histologically. j On the other hand, Wood and Gloyne, My own limited experience tends to > (18) in 1931, were able to trace 12 cases show that tuberculosis, as a complica \ of tuberculosis, 10 of which were active, tion of asbestosis, is by no means un \ in a series of 57 cases of asbestosis; common; the risk may or may not be | and among 35 deaths from asbestosis equal to that in silicosis; but that there ` referred to in the Report of the Chief is a risk, the evidence quoted, and my f Inspector of Factories for 1931, (19) own observations, appear to establish tuberculosis was a complicating or beyond doubt. Other things apart, re - terminal factor in 11 cases. Among cognition of the existence of this risk is ; seventeen of my own definite cases of an important factor when considering - asbestosis, the majority of whom were what preventive measures should be not at work, six had tuberculosis, of taken to control this occupational 1 which four were active. disease. The existence of this risk A typical lesion of mild activity, establishes that no person with tuber with an early stage of pulmonary as culosis in any form should be allowed bestosis, was present in one of my to enter the industry, nor should any cases who had been exposed to asbes one in whom tuberculosis at a later tos dust for 10 years; but the work, stage is detected be permitted to eon- 132 THE JOURNAL OF INDUSTRIAL HYGIENE [', no. 4 tinue in the industry. The risk here is to the other workers, as well as to themselves. Prognosis An interesting feature of this dis ease is the length of time which may elapse between exposure to the dust and a fatal termination, and the fact that this period is only one-half of that in silicosis. Apparently the dust gains access to the lungs and produces pul monary fibrosis as the result either of actual mechanical trauma, or of a toxic effect comparable to that exerted by silica in cases of silicosis; asbestosis bodies appear to lie inert in the tissues. The dust particles, once they have gained access, continue to injure the lungs, and the disease is a progressive one, which, if sufficient dust is present, ends fatally, the end being determined by some intercurrent complication, such as acute broncho-pneumonia or phthisis. Symptoms of pulmonary asbestosis as a general rule first appear some 5 to 15 years after the first exposure to dust, the time depending largely upon the nature and concentration of the dust; in one of my cases symptoms developed within 1 year after exposure commenced; but in other cases, ex posed to a minimum of dust, no symp toms have developed within 10 years of the first exposure. In an established case of asbestosis with symptoms, the dyspnoea is usu ally out of proportion to the clinical findings as regards fibrosis, while in a case of silicosis, one has the impression that dyspnoea, even though the clini cal findings of fibrosis are advanced, becomes manifest only on exertion. Again, a case of simple silicosis often looks well, declares that he is well, and is even offended when any reflection is cast upon the soundness of his lungs. In contrast to this, a case of asbestosis is cyanotic, emaciated, anxious, and often obviously going downhill. Such, then, is the clinical picture of the state of sufferers from asbestosis. Only by an extension of meaning could the word "sufferer' be applied to anyone with simple silicosis. Summary Clinical, radiological, and pathologi cal findings of the occupational disease, asbestosis, have been presented. This disease must be grouped with silicosis as a very serious pneumoconiosis. The average length of employment in fatal cases is only one-half that of silicosis. A diagnosis, which is most likely to be made during the winter months, when acute respiratory complications occur, must depend upon a combina tion of factors: (a) opportunities for inhaling asbestos dust, (b) the occur rence of asbestosis bodies in the spu tum, (c) clinical and radiological find ings of fine, diffuse, pulmonary fibrosis commencing at the bases; the character istic radiological findings are probably the most important reliable single piece of evidence in early diagnosis. The clinical features of the disease indicate that the onset of symptoms usually occurs after some 5 to 10 years of exposure to the dust: the degree of dyspnoea and emaciation, the com plexion, the absence of haemoptysis, and the very scanty expectoration, are all characteristic features. Inhalation of asbestos dust must be expected sooner or later to produce pulmonary fibrosis, depending upon July, 1933} (a) length o and concent The histo sis are esser interstitial areas of. act (b) the pre bestosis boc or in clump The presbodies in ' merely of p tos dust, : j. Merswe: C. W.: Dust o pressio Londor 1930. 2. Eixmax, monar} Med., 1 3. Eelmax. Practic p. 116. 4 OWVER. its Cl 1927, 9, 5. Paxcoas' E. P.: Furthe logical 1931, i 6. Wood, V Radioc grams Asbest 7. Glotxe. to the ence 1930, : ?. SCHCSTE sis in tferiol. $. Stefas' in th.-: to 5 :: sU Pa 10. GtCTN'E Lance V1' a;-' A'. ' - zv> no. 4 m is is lungs, sbestosis )Usj and Such, the state Only by u!d the anyone ithologi. 1 disease d. This silicosis coniosis. meat in that of likely to months, lications ombinaities for ip oecur- spucai find> fibrosis mracterprobably gle piece ; disease Tuptoms 10 years iegree of he com.oprysis, :ion, are oe produce 5 upon jviy, MS) PULMONARY ASBESTOSIS 1S3 j-a) length of exposure, and (b) nature have any clinical significance; if the : ^d concentration of the dust. bodies occur radially arranged in ) The histological features of asbesto- clumps, they suggest disintegration is are essentially (a) a diffuse chronic of pulmonary tissues. interstitial fibrosis of the lungs, with Pulmonary asbestosis, once estab - areas of acute catarrhal changes, and lished, is a progressive disease with a ? (b) the presence of characteristic as bad prognosis; its treatment can only - bestosis bodies, appearing either singly be symptomatic. . or in clumps. The tuberculosis risk in asbestosis The presence of isolated asbestosis must be reckoned with, even though bodies in the sputum is indicative time has yet to indicate whether it is merely of previous exposure to asbes- less, equal to, or perhaps even greater , tos dust, and does not necessarily than that in silicosis. BIBLIOGRAPHY 1. Mbmwether, E. R. A., and Price, C. W.: Report on Effects of Asbestos Dust on the Lungs and Dust Sup pression in the Asbestos Industry. London, H. M. Stationery Office, 1930. 2. Ellman, P.: Reports on Cases of Pul monary Asbestosis. Proc. Royal Soc. Med., 1930-31, 24,526,541,699. 3. Ellman, P.: Cbest Disease in General Practice. London: H. K. Lewis, 1932 p. 116. 4. Oliver, T.: Pulmonary Asbestosis in its Clinical Aspects. Thia Jour., 1927,9, 4S3. 5. Pancoast, H. K., and Pendergrass, E. P.: Review of Pneumoconiosis. Further Roentgenological and Patho- ' logical Studies. Am. Jour. Roentgen, 1931, 28, 556. 6. Wood, W. B.: Pulmonary Asbestosis: Radiographic Appearances in Skia grams of the Chests of Workers in Asbestos. Tubercle, 1929, 10, 353. 7. Glotne, S. R.: The Reaction oi Tissues to the Asbestos Fibre with Refer ence to Pulmonary Asbestosis. rbid., 1930,11,151. 8. Schuster, N. H.: Pulmonary .Isbesto sis in a Dog. Jour. Path, and Bacteriol., 1931,34,751. 9. Stewart, M. J.: Asbestosis Bodies in the Lungs of Guinea Pigs after 3 to 5 Months' Exposure in 3a Asbesto sis Factory. Ibid., 1930, 33, S43. 10. Glotne, 5. R.: The Asbestosis Body. Laacest, 1932,1,1351. 11. Stewart, M. J., and Haddow, A. C.: Demonstration of Asbestosis Bodies in Material obtained by Lung Punc ture and in the Sputum. Jour. Path, and Bacteriol., 1929,32,172. 12. Glotne, S. R.: Presence of Asbestos Bodies in the Faeces in a Case of As bestosis. Tubercle, 1930, 12, 15S. 13. Stewart, H. L., Bucher, C. J., and Coleman, E. H.: Asbestosis, a Re port on Two Cases. Arch. Path., 1931,12,916. 14. Stewart, M. J., Tattersall, N., and Haddow, A. C.: On the Occurrence of Clumps of Asbestosis Bodies in the Sputum of Asbestosis Workers. Jour. Path, and Bacterid., 1932, So, 737. 15. Ttlecote, F. E.f and Dunn, W. J. 3.: A Case of Asbestos-like Bodies in the Lungs of a Coal Miner who had never worked in Asbestos. Lancet, 1931,2, 632. 16. Kettle, E. H.: The Interstitial Reac tions caused by Various Dusts and their Influence on Tuberculous Infec tions. Jour. Path, and Bacteriol., 1932, So, 395. 17. Merewetser, E. R. A.: The Occur rence oi Pulmonary Fibrosis and other Pulmonary Affections in Asbestos Workers. This Jour.. 1930. 12, 253. IS. Wood, W. B., and Glotne. S. R.: Pul monary Asbestosis complicated by Pulmonary Tuberculosis. Lancet, 1931, 2, 954. 19. Annual P,,eport, Chief Inspector or Factories, 1931. London. H. M. Sta tionery Office, 1931, p. 112. i t i *; + - .av; ir ii% ;