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FILE NAME: Owens Illinois Library (OWL) DATE: 1933 DOC#: OW LOll DOCUMENT DESCRIPTION: Relevant Article with Bibliography & Abstracts from The Journal of Industrial Hygiene and Toxicology THE JOURNAL OF INDUSTRIAL HYGIENE EDITORS DAVID L EDSALL. M. D.. S. D., United States EDGAR L. COLLIS, M. D., M. R. C. S., Great Britain VOLUME XV JANUARY, 1933--NOVEMBER, 1933 THE PUBLISHED BY WILLIAMS & WILKINS Baltimore, Md. J COMPANY SUBJECT IN D E X TO ARTICLES. VOLUM E X V This is asubject index to all the reading m atter in the Journal of I ndustrial H ygiene, and one should, therefore, look for the subject word, with the following exception: "B ook Notices" are indexed under this title on page 489. The name of the author follows the sub ject entry in parenthesis. For author index, see page 491. Aiirasive, sand and m etallic, blasting as industrial health hazard (Bloom field and Greenburg).......................... 184 Aiu Conditioning, relation to comfort, health, and efficiency (H ayh u rst)... 98 Aik Pollution, sulfur dioxide in P itts burgh air (Schade).............................. 150 'Amikstosis, Pulmonary, clinical, ra diological, and pathological fea tures and risk of tuberculous infec tion (Ellman)........................................ 165 C\ tutoHvdrates, relative fatigue re covery value of (Laird).................... 89 Cakiion Monoxide poisoning from an I stove (Barker)............................... 238 production of, from paint in sealed ompartments (Frederick, Dudley, .ml Edtned).......................................... 1 Carmin Tetrachloride poisoning in 'hnmnooing and dry cleaning Midler).................................................. 418 Cuc inooenicity of mineral oils, rela- ion of, to certain physical and chemical characteristics o f these iU (Lyth)........................................ 226 Cusrmno, effect of, on rate of cooling of the body (W eeks)............ ................ 383 Coal Dust, bituminous, experimental inhalation of, and effects upon pri mary tuberculous infection in guit.o.-i pigs (Gardner, Cummings, and !)o\vdi................................................... 456 sui-ensation for industrial diseases, * time limitation in(M ayers).............. 466 ; Conuvi; by conduction and convection ,W<vlis and De Berry)...................... 34 #f i-.lv, effect of clothing on Week's).....................................................383 vorr-'v Mills, dermatitis in, due to .-i.i-h {.Schwartz and P ool).......... 214 CamiiTK Dust, study of workers ex- :......I to inhalation of (GudjonsII i .................................................... 27 (N avtuTis in cotton mills due to var- iSehwartx and P ool)................. 214 ** *-*- industrial, tim e lim itation in . ' ensation for (M ayers).............. 466 ' mvixii, carbon tetrachloride im; in shampooing and, ''lier).................................................... 418 D ust and fumes, lead, in air of streets, automobile repair shops and indus trial establishments (Bloomfield and Isbell)........................................ 144 bituminous coal, experimental inha lation of, and effects upon primary tuberculous infection in guinea gigs (Gardner, Cummings, and towd)............................................... 456 certain silicate, effects of, on lungs (Dreessen).......................................... 66 cryolite, study of workers exposed to inhalation of (Gudjonsson)............ 27 retained by the tracbeotomized cat (Ishikawa and Drinker).................. 57 silica, mortality of group exposed to, compared with th at o f general pop ulation and group exposed to dust not containing silica (Collia and Yule)................................................. 394 Fatigue recovery value of carbohy drates (Laird).................................. 89 F umes and dust, lead, in air o f streets, automobile repair shops and indus trial establisnments (Bloomfield and Isbell)............ .......... 144 Gonorrhea and syphilis, dealing with, as industrial problems(Clarice).... 79 H aematuria, chemical; from handling 5-chloro-ortho-toluidine (Currie).. 205 Health Hazard, sand and metallic ab rasive blasting as an (Bloomfield and Greenburg)............................... 184 H oods, local exhaust, importance of velocity characteristics in design of (Dallavalle)...................................... 18 Ionization, influence of atmospheric on human organism (Brandt).............. 354 Ionized Air, influence of respiration and transpiration on ionic content of air in occupied rooms (Yaglou, Benjamin, and Brandt). 8 observations on subjects before, dur ing, and after exposure to (Yaglou, Brandt, and Benjamin).................. 341 K elley D ust T rap, see Silicosis hazard. 487 THE JOURNAL OF INDUSTRIAL HYGIENE Vo l u m e XV JULY, 1933 N umber 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, County Borough o f East Ham, London, etc. THE close study which has been devoted to silicosis, resulting from exposure to silica dust, has Published fairly clearly the clinical .md pathological results which follow, together with the greatly increased predisposition to succumb to tubercu losis. Similar close study is to-day Wing given to the effects which follow ing the last few years, some of which I have already reported (2, 3). While these findings are in close agreement with those of other observers they help to establish the existence of asbestosis as a disease with definite characteristics distinguishing it from silicosis. Clinical F eatures upon the inhalation of another dust, 'h t arising when asbestos fibres are manipulated. A full description of the mineral asbestos, and of the in dustries in which it is employed, has l*xn given by Merewether and Price 1... Xo further reference to this side i 'bo question therefore is needed. This paper is restricted to presenting h clinical, radiological, and patho*vic:il findings in asbestosis, based 'ii an experience of cases seen dur- _ ` 'civrd 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 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 WDyspnoea.--Dyspnoea is one of the 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 my 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 early; 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 not 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 f o * 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 asbestosis 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, emaciation and loss of weight out of all 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 July, 1988] PULMONARY percussion note is impaired, especially at the bases, diminishing as the apex is approached. Auscultation betrays diminution of breath sounds at the base, although harsh breath sounds with prolonged expiration may be heard over the upper zones, indicative of compensa tory emphysema. The adventitious sounds are almost characteristic of the disease, comprising fine, dry, crackling rles; they are usually heard over the bases and in the axillary region. Pleu ral friction sounds, due to associated basal pleurisy, are not uncommon. The physical signs in the average case are, in fact, those of basal fibrosis, spreading, in more advanced eases, upwards, although they are usually confined to the lower and middle zones. The apex is usually free; and the upper lobes are not infrequently emphy sematous. Case t .--Female, aged i t . She worked in an asbestos factory for 4 years as an mat tress maker. She had to sew asbestos cloth, and then stuff it with asbestos fibre. The stuffing had to be shaken in order to spread it out, thus producing dust; then the mat tress required thumping to distribute the thickness of the packing, with the further production of dust. She had 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 January 2, 1931, she stated that her illness commenced 6 months previously with a dry, hacking cough which was associated with a loss of weight from 147 lbs. to 130 lbs. Two months ago she became conscious of short ness of breath on exertion, which became progressively worse. She complained of iom pain at the base of the left lung, which was worse on inspiration. There were no sweats and no haemoptysis. Clinical examination.--The patient was thin and pale, with cyanosed lips. There July, 1938] PULMONARY ASBESTOSIS 167 * percussion note is impaired, especially at the bases, diminishing as the apex is approached. Auscultation betrays diminution of breath sounds a t the base, although harsh breath sounds with prolonged expiration may be heard over the upper zones, indicative of compensa tory emphysema. The adventitious sounds are almost characteristic of the disease, comprising fine, dry, crackling rles; they are usually heard over the bases and in the axillary region. Pleu ral friction sounds, due to associated basal pleurisy, are not uncommon. The physical signs in the average case are, in fact, those of basal fibrosis, spreading, in more advanced cases, upwards, although they are usually confined to the lower and middle zones. The apex is usually free; and the upper lobes are not infrequently emphy sematous. Cate 1.--Female, aged i t . She worked in an asbestos factory lo t 4 years as an mat tress maker. She had to sew asbestos cloth, and then stuff it with asbestos fibre. The stuffing had to be shaken in order to spread it out, thus producing dust; then the mat tress required thumping to distribute the thickness of the packing, with the further production of dust. She had 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 January 2, 1931, she stated that her illness commenced 6 months previously with a dry, hacking cough which was associated with a loss of weight from 147 lbs. to 130 lbs. Two months ago she became conscious of short ness of breath on exertion, which became progressively worse. She complained of som^ pain at the base of the left lung, which was worse on inspiration. There were no sweats and no haemoptysis. Clinical examination.--The patient was thin and pale, with cyanosed lips. There 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, chiefly over the left base. X-ray examination revealed restricted diaphragmatic movements, especially on the left side. Linear striation at the bases was increased, with a faint homogeneous opacity, especially on the right side, where a fine punctate mottling could be observed. A little glairy, tenacious, mucoid expec toration was obtained, in which were found a few asbestosis bodies and dust fibres, but no tubercle bacilli. Diagnosis.--The case is one of an early degree of pulmonary asbestosis (Stage 1). R adiological F eatures Radioscopio examination of the chest, followed by a technically satis 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 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 of a fine diffuse fibrosis, which has been claimed to be characteristic of asbesto sis; but other allied dusts capable of producing pulmonary fibrosis may pos sibly lead to a condition indistinguish able from th at of asbestosis. Cer tainly Pancoast and Pendergrass (5) doubt whether anyone viewing a num ber of radiograms, indicative of pneu moconioses, sustained in several in- 168 THE JOURNAL OF INDUSTRIAL HYGIENE [xv, no. 4 dustries could select those of asbesto- In the fourth and final stage, the sis subjects; however radiograms of fine punctate mottling can be observed pulmonary asbestosis are certainly to have spread beyond the limits of the very characteristic. lower zone to the middle and even Dr. Stanley Melville has cooperated upper zone, but the apices usually closely in the study of my cases from remain free. This fine diffuse punc the radiological aspect. Roughly four tate mottling stands out in definite stages in order of progression of the contrast to the coarse nodular mottling disease have been observed. In the seen in silicosis. first stage, the movement of the dia This diffuse mottling, so distinctive phragm on one, and sometimes on of asbestosis, has been described as both, sides, is restricted; the root presenting a "ground glass" appear shadows are unusually heavy; and the ance by Burton Wood (6), and by basal linear striation on one or both Merewether as the veiled appearance sides is increased. The right chest has of the involved zone. StaflSv Mel not been observed to be specially in ville says the impression is that of a volved more than the left; indeed the dirty, blurred smearing of the involved left base on a film is normally some zones, as though a piece of india-rubber what obscured by the heart shadow, had been rubbed across the film. and is not so visible. The trachea is The radiological features thus con centrally placed; the heart is usually firm the clinical findings th a t the dis normal in shape, size, and position; ease is characterised by a fine diffuse but the costo-phrenic and even the fibrosis, commencing at, and involving cardio-phrenic angle may be ill defined. principally, the bases of the lung. Close examination of the film may de When tuberculous infiltration com tect some loss of translucency, and a plicates asbestosis, it can usually be fine homogeneous opacity or haze at detected and distinguished from the one or both bases. underlying fibrosis, just as in cases of In the second stage the homoge silicosis. neous opacity becomes more obvious, and a fine punctate stippling may be Case t . --A female, aged SS.--This woman detected at one or both bases, while the basal linear striation is more obvious, with very definite restriction of diaphragmatic movements and some worked in an asbestos factory from 1016 to 1921, had been quite healthy previous to working there, and had never had chest trouble. In 1919, cough and dyspnoea developed and became worse, but she con times blurring of the diaphragmatic tinued at work until 1921 when she was angles. The inter-lobar pleura is us compelled to give it up. In 1921 she was ually thickened, and in my experience notified as a case of pulmonary tuberculosis; i her weight was then 119 lbs.; i t is now 99}. j:l frequently drawn down to the base by She has twice been in a sanatorium; al- `S the fibrosis. though the sputum has been examined on ffi In the third stage definite evidence numerous' occasions, tubercle bacilli have J S of pleural involvement may be present, not been found. ,9 with or without mediastinal displace Clinical examination.--I first saw her in 4 9 May, 1930, when there was present cough, ment, depending upon the inequality dyspnoea, and occasional sweats. She was '9 of fibrosis in the two lungs. thin and emaciated, nnd her face was cya- 9 July, 1933] PULMONARY mixed. The chest expansion was poor, and the apices were retraeted. Expiratory signs were prolonged in the upper zones, Imt diminished in the lower zones; dry, i-ruckling, scattered crepitations were heard throughout both lungs, but especially over the left. The heart was drawn over to the left side. The sputum, carefully examined by Dr. Schuster in June, 1930, was found to contain asbestosis 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 asbestosis. In January, 1932 there was evidence of bilateral pleu risy, with the heart, mediastinum, and tra chea displaced to the left. The appear ances were typical of asbestosis, 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 p atient exhibits an advanced degree of asbestosis. 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. Case 9.--A fem ale, aged 98. 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, whici had persisted for 4 years. These symptoms liecame progressively worse, and were asso ciatcd with hiss o f weight. The patient came under observation ai the end of 1931, when she was thin an< emaciated, and stated that she had lost ' pounds in weight during the last 6 months Her face was somewhat cyanosed. Clinical E xam ination.--The chest expan sion was poor, w ith definite dullness on bot bases, especially the left, which decrease as the apices were approached, where n July, 1933] PULM ONARY ASBESTOSIS 169 nosed. The chest expansion was poor, and the apices were retracted. Expiratory signs were prolonged in the upper zones, hut diminished in the lower zones; dry, crackling, scattered crepitations were heard throughout both lungs, but especially over the left. The heart was drawn over to the left side. The sputum, carefully examined hv Dr. Schuster in June, 1930, 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, 19:12 there was evidence of bilateral pleu risy, 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 1 suspicion of super-added tuberculous infection, though no bacilli have yet been found. appreciable impairment of percussion was detected. Breath sounds were diminished a t both bases, where fine, dry', crackling r&les were heard, extending well up into the axillae. The expiratory sounds were pro longed in the upper zone; and a few pleural friction sounds were heard a t the left base. X-ray examination in April, 1932, re vealed restricted movement of both sides of the diaphragm, with evidence of pleural thickening a t both bases. The right lung showed basal fibrosis, with characteristic punctate mottling of the lower zones. The left lung showed fibrosis and mottling of the lower and middle zones. The mottling was Fio. 1.--Case 2. Ashestosis bodies in clumps in the sputum. Case S.--A female, aged 26. 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 at the end of 1931, when she was thin and emaciated, and stated that she had lost 8 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 bases, especially the left, which decreased as 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, but the trace present was tenacious and muco purulent. Tubercle bacilli were persist ently absent, but asbestosis bodies and fibres were present. At a subsequent X-ray examination in January, 1933, the mottling detected definitely indicated an increased spread of the Abrutie condition in both lungs during comparatively short period; the middle zones of both lungs wre now completely involved; but there was no deAnite evidence of inAltration. Diagnosis.--This case shows deAnite and k /w ! *-I I ,r Fig. 2 Fro. 3 F ig. 2.--Case2. Fine punctate m ottling distributed in all zones, th e apices rem aining free (stage 4). A suspicious annular shadow in th e left infraclavicular region is suggestive of a cav ity . F i g . 3.--Case 2. Same p a tie n t some 14 m onths later. There is very definite ex ten sio n ^feih e disease. W hilst th e appearances are ty p ical of asbestosis, th e m ottlin g in th e u pper zones of b o th lungs suggests th e pos&ibilitjtfjSv a superadded tuberculous infection. T he annular shadow in the left infraclavicular region is now very well defined. CO is* <. July, 1033] PULMONARY ASBESTOSIS 172 THE JOURNAL OF INDUSTRIAL HYGIENE [xv, no. 4 progressive spread of fibrosis in both lungs in less than 9 months. change. In addition to the dense fi brosis, inflammatory cat arrhal changes P athological F eatures* 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 may be observed, with desquamation of alveolar and bronchiolar epithe lium, and thickening of the alveolar and bronchiolar walls. Here asbesto sis bodies tend to be fewer in number. Foreign body giant cells, distinct from tuberculosis giant cells, may be present in the connective tissue. Gloyne, (10) who has recorded these cells, and termed them "asbestosis giant cells,'' suggests th at they present an attem pt 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 cascading ap pearance of tuberculosis giant cells. tous; this compensatory em physem a Case 4---A female, aged SI. This woman may often be detected clinically and radiologically. Microscopic appearances.--The in terstitial tissue of the lungs is every where increased, so much so th a t in 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 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 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. to the naked eye to have escaped the Early in 1931 she consulted a doctor, who apices, much fibrosis may be seen in notified her as suffering from pulmonary them on lung section. In and around tuberculosis. Clinical condition.--When seen she was the densely fibrous areas, asbestosis obviously ill, thin and wasted, very dysp- ' bodies are found in profusion; they noeic, while her face was somewhat cya- j tend to occur in radially arranged nosed. Sputum contained tul>erele bacilli t clumps. and asbestosis bodies, which were found in I Carbon pigment is present in vary clumps on one occasion. f There were physical signs in the lungs of | ing quantities. Advanced areas of advanced phthisis, with cavitation in the 9 fibrosis can be found, associated with left upper lol>e, and, some months later, f dilated bronchioles and bronchiectatic definite physical signs appeared in the 1 right upper lobe. At the bases physical m *I am indebted to Professor M. J. Stewart signs of a basal fibrosis, compatible with for his valuable help in this section. asbestosis, could he detected, v iz .d u lln e ss , M July, 19S3\ PULMONAR weak breath sounds, and dry, crackling rales, rnther different from the riles in the upper zones. The signs were, however, overwhelmingly those of tuberculosis. An X -ray exam ination in A pril, 1931, showed definitely restricted diaphragmatic movements on both sides. There was some dorsal scoliosis, the heart tending to be in the hollow of the concavity. The trachea was drawn to the left. The right lung, was dear, whilst the left lung showed definite evidence of tuberculous infiltration of the upper and middle zones, with cavitation in the left upper zone. There was evidence F io. 6.--C ase 4. Foreign body g ia n t c e ll. Note asbestos body within the cell. of bilateral basal fibrosis, w ith pleural involvement of the left base. The patient had institutional treatm ent in hospital and a t a sanatorium for fi m onths. In June, 1932, sh e discharged herself ironthe sanatorium and w ent home; sh e \vn then acutely ill, and had advanced physirnl signs of tuhcreulosis in hnth lungs. Sh< died on August 30th, 1932. Post mortem examination was made by Dr. S. R. G lovnc whose findings were afollows: the le ft pleural sac w as found to be com pletely obliterated by adhe sions, except at the extreme base, where there was a sm all free sac with greatly thickened pleura containing yellowish tu !>ercles, and covered here and there wit* July, 1933] PULM ONARY ASBESTOSIS 173 weak breath sounds, and dry, crackling rales, rather different from the rales in the upper zones. The signs were, however, overwhelmingly those of tuberculosis. An X -ray examination in April, 1931, showed definitely restricted diaphragmatic movements on both sides. There was some dorsal scoliosis, the heart tending to he in the hollow of the concavity. The trachea was drawn to the left. The right lung, was dear, whilst the left lung showed definite evidence 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 wax 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, Fid. 6.--Case 4. Foreign body giant cell. Note asbestos body within the cell. of bilateral basal fibrosis, with pleural involvement of the left base. The patient had institutional treatm ent in hospital and at a sanatorium for 6 months. In June, 1932, she discharged herself from the sanatorium and went home; she was then acutely ill, and had advanced physical signs of tuberculosis in both lungs. She died on August 30th, 1932. Post mortem examination was made by Dr. S. R. Glovne whose findings were as follows: the left pleural sac was found td be completely obliterated by adhe sions, except at the extreme base, where there was a small free sac with greatly thickened pleura containing yellowish tu bercles, and covered here and there with Fig. 7.--Case 4. Section showing diffuse asbestos fibrosis with ashestosis bodies in clumps, 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 asbestosis, almost confluent in the lower lol e. The upper loin* was completely involved in tuberculosis with several ragged cavities, and was practically destroyed by the cavi ties. The lower lolc showed a few caseous tubercles; in the upper part one of these was breaking down to form a small cavity. The right lung also showed extensive areas of asbestosis. In the upper lybe there'were numerous caseous deposits of'tubercle from the size of a pea to that of a walnut. Mid dle and lower lobes also showed a few 174 TH E JOURNAL OF INDUSTRIAL HYGIENE no. 4 minute discreet nodules of tubercle. No lesions in any other system. Diagnosis.--W hilst the signs of tubercu losis tended to mask those of asbestosis, there was little doubt th at this ease was, in all probability, originally a ease of pure --probably iron silicate--derived from body tissues, oxyhacmoglobin being the chief source. In addition to being found in the sputum and lung juice, (11) they have been found in the fe pulmonary asbestosis complicated by an advanced degree of tuberculosis. Post mortem examination of the lungs showed advanced asbestosis in both lungs; cluni|>cd bodies of asbestosis had l>een observed in ces (12), and even in the spleen, (13) which raises the question as to how they gained access to this organ. Pre sumably they travelled either by em the alveoli and on one occasion in the bolic spread in the blood stream, or by sputum. phagocytic cells. The bodies have Asbestosis B odies also been found in the upper abdom inal lymph glands (M. J. Stewart, Highly characteristic golden-yellow personal communication). bodies are found in the sputum and The presence of asbestosis bodies in fibrosed lungs of asbestos workers. the feces is as pointed out by Gloyne They have been present in all autopsies of practical value where no sputum is upon cases of pulmonary asbestosis. available, since, as in cases of phthisis, They vary in size and shape; but, the sputum may have been swallowed, characteristically, they have bulbous rather than coughed up. enlargements at the extremities, with The bodies are best seen with an oil a regularly or irregularly segmented immersion lens, and show up clearly body, resembling dumb-lwlls; when without staining as golden-yellow fractured they are club-shaped. The structures. They can, however be appearance of fully formed bodies has stained by haemotoxylin, by potas been aptly compared by Gloyne to sium ferrocyanide, and hydrochloric beads on a necklace; the beads vary in acid, giving prussian blue reaction, and size, and represent the irregularly by ammonium sulfide. segmented Ixidy. These bodies have Asbestosis bodies in clumps.--The boon found by various observers to bodies may be found in the lung tissue vary in length from 20 to over 200 either singly or in clumps, and may microns. An asbestos fibre forms occur similarly in the sputum, al the central core of each body, and can though they more usually are found in frequently be detected (10). The the sputum singly or in groups of two golden-yellow material covering each or three. The bodies tend to be fibre contains an iron substance, which scanty if there is little bronchial secre gives a pnissian blue reaction; prob tion; and, given a pu'monary fibrosis, ably it is a silicate, which protects the profusion of bodies in the sputum the fibre from further change. When appears to show a tendency' to vary stained with ammonium sulfide, the directly with the extent of the disease. central core of an asbestos fibre stains When the.bodies are more abundant in lightly against a well stained body. the sputum, they may occur in radially , Asbestosis bodies are probably as arranged clumps; such an occurrence | bestos fibres which have become coated indicates disintegration of lung tissue | with colloidal golden-yellow material by either simple suppurative broncho- 1 July, 1983] PULMONARY pneumonia, or secondary tuberculous infection (14). This occurrence of bodies in clumps in the sputum is com parable 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, who had never worked in asbestos, and of a Lancashire coal-miner. Appar ently other dusts may simulate asbes tos fibres, and lead to similar reac tions with the lung tissues. A recent observation by K ettle (16) is interesting and noteworthy in this connection: "Crystalline silica heavily coated with iron (silica, 59.9 per cen t.; ferric oxide, 40.1 per cent.) and injected into the tissues appeared to be ns inert as pure ferric oxide itself. It would appear that the silica is prevented from going into solution by its very adequate coating o f 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 the result of solution from the surface of the spicule before it is rendered inert by the coating of iron." Kettle records the fact that asbestosis bodies injected into the subcutan eous tissues of mice arc as inert and harmless as the iron coated crystals of siliia. This protective action of the colloid substance is a point of consid erable interest. Asbestosis bodies in sputum.--The July, 1933] PULMONARY ASBESTOSIS 17St pneumonia, or secondary tuberculous infection (14). This occurrence of bodies in clumps in the sputum is com parable to the presence of elastic tissue in phthisis (M. J. Stewart). What have been called "pseudo-as hes! os bodies" (15) have recently been recorded as found in (he lungs of a coal miner working in the mines of Alabama, who had never worked in asbestos, and of a Lancashire coal-miner. Appar ently other dusts may simulate asbes tos fibres, and lead to similar reac tions with the lung tissues. A recent observation by K ettle (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 he 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 the result of solution from the surface of the spicule Indore it is rendered inert by the coating of iron." Kettle records the fact that asbesto sis bodies injected into the subcutan eous tissues of inice are as inert and harmless as the iron coated crystals of siliia. This protective action of the colloid substance is a point of consid erable interest. Asbestosis bodies in sputum.--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; and (d) asbestosis bodies in sputum, feces, or lung tissue. I t 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 34. She was en gaged in an asbestos factory from 1911 to 1917. She was first seen in September, 19X0 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 cough, 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 |>crsistcd, with some muco-purulcnt expectoration, half an ounce in 24 hours; it was never blood-stained. There were severe night sweats, and the appetite was poor. Lassitude was present. Asbestos corns were present, especially on the hand and elbow. ' Clinical examination.--Physical signs in the chest were mainly at the base, and t.vpi- 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 thickening at the base, with lowering and thickening of the inter-lobar septum. The basal linear striation was exaggerated, and there was some ill defined mottling of all zones. On bodies in clumps. The condition suggested a rapid, complicating tuberculous process. X-ray examination now showed restricted movementof the right side of the diaphragm, and increased fibrosis a t the right base. On the left side there was infiltration of the upper and middle zones, with excavation in the upper zone, with pleural involvement, and basal fibrosis. Diagnosis.--The case was originally one of pure pulmonary asbestosis, complicated later by tuberculosis. Here the tuberrulo- the left side some fibrosis was detected at sis was implanted upon an asbestosis. The the base. clumping of the asbestosis bodies indicates The tenacious mueo-purulentsputum was disintegration of lung tissue. found to contain numerous and mixed organisms, mainly bacillus friedlander and Case 6.--A male, aged 43. This man pneumococcus. No tubercle bacilli were worked ns a card-room superintendent in an round. Asbestos fibres and asbestodj asbestos factory for 9 years, 1920 to 1929. bodies were present. His work brought him into contact with a All symptoms hail become much aggra high concentration of dust. He remained vated by July, 1932, and the weight had free from chest trouble until 1924, when he ! dropped from 113 lb. to 96 lb. The pulse became conscious of mild dyspnoea on exer was rapid, and there was evening pyrexia. tion, with an irritating, dry cough. The Sputum increased in amount, and tubercle symptoms grew gradually worse, until in bacilli were found in October, 1932, after 1929 he was so breathless on the slightest frequent examinations. Asbestosis bodies exertion th a t he was compelled in October of great variety were present, with definite to cense work; he was then confined to bed v, no. 4 July, 1933] BT & r 3 P P 3 3 IX6^; &&? & * dfi s- ^ s a 3- ? o eu o - 33- . *y3SC 3= no. /&-. v*?V PULMONARY ASBESTOSIS F o. 9 F ig . 10 F ig . 9.--Case 5. N ote th e c h a racteristic m o ttlin g w ith bilateral basal fibrosis. T he rig h t in terlo b ar septum eun be seen to be thickened and below its norm al position, h av in g been draw n down by the basal fibrosis. T h ere is no evidence of tuberculous infil tration of the parenehvma of either lung. F ig . 10.--Case 5. Same case nearly 2 years la te r. N ote now the definite tuberculous in filtra tio n involving the left upper and middle zones w ith excavation. This has com plicated the original pure ashestosis. Extension of the fibrosis of the right lower zone can he seen. because of right-sided pleural effusion. Me now suffered from progressive anorexia and palpitations; he was breathless even a t rest; the face was cyanosed, with an earthy com plexion; he was obviously wasted, and his weight had fallen from 203 lb. to 131 lb. Marked clubbing of the fingers was present. Clinical examination.--The apices were contracted. The right side was practically immobile and the chest was flat. Move- X-ray examination showed the right dia phragm almost completely obscured, while the movements of the left were very re stricted. The trachea was slightly drawn over to the right There was a dense opacity over the greater part of the right heinithorax, consistent with anencystcd effusion. F in; punctuate stippling was seen over the area not covered by the dense opacity a t the right base. The left lung showed character dence of a right-sided tuberculous empyema with advanced bilateral pulmonary asliestosis. Tubercule bacilli were found in the pus, the fluid of which was clear and straw coloured when a paracentesis was done by me. Diagnosis.--The case was clearly one of advanced pulmonary asbestosis, compli cateti by tul>crculous pleurisy. Apparently there was some disintegration of lung tissue, * - Fio. 11.--Case 6. Showing asbestosis bodies in clumps. The central asliestos fibre is well shown in the long curled body. (I am indebted to Prof. Matthew J. Stewart for the microphotographs of asbestosis bodies in clumps in Cases 5 anti 6.) ment of the left base was very restricted. There was dullness over the whole of the right chest and the left base. Breath sounds were diminished over the whole of the right chest, and some fine rales were heard a t the base. The breath sounds over the left chest were coarse, and the expira tion was definitely prolonged. Fine, charac teristic, crackling rles were heard over the left base and in the axilla. istic fine punctate mottling, involving the lower ami middle zones. Numerous asbesto.sis bodies, both singly and in clumps, were found in the sputum; but repeated examinations for tulierde ba cilli were negative. Nevertheless, exami nation of pleural fluid showed it to be a clear tuberculous exudate. This patient died on February 11, 1933. An autopsy by D r. 8. R. Gloy ne showed evi- Fic. 12.--Case 7. Macro- since the asbestosis bodies were found clumps. Case 7.--.1 rough-haired terrier dog, gears old. This terrier was kept for rattit purposes in an asbestos factory, where spdnt the greater part of his life, and v exposed to asbestos dust during most of ' time. He developed a cough, and inert ing dyspnoea for 2 years, during the las* months of which he became thin and em: ated. The dyspnoea became so distress July, 1933] PULMONARY ASBESTOSIS 179 iWnce of a righ t-sid ed tuberculous em pyem a with advanced Inlateral pulmonary asbestosis. T u b crcule hurilli %verc found in the pus, the fluid of which was clear and straw coloured when a paracentesis was done by me. D iagnosis.--The case was clearly one of advanced pulmonary asbestosis, com pli cated by tul>erculous pleurisy. A pparently there was som e disintegration of lung tissue, th at the dog was Ipthallcd ill its own inter est. The thoracic organs, trachea, heart, and lungs (through the courtesy of Dr. Kerr who obtained them for me) were k in d ly exam in ed by D r. N . h'ch u ster, w hose findings have been reported elsewhere (8), but m ay be briefly sum m arized here. The m acroscopic appearances showed that, w hilst there was no sign of acute pleu risy, there was a general opacity of the vis- F ic . 12.--C ase 7. M acroscopic ap p earan ce o f d o g 's lu n g since the asbestosis bodies were found in clum ps. Case 7.-- .1 rough-haired terrier dog, 10 gears old. T his terrier was kept for ratting purposes in an asbestos factory, where he spdnt the greater part of his life, and was exposed to asbestos dust during m ost of the time. He developed a cough, and increas ing dyspnoea for 2 years, during the last 6 m onths of which he became thin and em aci ated. The dyspnoea became so distressing ceral pleura, w ith patches of localized pleural thickening, am i bands of adhesions between the lolies. T he lungs had lost their usual spongy consistency; on section there was evid en ce of diffuse fibrosis under the pleura. The bronchioles were dilated; car bon pigm ent was to be seen scattered throughout the lung. Evidence of any acute inflam m atory process was com pletely absent. M icroscopic exam ination revealed much 180 TH E JOURNAL OF INDUSTRIAL HYGIENE [xv, no. 4 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 asbestosis 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 ease of this dog were closely allied to those of asbestosis in the human lung, two noteworthy features were absent--asbestosis bodies, and evidence of acute inflammation. A possible relationship lietween the formation of asbestosis bodies and an acute inflamma tory exudate might suggest itself, had not asbestosis bodies l>een 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 show ing asbestos fibres. (Microphotograpn 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 13J 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 tu n ity a?- Ihe first of inhaling asbestos dust, since it was only at the factory with the night watchman. This absence of asl>estosis bodies was also observed by Stewart in 3 rats from an asbestos factory, although fibres were pres en t in the lungs. Gloyne, however, after careful search, has found one small body, together w ith numerous fibres, in the lungs Fig. 14.--Case 7. Foreign body giant cell. Note coarse stippled pigmented ap pearance. The presence of asbestos fibres, represented by fine lines can just be seen. (M icrophotograph by Dr. \V. Susman, Pathological Department, Manchester Uni versity.) T he T uberculosis Risk in Asbestosis Tultorculosis is generally recognised as the most serious risk to which silico tic patients are exposed; but the ques tion of tuberculosis complicating asbestosis lias remained rat her 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] PULMONAE feature in contra-distinction to sili cosis. R ecently, however, Professor K ettle, (16) working experim entally with ani mals, finds that silica and asbestos dusk belong to a group of active substances which produce lesions when introducer, into the subcutaneous tissues; they both produce serious pulmonary fibro sis, and both assist the growth of tuber cle bacilli. Clinical evidence would seem to support this experim ents work, as there is little doubt that aL increasing number of cases of tubercu losis are being seen in subjects exposed to asbestos dust. Such cases m ay not be m et with in an examination of workers at work with no symptoms they tend rather to be seen amonp those who have left work and are at tending clinics. Hence Merewether (17) in 1930, found only .4 active cases of tuberculosis in an examination of 374 asbestos workers actually at work, and formed the impression that there was no outstanding susceptibility to tuberculosis among these workers. On the other hand, Wood and Gloyne (18) in 1931, were able to trace 12 cases of tuberculosis, 10 of which were active, in a series of 57 cases of asbestosis, and among 35 deaths from asbestosis referred to in the Report of the Cbier Inspector of Factories for 1931, (19, tuberculosis was a com plicating or terminal factor in 11 coses. Amonr seventeen of my own definite cases c asbestosis, the m ajority of whom were not at work, six had tuberculosis, o which four were active. A typical lesion of mild activity with an early stage of pulmonary as bestosis, was present in one of my cases who had been exposed to asbes tos dust for 10 years; but th e work July, 19S3] PULMONARY ASBESTOSIS 181 feature in contra-distinction to sili cosis. Recently, however, Professor Kettle, (16) working experimentally with ani mals, finds th at silicaand asbestos dusts belong to a group of active substances which produce lesions when introduced into the subcutaneous tissues; they both produce serious pulmonary fibro sis, and both assist the growth of tuber cle bacilli. Clinical evidence would seem to support this experimental work, as there is little doubt that an increasing number of cases of tubercu losis are being seen in subjects exposed to asbestos dust. Such cases may not be met with in an examination of workers at work with no symptoms; they tend rather to be seen among those who have left work and are at tending clinics. Hence Merewether, (17) in 1930, found only .4 active cases of tuberculosis in an examination of 374 asbestos workers actually at work, and formed the impression that there was no outstanding susceptibility to tuberculosis among these workers. On the other hand, Wood and Gloyne, (18) in 1931, were able to trace 12 cases of tuberculosis, 10 of which were active, in a series of 57 cases of asbestosis; and among 35 deaths from asbestosis referred to in the Report of the Chief Inspector of Factories for 1931, (19) tuberculosis was a complicating or terminal factor in 11 cases. Among seventeen of my own definite cases of asbestosis, the majority of whom were not at work, six had tuberculosis, of which four were active. A typical lesion of mild activity, with an early stage of pulmonary as bestosis, was present in one of my cases who had been exposed to asbes tos dust for 10 years; but the work, which consisted in coating lead pipes, did not entail exposure to high dust concentrations. Tubercle bacilli and asbestosis bodies have been found in sputum. This case has been watched for 3 years, during which the tubercu losis has remained stationary. In this connection Wood and Gloyne (18) have pointed out that obolescent tu berculosis may remain quiescent in spite of exposure to asbestos dust. Another case, one of pure pulmonary asbestosis, (case 5) under my care has, during the last few months, developed pulmonary tuberculosis, which I can say quite definitely, from clinical, radiological, and sputum controls, has been implanted upon the asbestosis with decided aggravation of all symp toms. Among my series, serial skia grams raise the suspicion of superadded tuberculous infiltration in 2 cases. I am further informed by Pro fessor Stewart that at autopsy, when no microscopic evidence of lung tuber culosis has been observed, tuberculosis may be found histologically. My own limited experience tends to show that tuberculosis, as a complica tion of asbestosis, is by no means un common; the risk may or may not be equal to that in silicosis; but that there is a risk, the evidence quoted, and my own observations, appear to establish beyond doubt. Other things apart, re cognition of the existence of this risk is an important factor when considering what preventive measures should be taken to control this occupational disease. The existence of this risk establishes that no person with tuber culosis in any form should be allowed to enter the industry, nor should any one in whom tuberculosis a t a later stage is detected be permitted to con- 182 THE JOURNAL OF INDUSTRIAL HYGIENE few, no. 4 tinue in the industry. The risk here is to the other workers, as well as to themselves. P rognosis 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. S ummary 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] PULMONAR (a) length of exposure, and (b) nature and concentration of the dust. The histological features of asbesto sis are essentially (a) a diffuse chronii interstitial fibrosis of the lungs, with areas of acute catarrhal changes, and (b) the presence of characteristic as bestosis bodies, appearing either singly or in clumps. The presence of isolated asbestosi. bodies in the sputum is indicative merely of previous exposure to asbes tos dust, and does not necessarily BIBL1 1. M erew et h er , E. R. A., and Prici C. W.: Report on Effects of Asbestc Dust on the Lungs and Dust Su; pression in the Asbestos Industry London, H. M. Stationery Office 1930. 2. Ellman, P.: Reports on Cases of Pul monary Asbestosis. Proc. Royal Sot Med., 1930-31, 4 ,526,541,699. 3. Ellman, P .: Chest Disease in Genen Practice. London: H. K . Lewis, 193 p. 116. 4. Oliver, T.: Pulmonary Asbestosis i. its Clinical Aspects. This Jour. 1927, 9, 483. 5. Pancoast, H . K ., and Pendergrass E. P .: Review of Pneumoconiosis Further Roentgenological and Pathi logical Studies. Am. Jour. Roentgei 1931, 26, 556. 6. Wood, W. B.: Pulmonary Asbestosi Radiographic Appearances in Ski grams of the Chests of Workers ii Asbestos. Tubercle, 1929, 10, 353. 7. Gloyne, S. R.: The Reaction of Tissui to the Asbestos Fibre with Refci ence to Pulmonary Asbestosis. Ibid 1930,1 1 ,151. 8. Schuster, N. H .: Pulmonary Asbest' . sis in a Dog. Jour. Path, and Ba< I teriol., 1931,34,751. 9. Stewart, M. J .: Asbestosis Bodi in the Lungs of Guinea Pigs after to 5 Months' Exposure in an Asbest sis Factory. Ibid., 1930,33,848. 10. G loyne, S. R .: The Asbestosis Bod July, 1933] PULMONARY ASBESTOSIS 183* (a) length of exposure, and (b) nature and concentration of the dust. The histological features of asbestosis are essentially (a) a diffuse chronic interstitial fibrosis of the lungs, w ith areas of acute catarrhal changes, and (b) the presence of characteristic asbestosis bodies, appearing either singly or in clumps. The presence of isolated asbestosis bodies in the sputum is indicative merely of previous exposure to asbes tos dust, and does not necessarily have any clinical significance; if the bodies occur radially arranged in clum ps, they suggest disintegration of pulmonary tissues. Pulmonary asbestosis, once estab lished, is a progressive disease w ith a bad prognosis; ittreatm en t can only be sym ptom atic. The tuberculosis risk in asbestosis m ust be reckoned w ith, even though tim e has y et to indicate whether it is less, equal to, or perhaps even greater than that in silicosis. BIBLIOGRAPHY 1. Merbwether, E. R. A., and P rice, 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, t 4,526,541,699. 3. Ellman, P .: Chest Disease in General Practice. London: H. K. Lewis, 1932 p. 116. 4. Oliver, T .: Pulmonary Asbestosis in its Clinical Aspects. This Jour., 1927,9 , 483. 5. Pancoast, H. K ., and P enderorass, E. P.: Review of Pneumoconiosis. Further Roentgenological and Patho logical Studies. Am. Jour. Roentgen, 1931, 6, 556. 6. Wood, W. B.: Pulmonary Asbestosis: Radiographic Appearances in Skia grams of the Chests of Workers in Asbestos. Tubercle, 1929, 10, 353. 7. Gloyne, S. R .: The Reaction of Tissues to the Asbestos Fibre with Refer ence to Pulmonary Asbestosis. Ibid., 1930,11,151. 8. Schuster, N. H.: Pulmonary Asbesto. sis in a Dog. Jour. Path, and Bacf teriol., 1931,34,751. 9. Stewart, M. J.: Asbestosis Bodies in the Lungs of Guinea Pigs after 3 to 5 Months' Exposure in an Asbesto sis Factory. Ibid., 1930, SS, 848. 10. Gloyne, S. R .: The Asbestosis Body. 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, Si, 172. 12. Gloyne, S. R.: Presence of Asbestos Bodies in the Faeces in a Case of As bestosis. Tubercle, 1930, It, 158. 13. Stewart, H. L., Bucher, C. J., and Coleman, E. H .: Asbestosis, a Re port on Two Cases. Arch. Path., 1931, It, 916. 14. Stewart, M. J., T attersall, N., and H addow, A. C.: On the Occurrence of Clumps of Asbestosis Bodies in the Sputum of Asbestosis Workers. Jour. Path, and Bacteriol., 1932,35,737. 15. T ylecote, F. E., and D unn, W. J. S.: A Case of Asbestos-like Bodies in the Lungs of a Coal Miner who had never worked in Asbestos. Lancet, 1931, i, 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, 35, 395. 17. M erbwether, E. R. A.: The Occur rence of Pulmonary Fibrosis and other Pulmonary Affections in Asbestos Workers. This Jour., 1930, It, 253. 18. Wood, W. B., and Gloyne, S. R.: Pul monary Asbestosis complicated by Pulmonary Tuberculosis. Lancet, 1931, t, 954. 19. Annual Report, Chief Inspector of Factories, 1931. London, II. M. Sta- : n fr 10*1 it*" 152 TH E JOURNAL OF INDUSTRIAL HYGIENE Altitude, polymorphonuclear-lympho cyte ratio at 5750 feet (Stammers). 140 Amyl Acetate, investigation of toxic action of acetic acid esters (Blina).. 125 vapors, colorimetric determination of, in air (Koreman).......................... 38 Amyl Alcohol vapors and amyl acetate vapors, colorimetric determination of, in air (Koreman).......................... 38 Amyl N itrite and cyanide poisoning (Chen, Rose, and Clowes)............... 124 Aniline cancer (Berenblum).............. . 26 dye workers, occupational cancer in (B iittn e r )........._............... 65 poisoning, chronic, clinic and diag nostics of, (Genkin and Raschew- skaja)...................................................... 96 tumors of bladder, treatment of (Muller)................................................. 66 Ankylostomiasis in German coal mines (Bruns)................................................... 55 Anthracosis, silico- (Cooke).............31, 79 Anthrax (Sm yth)........................................ 132 notes on industrial (Eurich)............... 132 Antimony oxide workers, health of (Oliver).................................................. 96 poisoning from enam elled vessels........ 120 Arsenical and fluorine insecticides, re lative toxicity of some (Smyth and Sm yth)................................................... 5 Arseniuketted hydrogen poisoning due to action of water on metallic arsenides (Bomford and H unter).. 32 Arsine poisoning, chronic, case of (Dassel).................................................. 120 poisoning from action of water on metallic arsenides (Bomford and H unter).................................................. 121 Arthritis, influence of conditions in home and workshop on course of chronic rheumatic, infective (Edstrom)........................... 26 rheumatoid- and osteo-, social and in dustrial aspects of (F ox).................. 63 Arsenic, zinc, copper, lead compounds in atmospheric dusts, and sources (Dunn and Bloxam ).............................131 Asbestosis bodies, occurrence of clumps of, in sputum of asbestos workers (Stewart, Tattersall, and Haddow)................................................ 78 lung, infra-red photomicrographs of the<(Gloyne)................... _................... 103 morbid anatomy and histology of (Gloyne)................................................. 127 pulmonary (E llm an).............................. 43 silicosis and.............................................. 6 Asbestos workers, occurrence of clumps of asbestosis bodies in spu tum of (Stewart, Tattersall, and Haddow)................................................ 78 Asphyxia, fundamentals of (Hen derson)................................................... 118 Asthma from sensitization to chromium (Joules).................................................. 5, Asthma pollen, and hay fever, effect of air filtration in (Nelson, Rapport, and Welker)................................... 108 pollen, hay fever and, treatment of, by air-conditioned atmosphere (Gay).............................................. 108 Atmosphere, ionization of, and its bio logical effects (Roller)................... 52 Atmospheric D usts, zinc, copper, lead, and arsenic compounds in, and sources (Dunn and Bloxam).......... 131 Atmospheric Pollution by smoke and toxic gases (Kimpflin).................... 80 eighteenth report, 1932...................... 130 motor fumes and, (Regan)................ 9 particles suspended in air (Rochaix).. 132 seventeenth report, 1930-1931........... 9 sulfur dioxide in industrial commu nity air (Betz, Holden, and Handy)............................................ 124 see algo Air pollution Australia, chemical analysis and path ology of lungs of coal miners in New South Wales (Bradham and Taylor)............................................ 103 Bakers' Eczema and its causes (Teleky and Zitzke)...................................... 80 and sensitiveness to lactic acid (Ken e d y ) .............................................. 46 Basophilic Granulation o f erythro cytes in cases of contracted kidney (Litzner)................................. 29 of erythrocytes, and industrial dust (Mertenskotter).............................. 36 of erythrocytes in men without lead exposure (Seitz).............................. 30 Benzene and benzine vapors, quanti tative poisoning from (Bamesreiter)........................................; ... 68 colorimetric process for determina tion of, (Gavrilov)...................... 8 leucemia following exposure to (Emile-Weil)................................... 67 leucemia in map.and in white mice (Lignac)........................................... 67 poisoning, experimental chronic ben zol poisoning, (Sartorius and Sudhues)........................................ 121 poisoning from adhesive dissolved in (de Balsac and Agasse-Lafont)-- 121 Benzol, see Benzene Beryllium, apparatus for producing low dust concentrations of constant composition and method for microgravimetric determination of dust, use of method in studying dust from production of (Weber and Engelnardt).................................... . ........ 104 Bladder and prostate, cancer of, in cer tain occupations (Henry, Kennaway, and Kennaway)...................... 65 treatment of aniline tumors of (Mailer)........................................... 5 SUB Blackdamp and carbon monoxide, for mation of, from coal a t ordinary temperatures (Haldane and Makgill).......................................................... Blood picture, industrial (Massione)... polymorphonuclear-lymphocyte ra tio at altitude of 5750 feet (Stammers)...................................... pressure in healthy young male adult (Treadgold)...................................... pressure, influence of muscular work in high mountains upon venous pressure (Vigliani)........................... B uffer influence upon response of stri ated muscle to caffeine stimulation in fatigue studies (Cheney)........... Burns and scalds, treatment of, with especial reference to use of tannic acid (Mitchiner).............................. extensive cutaneous (M clver)............. tannic acid treatment of (M artin)... treatment of old unhealed (Davis and Kitlowski)......................................... treatment of shock and toxemia; heal ing wound, reconstruction (Bettm an)........................................................ treatment of. with gentian violet (Connell, Fatheree, Kennedy and McSwain........................................... Cadmium poisoning (W able).................... Caffeine stimulation, buffer influence upon response of striated muscle to, in fatigue studies (Cheney)........... Cage, winding-engine controls (Winstanley)............................................ 1 Caisson workers, proposed Swiss regu lations for prevention of accidents among, and German ordinance for protection of workers in compressed air............................................................. Cancer, aniline (Berenblum).................... lung, among chromium workers (Lehmann)............................................. lung, and diseases of lung, caused by dust, increase of (Berbunger)............ lung, in miners of Jachymov (Joachimstal). (Pirchan and Sikl)___ occupational, m aniline dye workers (Biittner)......................................... ' of bladder and prostate in crtain oc cupations (Henry, Kennaway, and Kennaway)....................................... tar, (Caligaris).................................... >. tar (David).......................................... tar, review of recent literature (See- see also Tumors Carbon are as source of artificial sun shine, ultraviolet, and other radia tions (Greider)...................................... Carbon Bisulfide, see Carbon disulfide Carbon Dioxins-air mixtures, deter mination of hydrocyanic acid in (Cupplea).......................................... SUBJECT PAO B lackdamp and carbon monoxide, for mation of, from coal at ordinary temperatures (Haldane andM ak- g ill)........................................................... 122 B lood picture, industrial (Massione)... 85 polymorphonuclear-lymphocyte ra tio at altitude of 5750 feet (Stammers)....................................... 140 pressure in healthy young male adult (Treadgold)....................................... 141 pressure, influence of muscular work in high mountains upon venous pressure (Vigliani)............................. 86 B uffer influence upon response of stri ated muscle to cafleine stimulation in fatigue studies (Cheney)........... 50 B urns and scalds, treatment of, with especial reference to use of tannic acid (Mitchiner)................................ 93 extensive cutaneous (Mclver)........... 138 tannic acid treatm ent of (M artin)... 138 treatment of old unhealed (Davis and Kitlowski)......................................... 139 treatm ent of shock and toxemia; heal ing wound, reconstruction (Bett- m a n )................... 139 treatment of. with gentian violet (Connell, Fatheree, Kennedy and McSwain.............................................. 64 Cadmium poisoning (W ahle).................... 71 Caffeine stim ulation, buffer influence upon response of striated muscle to, in fatigue studies (Cheney)........... 50 Cage, winding-engine controls (WinStanley)................................................... 137 Caisson workers, proposed Swiss regu lations for prevention of accidents among, ana German ordinance for protection of workers in compressed air.............................................................. Cancer, aniline (Berenblum)............... lung, among chromium workers (Lehmann)........................................ 65 lung, and diseases of lung, caused by dust, increase of (Berblinger)....... 74 lung, in miners of Jachymov (Joacnunstal). (Pirchan and Sikl)__ 64 occupational, in aniline dye workers (B ttttner).......................................... 65 of bladder and prostate in certain oc cupations (Henry, Kennaway, and Kennaway)........................................ 65 tar, (Caligaris)..................................... 65 ta r (David)........................................... 25 tar, review of recent literature (See25 see also Tumors Carbon arc as source of artificial sun shine, ultraviolet, and other radia tions (Greider)................................. 18 Carbon B isulfide, see Carbon disulfide Carbon DioxiDE-air mixtures, deter mination of hydrocyanic acid in (Cupples)........................................... 38 IND EX 153 _ PAll* Carbon Dioxide, effect of, on bacterial growth with reference to the pres ervation of fish. (Coyne)............. 25 experiments in chambers protected from air raids (Quasebart)............ 87 precise automatic apparatus for con tinuous determinations of, in air (Thomas).......................................... 106 reducing inflammability of fumigants with (Jones)..................................... 85 Carbon Disulfide and hydrogen sul fide, intestinal diseases following chronic inhalation of (Weise)........ 32 industrial poisoning by, in Italy (Ranalletti)....................................... 5 pathology of industrial poisoning with (Gianotti)................................ 120 poisoning simulating intracranial tu mor (Baader).................................... 120 Carbon Monoxide and blackdamp, for mation of from coal at ordinary temperatures (Haldane and Mak- giU).................................................... 122 and its relation to aircraft (White)... 5 burning of, by heart and skeletal mus cles (Fenn and Cobb)...................... 122 colloidal sulfur and, (Vita and Salmoiraghi).......................................... 123 content of blood, effect of smoking on (Hanson and Hastings)................... 99 detection of traces of, m air (Acker- mann)................................................ 106 determination by use of iodine pentoxide-oleum suspensions and io dine-oleum solutions (Schlpfer and Mosea)................................................. 38 effects of repeated exposure to, (Killick)............................................. 27 inflammable gases produced by ther mal decomposition of plastic insu lators in an electric arc (Littlefield and Yant)........................................... 85 in garages (Sundberg and Ljung- holm)................................................. 123 methylene blue, a synergist, not an antidote for (Haggard and Green berg)............................................. 99 "normal" content of the blood (Gettler and M attice)............................... 50 poisoning, chronic, animal experi ments on, (Buresch).......................... 27 poisoning, cnronic,_ hypertrophy of heart in acclimatization to (Camp bell)..................................................... 99 poisoning, effect of methylene blue on hydrocyanic acid and (Brooks)__ 27 poisoning from motor-car fumes (Owens)............................................... 27 poisoning, influence on antibodies of chronic (Sudhues).........................., 26 poisoning, methylene blue as antidote to (Brooks)....................................... 122 poisoning, methylene-blue solutions in treatment of (Geiger)................... 67 poisoning, series of chronic cases (Symanski).......................................... 67 6 THE JOURNAL OP INDUSTRIAL HYGIENE The relative toxicity of fluorine and arsenical insecticides was determined by feeding to white rats various accurately measured amounts of cyrolite, barium, fluosilicate, and lead arsenate, mixed with their food for 16 weeks. The arsenical com* pound was found to be several times as toxic as the fluorine compounds.--L. T. P. D eratization of A ustralian Coasting Vessels bt S ulfur. G. A. Murray. Bull Office Internal. d'Hyg. Pub., 1932, vol. 24, pp. 8b7-65l. Gaseous F umigants for S h ips. C. Maselli. Bull Office Internal. d'Hyg. Pub., 1932, vol. 2b, pp. 652-866. D eratization of Vessels bt Mixed Oxides of Carbon. Sanneman. Bull. Office Internal. d'Hyg. Pub., 1932, not. 2b, pp. 6bl~6bb. S olforkose in Ship F umioation. Hamel. Bull. Office. Internal. d'Hyg. Pub., 1932, vol. 2b, pp. 645-68. Injur ies D ue to Work with T oxic Woods, with P articular R eference to a N um ber of B razilian S pecies. F. W. Freiee. Arch. f . Gewerbepath. u. Gewerbehyg., 1932, vol. 3, pp. 1-lbSymptoms and chemical substances asso ciated with certain commercial woods are correlated. DUST HAZARDS AND T H EIR EFFECTS T he D ust H azard in P orcelain Works. silicosis. A number of other employments A. Hofbauer-Flatzeck. Abelr, as follows in porcelain works are given which are dust from Zenlralbl. f. Gewerbehyg., 1932, vol. free. The medium and severe forms of 19, pp. 105-111 in Bull. Hyg., 1932, vol. 7, silicosis were found only in workers who had p. 697. been exposed to dust for over 11 years. In The author here reports the results of many cases the disease occurred many years 1,339 X-ray examinations of porcelain work after a comparatively short period of work ers of the Bavarian town of Selb. The re with exposure to dust, and particulars are sults are tabulated according to the classes given of 3 cases in which severe silicosis oc of work grouped with regard to the dust curred 40 years after work which exposed to hazard, and the number of years a worker dust. The periods of work were only from was employed in that class, and in cases 4 to 9 years and there had been no exposure where silicosis was found it is shown as to dusty work after that. This long latent slight, medium, or severe. The mortality period requires further investigation. from pulmonary tuberculosis among the general population of Selb was in 1930 ab o u t1' ' S ilicosis and Asbestosis. Home Office, three times as high as in Bayern, and the H. M. Stationery Office, 1932. number of new cases more than twice as "The object of this Memorandum is to many as in the neighbouring town of Stettin. set out briefly what the disease (silicosis) is, The author considers that unless medical how and where it is produced, the means men understand more about the nature of which can be taken to prevent it, the pro the work in porcelain works, there is a tend vision made for compensation, and the ency to regard cases of pure tuberculosis arrangements for the medical examination as silicosis, and overlook cases of silicosis and certification of workmen." ' which have occurred after a long latent "W ithin recent years it has been found period. that asbestos dust produces a fibrosis of the In grouping the occupations some diffi lungs (known as asbestosis) which resem culty was experienced, as the same word bles silicosis in many ways. A note on this is used in different parts of Gcmany to disease is included." describe different kinds of work, in which Of particular interest is the following: the dust hazard may not be so great. Of "During the last three years there have been 231 potters examined only 90 were free of 80 cases (silicosis), including 30 deaths, silicosis, and there were 33 light cases, 39 amongst workmen employed in ganister medium, and 69 severe, while in 108 porce mines and silica brick works; 179 cases in lain painters there was not a single case of cluding 25 deaths, in the getting and manipu- A lation of sandstone a t quarries and o n ; ises worked in conjunction therewith eases, including 87 deaths, in the pc industry; 81 cases, including 32 deatl the metal industries, including metal g isg and sandblasting; and 91 cases, incl 20 deaths, in coal mines." It is a regrettable fact th a t while we i United States, have abundant evidem day of instances of both diseases we not even an approximate idea of our tistics thereon. An excellent bibliography of 14 refer to British publications, mostly govern tal, is appended. Observations a nd St u d ie s on Silico D iatomaceous S ilica. R. T. Legg> E. Bosencrante. Am. Jour. Pub. h Ocl., 1932, vol. 22, pp. 1055-1060. This paper summarizes the finding recommendations of an investigation ` silicosis hazard among workers enga, mining diatomaceous earth in Santa B: County, California. The deposit is posed of fossilized diatomes and n algae, and contains about 85 per cen silica. Workers are Mexican In< selected by physical examination, ar authors state th a t these people hav highest tuberculosis rate in this cm One hundred and eight were given . examinations. T he ages ranged from 56 years, and length of employment leas than 1 to more th a n 5 yean, 33 per having worked there 5 years. Pneu? niosis of various degrees was present i per cent, of the cases, 60 men showing pneumoconiosis, 15 moderately adva and 6 in the advanced stage of the dis The men were in excellent physics' dition. The m ost striking physical found in 73 per cent, of the men, was cli fingers which tw o-thirds of the wo developed in the first year of employ Dust concentrations were determii the U. 8. Bureau of Mines, b u t unfortur aie not included in this paper. The is a valuable contribution to the liter on the silicosis hazard from amo silica.--T . H. Molding P ow der as a C ause o r P' nart D ust D isease. A. Abr STINO rratj, lost, lelli. vol. )DS, ITMw, er~ soire ts at of ,d n '3 S ) i i i ABSTRACTS 7 lation of sandstone a t quarries and on prem ises worked in conjunction therewith; 322 cases, including 87 deaths, in the pottery industry; 81 cases, including 32 deaths, in the metal industries, including metal grind ing and sandblasting; and 91 cases, including 20 deaths, in coal mines." It is a regrettable fact that while we in the United States, have abundant evidence to day of instances of both diseases we have not even an approximate idea of our sta tistics thereon. An excellent bibliography of 14 references to British publications, mostly governmen tal, is appended. Observations and Studies on Silicosis bt D iatomaceocs Silica. R. T. Legge, and E. Rosencrantz. Am. Jour. Pub. Health, Oct., lOSt, vol. t t , pp. 1056-1060. This paper summarizes the findings and recommendations of an investigation of the silicosis hazard among workers engaged in mining diatomaceous earth in Santa Barbara County, California. The deposit is com posed of fossilized diatomes and marine algae, and contains about 85 per cent, free silica. Workers are Mexican Indians, selected by physical examination, and the authors state that these people have the highest tuberculosis rate in this country. One hundred and eight were given X-ray examinations. The ages ranged from 19 to 56 years, and length of employment from less than 1 to more than 5 years, 33 per cent, having worked there 5 years. Pneumoco niosis of various degrees was present in 68.5 per cent, of the cases, 60 men showing early pneumoconiosis, 15 moderately advanced, and 6 in the advanced stage of the disease. The men were in excellent physical con dition. The most striking physical sign, found in 73 per cent, of the men, was clubbed fingers which two-thirds of the workers developed in the first year of employment. Dust concentrations were determined by the U. S. Bureau of Mines, but unfortunately e not included in this paper. The article a valuable contribution to the literature on the silicosis hazard from amorphon silica.--T. H. Molding Powder as a Cause op P ulmonabt D ust D isease. A . Abraham. Abatr. as follows from Klin. IVochschr., 19St, vol. 11, pp. 1110-lllS, in Chem. ' Abstr., lOSt, vol. t6, p. 6036. Four case reports on injury from the manufacture of clay molding powder con taining quartz, 31.17 per cent., feldspar, 50.4 per cent., and soluble silica, 1.79 per cent.; and lime molding powder containing quartz, 0.87 per cent., feldspar, 0.43 per cent., and soluble silica, 1.29 per cent. Cement D ust Inhalation and Spread op T uberculosis in Guinea-pio Luncs. J. Grober, and G. Riemerschmid. Abstr. as follows from Beilr. Klin. Tuberk., 10S1, vol. 78, pp. ttt- tS l, in Chem. Abstr., lOSt, vol. S6, p. 6011. A series of guinea pigs was placed in the dustiest region of a cement establishment for 5 months after which it was found that the ash content of the lungs was greater than that of control animals while the cal cium content of the lungs hardly differed from th at of the cement-free animals. Twenty-four cement animals and an equal number of controls were injected intraperitoneally with human tubercle bacilli. The cement animals revealed the usual spread of tuberculosis but they rarely, in contrast to the non-cement animals, showed tubercu lous changes in the kidneys or adrenals and still more rarely in the lungs, pleura, heart or bronchial glands. The pulmonary con dition in the cement animals appeared to be less progressive than th a t of the controls. Whether this was due to a local deposition of calcium substances resulting in a chem. influence upon the lung tissue or a general change in the body as a whole requires ex planation. Observations on the P neumoconioses. E. H. Kettle. Abstr. asfollowsfrom Brit. Med. Jour., 19SS, Aug. IS, pp. S81-8S, in Bull. Hyg., lOSt, vol. 7, p. 607. A thoughtful consideration is presented of present knowledge on dust diseases of the lungs. Most is known regarding the action of silica dust; still it is not clekr whether the characteristic nodule originates in the lo calization of silica-containing phagocytes in pulmonary adenoid tissue, or as collagen de posited about silica-containing phagocytes 42 THE JOURNAL OF INDUSTRIAL HYGIENE ABS also presented. In connection with granite dust (25 to 40 per cent, quartz) the author points out that silicosis develops much more slowly than in an exposure to pure quartz dust and attributes this slower reaction to the possible neutralizing or inhibiting effect of the other constituents of granite. Atten tion is invited to the limitations of our present knowledge of many of the problems involved in pneumoconiosis and the need for more study of different types of dust both in the pure state and in measured com binations.--J. J. Bloomfield. Siucosis or Pneumoconi0818 in Vermont Gbanite Cutters and Slate Workers. Edward J . Rogers. New England Jour. Med., August 4, 1999, vot. tOV, pp. 909-908. The author, who is the Medical Director of Vermont Sanatorium, has had excellent opportunity to observe pneumoconiosis and silicosis in Vermont during the twenty years of his service. He states that silicosis has been found by Jarvis, Russell, and others to be present in nearly all granite cutters. He quotes Russell that Italian and Swiss form the higher percentage of workers, the Scotch next, and Americans third. The amount of silicosis found appears to be directly proportional to the concentra tion of dust to which the worker is exposed. He comments on the absence of physical signs of disease in the chest and emphasizes the importance of dyspnea as an early symptom. Subsequent symptoms are dis turbance of digestion, loss of weight, defi nite fatigue, and pleurisy. Occasionally the patient has a frank hemorrhage. There is also fever, which is not apt to be high. The prognosis of tuberculosis in Silicosis is bad. Men break down with it several years after leaving their dusty work. The author states that the amount of free silica in slate dust is probably greater than in granite dust. Finely powdered slate is, therefore, very dangerous to those exposed to inhaling it. However, the author is under the impression that the death rate from tuberculosis in the slate district is not as high as in the granite district. He points out that workers in marble dust appeared free of pneumoconiosis and tuber culosis.--W. 1. Clark. Severe Silicosis in R elation to Woszmen's Compensation Laws. B. Btisi. her. Schrifl. a. d. Gesamlgeb. d. Genttbehyg. No. 49,1999, pp. 84. This monograph on the relation betweea the X-ray and clinical findings in silicon* is founded on the author's examination of 450 workmen who were exposed for seversl years to the inhalation of dust containing silica. Of these 338 were miners. Of M cases the author gives a ifisumfi of the pi*cedings, of the X-ray, and the clinical find ings. As an objective test of the respira tory function he notes the time which the patient is able to hold his bTeath during which time his heart action is observed, and he watches toward the end of that time for symptoms of congestion such as accelera tion of pulse, breathing rates, and swelling of the arm veins. During the entire exami nation breathing rates are observed. In all the cases he shows statistically that small chest expansion and small lung displace ment are not necessarily typical for silicosis. The author reports 63 cases in which he finds a discrepancy between the X-ray sad the respiratory function excluding all cases ; of insufficiency from other etiology thaa l silicosis. In 30 of these 63 cases he finds a severe decrease in function with only slight h signs of fibrosis; in 33 cases the X-rays show I a silicosis of second to third degree without | marked change in the respiratory function. I From this he reasons that it is not the fibre- I sis which produces the clinical signs of I silicosis and he agreeB with Reichman that I emphysematous silicosis is not compenaa- 8 tory but a result of shrinking, traction, and 8 resistance. This in itself perhaps causes 8 a decrease of function so that in the most 8 severe cases emphysematic parts and tent- 1 like tractions of the lungs due to shrinking 8 are almost detectable in the X-ray. Re 8 advances the theory that changes in the , 8 permeability of the walls of the alveoli v j result from mechanical irritation by dust particles. He attempts to explain the fact that partioles of other dusts do not prodoe* d H the same effect on the respiratory function; and believes that since phagocytosis of M U silica particles is slower than for otbef dusts, these latter remain in the alveoli n iy ^ H shorter time than does silica. His explsastion is not altogether convincing since the i S H tSeet of silica inhalation on the respirato 'action is not only quantitatively b qualitatively different from the effect .her dust. Rcintker admits th at his theory of t. decrease in the permeability of the alve< being the reason for the decrease in resph lory function is only a conjecture, as neith the X-ray nor the histological find ngs so port bis theory. The author ends with demanding th a t t decrease in respiratory function must considered more thoroughly than it is n bymost German physicians who give exp opinion in cases of silicosis. He com psr the finding of fibrosis in cases of silicc to the finding of granulated erythrocytes lead poisoning, admitting the fibrosis oi as an indicator th at silicosis exists a t ; but he denies th at the degree of fibrosis < be used as a test for the gravity of the d cue.--K. Stfiber. Pneumoconiosis. J . R. TodhutUer and B. Dixon. Lancet, November 19, 19 p. 1199. Attention is drawn to pneumoconiosis o to other dusts than silica. Five cases ' quoted in detail; in one the authors cla the condition to be indistinguishable fr< silicosis; it occurred in a grease-mopper, a was associated with pulmonary tubercu sis. The second was somewhat similar, a occurred in a general laborer; the th. affected an emery-wheel grinder; so did ( fourth, which was associated with pulm aary tuberculosis; the fifth and sixth w similar, there was fibrosis and pulmon' tuberculosis after long exposure to em dust. The type of fibrosis, as seen pc mortem, while somewhat similar to that silicosis, seems to have been less defit Men so affected experience an undue n tality from respiratory diseases, and gren ` tare should be taken to safeguard them f the dust risk. There seems no good rea why such affected workers should not k awarded compensation, just as in the < i of silicosis.--E. L. C. Y Pulmonart Asbestosis. P . EUman. L m eel, 1999, February 4, PP- 969-69. The clinical, radiological, and pathol r cal features of pulmonary asbestosis ABSTRACTS 43 >*el of silica inhalation on the respiratory 'action is not only quantitatively but -joilitatively different from the effect of '.her dust. Beintker admits th a t his theory of the decrease in the permeability of the alveoli Vina the reason for the decrease in respira tory function is only a conjecture, as neither the X-ray nor the histological find ngs sup port his theory. The author ends with demanding th a t the Wrcase in respiratory function must be considered more thoroughly than it is now by most German physicians who give expert opinion in cases of silicosis. He compares the finding of fibrosis in cases of silicosis to the finding of granulated erythrocytes in lead poisoning, admitting the fibrosis only u an indicator that silicosis exists at ail, hut he denies that the degree of fibrosis can he used as a test for the gravity of the discsse.--K. Stttber. Pneumoconiosis. J . R. Todhunter and G. B. Dixon. Lancet, November 19, 1989, p. ms. Attention is drawn to pneumoconiosis due to other dusts than silica. Five cases are quoted in detail; in one the authors claim the condition to be indistinguishable from iticosis; it occurred in a grease-mopper, and was associated with pulmonary tuberculolis. The second was somewhat similar, and occurred in a general laborer; the third affected an emery-wheel grinder; so did the fourth, which was associated with pulmo nary tuberculosis; the fifth and sixth were similar, there was fibrosis and pulmonary tuberculosis after long exposure to emery dust. The type of fibrosis, as seen post mortem, while somewhat similar to that of silicosis, seems to have been less definite. Men so affected experience an undue mor tality from respiratory diseases, and greater care should be taken to safeguard them from the dust risk. There seems no good reason why such affected workers should not be awarded compensation, ju st as in the case of silicosis.--E. L. C. Pulmonary Asbestosis. P. Elltnan. Lan cet, 19SS, February 4, VP- 959-58. The clinical, radiological, and pathologi es! features of pulmonary asbestosis are discussed from the author's personal ex perience. Dyspnoea is an early symptom, associated with a hard, non-productive cough. Anorexia was not unusual, and loss of weight out of proportion to the physical signs was a distinctive feature. Asbestos corns on the skin of the hands were often noted. The characteristic changes con sisted of basal diffuse fibrosis, while the apices of the lungs were often hardly in volved. The condition tends to interfere with the functions of the lungs, and to pro gress to a fatal issue more inevitably than does simple silicosis. On the other hand the tendency to succumb to inter-current tuberculosis is not so pronounced in asbes tosis. Asbestos bodies are usually to be found in the sputum, and in the lungs post mortem. When these bodies are found in clumps, they usually indicate the occur rence of disintegration of lung tissue. Ap parently asbestos falls with silica into the group of active dusts which produce lesions in the tissues due to their toxic action after passing into solution. Such active dusts exert a definite influence on tuberculous infection, and assist the growth of the tuber cle bacillus. In the author's series of 17 cases, 6 had tuberculosis. Serial skiagrams are of gTeat value in following the progress of any case.--E. L. C. Silicosis and Allied D iseases o r the Lunob. M. J . Stewart. Lancet, 19SS, February 4, VP- 989-954. A discussion was started by Professor Stewart at the Liverpool Medical Insti tution upon pneumoconioses. He distin guished between anthracosis, silicosis, and asbestosis, particularly indicating how the pathological characteristics of the two last named varied. He claimed that asbestosis was a more serious disease, proving fatal after 13 to 15 years employment, as com pared with 32 or even 42 years in silicosis. Nevertheless, the tendency to tuberculosis was significantly less in asbestosis than in silicosis, a possible reason being that asbestosis was much more rapidly fatal, and so did not give tuberculosis a chance to develop. The tendency for pulmonary fibrosis in asbestos workers to be mainly a t the base may be due to the action of gravity causing the long fine fibres to 44 THE JOURNAL OF INDUSTRIAL HYGIENE pass downwards in the lung rather than in any other direction. An interesting dis cussion followed, to which Professor Dible and Professor Beattie contributed. One interesting point was the extent to which women rather than men succumb to asbestosis.--E. L. C. I nfra-R ed P hotomicrographs op the Asbestosis Long. S. R. Gloyne. Tuber cle, 1933, vol. 14, no. S, pp. 908-309. Interesting infra-red photomicrographs are published in contrast with illustrations taken on ordinary plates. The infra-red method without doubt shows up asbestos bodies in lung sections in far finer detail than does ordinary microphotography. The interest in this note lies in the possibili ties it suggests of the use of infra-red pho tography in pathological work.--E. L. C. Occupation and R espiratort D iseases. A. E. Russell. South. Med. Jour., 1939, vol. 95, pp. 919-996. A summary of the knowledge on the rela tion between occupation and respiratory diseases is given. Some information is pre sented concerning the occurrence of silicosis in groups of granite workers. A steady rise in sickness and also in the prevalence of active cases of tuberculosis occurred in direct proportion to years of service in the industry and extent of dust exposure. These two groups of granite workers were exposed to an atmosphere containing 20 to 60 millions particles per cubic foot of air. The increase in morbidity and the preva lence of tuberculosis was not experienced by groups of workers who were exposed to less than 20 million particles per cubic foot of air. No such frequency of disability from tuberculosis occurred in other Industrie!, two of which, anthracite coal mining and cement manufacturing, were dusty. The incidence of pneumonia in these last two industries was less than th at of employees in general manufacturing. Workers in the granite and gold mining industries (both of which have silica dust hazards) had pneu monia in excess of those engaged in general manufacturing. I t was shown that the dust hazard in the granite industry became excessive with the introduction of pneu matic tools and th a t while the death rate from tuberculosis in the general population has decreased in recent years, in certain dusty trades there has been an increase during the same period.--A. E. Russell. Pneumoconiosis : A L ist op R eferences. Internal. Labour Office, Studies and Rep., Series F (Indust. Hyg.)No, 15,1939,pp. 76. "This work is published in separate edi tions in English, French, and Germancertain of the entries appear in French, the language in which the Bibliography was compiled. . . References are given under: (1) Pneumo coniosis (03 refs.), (2) General pathology (268 refs.), (3) Experimental Research (106 refs.), (4) Clinic (172 refs.), and (6) Pathol ogy (633 refs.). Indices by subject, country, and author follow. I t is difficult to see how anyone interested in industrial hygiene can afford not to have this book readily accessible. Authors and students will find it invaluable. (Available in America a t the World Peace Foundation, 40 Mt. Vernon St., Boston for 50 cents.) OCCUPATIONAL AFFECTIONS OF THE SKIN AND SPECIAL SENSES Copper D ermatitis. Erich Eisner. Abstr. from Dermal., Ztschr., Oct., 1939, vol. 64, p. 409, in Arch. Dermal, and Syph., Mar., 1933, vol. 97, p. 511. The author observed a patient in whom a lichenified eczema developed as a result of irritation from dust containing copper. Patch tests, as well as intra-cutaneous tests with copper sulphate solutions, were posi tive. T he D iaono8IS op Occupational D erma titis. R. M. B. MacKenna. Jour. Stats Med., 1933, vol. 41, no. 1, pp. 5-90. This paper is based on a series of 100 con secutive cases of occupational dermatitis seen in private practice. Seventy-one per cent, were males. When distributed by age the peaks are found to be: one under age 25, and a second between ages 30 and 40. Cases which develop dermatitis before 35 ABS possess to a greater degree than most a inherent susceptibility. Later in lif skilled workers may migrate to another fac lory, and meet with a new hazard, such, fo instance, as a French polisher who moved t a shop where the manager used turpentin substitute instead of turpentine, whic caused trouble; or again a painter who, a part of his work, was sent to paint a suga factory, and came in contact with dripping from sugar boilers and sugar dust; he d< veloped sugar dermatitis. In the series c cases bakers and confectioners stood toi with 24 per cent, of the cases, followed b French polishers with 17 per cent, and ct ment workers with 10 per cent. Exposur to oil claimed 8 per cent. Usually a perio of years is needed to sensitize to flour, bu 2 cases occurred after periods of 8 and 1 weeks respectively in different bakerie: Toxic absorption from septic foci is seldoi a factor in occupational derm atitis, whic usually commences as blebs on the fingei and back of one hand, which spread rapidl to the other, and then to th e forearms. T1 palms of the hands are seldom affectec The rest of the body is not often attacker but if the thighs are affected the attack i usually a severe one, mid if th e body, othr than the shoulders and upper third of th chest, is concerned, the dermatitis is usual] of great severity and wide distribution; bu such cases are rare. Prevention lies i selecting the workers, selecting material: and prophylactic measures. Much can b done in educating the workers with regar to the use of suitable cleansing material: Often the physician needs to visit the wori. shop to ascertain for himself th e nature < the hazard, which workers can seldom efi ciently describe. Differential diagnosi may be difficult; it is mainly concerned wit deciding whether or not the condition caused by occupation. In some cases t* lesions may be self-inflicted, but the malir gerer has seldom the skill to im itate derm titis lemons w ith success.--E. L. C. Tmf N urse in I ndustrt. I . H. Charlc Jour. State Med., 1933, voC. 41, no. pp. 47-59. The story is told how the Metropolis Life Insurance Company instituted i nursing service, which, far later, has spre ABSTRACTS 45 possess to a greater degree than most an to England. Groups of workers in factories, inherent susceptibility. Later in life business establishments or offices, are in killed workers may migrate to another fac sured en bloc for life, pensions, or sickness tory, and meet with a new hazard, such, for and accident. Cases of absence through instance, as a French polisher who moved to sickness are notified to the local nursing shop where the manager used turpentine association, perhaps the Queen's Institute substitute instead of turpentine, which for District Nursing, after a period of 2 caused trouble; or again a painter who, as days. On receipt of the call the nurse visits part of his work, was sent to paint a sugar and offers service. Each visit is paid for by factory, and came in contact with drippings the Insurance Company a t the rate of one from sugar boilers and sugar dust; he de shilling and fourpence. The nursing serv veloped sugar dermatitis. In the series of ice definitely decreases absenteeism, which cases bakers and confectioners stood top speeds up the productive capacity of indus with 24 per cent, of the cases, followed by try. Stress is, however, laid on the need for French polishers with 17 per cent, and ce co-ordinating all district nursing, so th at at ment workera with 10 per cent. Exposure one and the same time a health visitor may to oil claimed 8 per cent. Usually a period not be inquiring about a pre-school child, of years is needed to sensitize to flour, but and a school nurse, a district nurse, a tuber 2 cases occurred after periods of 8 and 12 culosis nurse, together with the industrial weeks respectively in different bakeries. service, be in attendance.--E. L. C. Toxic absorption from septic foci is seldom a factor in occupational dermatitis, which D ermatitis following the Wearing o r usually commences as blebs on the fingers D ted F abrics. B. M. Killick and J . T. and back of one hand, which spread rapidly Ingram. Lancet, January 14, 933, pp. to the other, and then to the forearms. The 71-30. palms of the hands are seldom affected. The authors give full particulars concern The rest of the body is not often attacked, ing a case of derm atitis resulting from a gar but if the thighs are affected the attack is ment which had been dyed black. I t had usually a severe one, and if the body, other been dyed solely with azo direct (substan than the shoulders and upper third of the tive) dyes, which are normally used. On chest, is concerned, the dermatitis is usually ``patch" investigation the patient exhibited of great severity and wide distribution; but a specific idiosyncrasy to the dye, while such cases are rare. Prevention lies in normal subjects, and individuals suffering selecting the workers, selecting materials, from other skin troubles, were negative. and prophylactic measures. Much can be The authors claim th at dermatitis arising done in educating the workers with regard from the use of paraphenylenediamine and to the use of suitable cleansing materials. allied chemicals is allergic in nature, rather Often the physician needs to visit the work than due to direct chemical irritation.-- shop to ascertain for himself the nature o4 E. L. C. the hazard, which workers can seldom effi-^V ciently describe. Differential diagnosis Anomalies in the I nterpretation of the may be difficult; it is mainly concerned with I ndustrial D ermatoses, ft. Proseer deciding whether or not the condition is White. Jour. State Med., 1933, ool. 40, caused by occupation. In some cases the no. 10, pp. 559-573. lesions may be self-inflicted, but the malin An interesting but somewhat discursive gerer has seldom the skill to imitate derma discussion upon occupational skin troubles titis lesions with success.--E. L. C. is presented. Workers may be made aller gic to many industrial agents which can Th^ N orse in Industry. I. H. Charley. cause skin trouble; b ut every catarrhal Jour. State Med., 1933, voL 41, no. 1, inflammation of the skin id not a sensitized pp. 47-53. eruption. If a skin affection is called The story is told how the Metropolitan eczema, the worker cannot establish a claim Life Insurance Company instituted its for compensation, as he can if it is chris nursing service, which, far later, has spread tened dermatitis. Once a worker is sensi- 78 TH E JOURNAL OF INDUSTRIAL H YG IENE [xv, no. 4 The author states th at radiologists morei originally described in T his Journal (vol. than any others need the salutary lessonsi 1, p. 183, and vol. 3, p. 231). Analysis of of the deadhouse to correct their visionary the ores showed them to contain 79 per interpretation of shadows, particularly of' cent, of manganese dioxide. The authors, those radiating from the roots of the lungs. however, somewhat unexpectedly attribute He states the unsatisfactory position today the toxic condition to the presence of 0.013 is due to lack of codperation between phy per cent, arsenic in the minerals. Such a sician, pathologist, chemist, and radiol small amount of arsenic present in dust ogist. would hardly be expected to exert any toxic Diagnosis.--The history, knowledge of influence.--E. L. C. working conditions, and the presence of emphysema with dyspnoea altogether out of On the Occurrence o r Clumps or Asbes- proportion to the amount of exercise, black tosis Bodies in the Sputum o r Asbestosv morning sputum and minimal physical Workers. M. J. Stewart, N. Tattersall, signs in the chest and the presence of and A.C.Haddow. Abstr. asfollowsfrom fibrosis in the roentgen examination are the Jour. Path, and Bacteriol., 1938, vol. 35, important points. pp. 787-741, in Bull. Hyg., Jan., 1983, vol. Prognosis.--If the diagnosis is made early 8, pp. 87-88. and the patient removed from the mine and The authors describe two cases in which, given an outdoor occupation, the disease in addition to single asbestosis bodies, a appears to be not only arrested but con large clump of some 20 to 30 bodies, more or siderable improvement in the lung condi less radially arranged with their bulbous tion and cardiac response takes place. extremities outward, were found. The Even the moderately advanced cases live appearance of the clumps was similar to many years in tolerable comfort. Infective what is seen in histologic sections of the conditions increase the gravity of the lung in cases of pulmonary asbestosis, disease. where clumps of bodies occur either within Prophylaxis.--Better ventilation, espe the lung alveoli or embedded in fibrous cially in dead-end places and cuttings, the tissue. universal adoption of wet drilling, and in The authors suggest that the finding of a special circumstances the use of respirators large clump or clumps of asbestosis bodies in will materially lessen the incidence of the sputum is a clear indication of disin anthracosis. tegration of lung tissue, either by a process Treatment.--The essentials are removal of of simple suppurative bronchopneumonia, the patient from the mine dust and to guard or as a result of secondary tuberculosis in against infection in an already damaged fection. They believe that the fact that lung. Gough, dyspnoea, etc. are treated the sputum is rather roughly treated may symptomatically. The author stresses the account for the rarity of these clumps; on use of various drugs and diet and when there the other hand they have never found is cardiac failure th use of venesection.-- broken-up portions which might be ex E. P. Pendergrass. pected to result from rough treatment. 1 The radial arrangement of the bodies with Poisoning bt Manganese Ores. Salmon the bulbous extremities at the periphery, and Planque. Ann. d'Hyg., Pub. Indust, indentical with that of the majority of the et Sociale, 19SS, vol. 11, pp. 196-800. clumps in lung sections, shows, the authors Some interesting cases are reported where consider, that such clumps are not artefacts men exposed to dust arising from mineral but formations built up in situ within the ores suffered from symptoms which pre lung alveolus from which they can only sented the picture of manganese poisoning. escape as a result of some secondary dis Four men were affected, who presented integrative process. \ symptoms of mental dullness, slow speech, The authors conclude that since these pain in the muscles of the limbs, and diffi- c<lumps, which are only rarely encountered, culty in walking and the steppage gait. p{oint to disintegration of lung tissue their The picture is undoubtedly the same as was p] resence in sputum is of far greater sig- July, 19SS] ABSTB nificance than the finding of single bodies.-- S. R. G. T he D ust H azard in the Cotton In dustry. F. Koelsch. Abstr. os follows from Arch.f. Gewerbepatk. u. Gtwerbehyg., 1988, vol. 3, pp. 899^411, in Bull. Hyg., Jan., 1933, vol. 8, p. 87. The quantity of dust found in cotton mills may vary widely, as much depends on the kind and quality of the cotton, on the number of machines, and on the effective ness of the exhaust ventilation. Chinese cotton gives off most dust. Among organic impurities in the dust are to be found the remains of seed pods and parts of fungi, and an analysis of the dust from American cotton shows about 50 per cent, of silica, and of the dust'from Egyptian cotton about 29 per cent. Some of this was sand. The author made some observations in a cotton mill where the rooms were spacious and well provided with exhaust ventilators and general ventilation, and where Ameri can long fiber cotton was used. Specimens of dust were taken at various places and counted with Owen's dust counter or the Zeiss konimeter. In a specimen taken near a carding machine there were 72 particles per cc. of air, of which about one-third were under 5m. and a microphotograph of this specimen shows very little dust and particu larly no fibers: this good result ia believed to be due to the effective exhaust ven tilation. DUST, SMOKE, S, AND VA AND ELD1 C ity Air Pollution and I ts Control. ' H. B. Heller. Aerologist, Feb., and Mar., 1933, vol. 9. In two articles the author gives a good ' informative resum of the air pollution problem for the lay reader, including con trol of combustion, physiologic and economic effects of pollution, and regulatory recom mendations. Possible dangers to health are rather broadly covered with embodiment of intangible results difficult of proof. Practical scientific control has outstripped ordinance requirements which should be extended to control of combustion, dust, July, 1933} ABSTRACTS 79 nificance than the finding of single bodies.-- S. R. G. T he D ust H azard in the Cotton I n* dustry. F. Koelsek. Abatr. as follow from Arch.f. Gewerbepath. u. Gewerbekyg., 1933, vol, S, pp. 399-411, in Bull. Hyg., Jan., 1933, vol. 8, p. 37. The quantity of dust found in cotton mills may vary widely, as much depends on the kind and quality of the cotton, on the number of machines, and on the effective ness of the exhaust ventilation. Chinese cotton gives off most dust. Among organic impurities in the dust are to be found the remains of seed pods and parts of fungi, and an analysis of the dust from American cotton shows about 50 per cent, of silica, and of the dust from Egyptian cotton about 29 per cent. Some of this was sand. The author made some observations in a cotton mill where the rooms were spacious and well provided with exhaust ventilators and general ventilation, and where Ameri can long fiber cotton was used. Specimens of dust were taken at various places and counted with Owen's dust counter or the Zeiss konimeter. In a specimen taken near a carding machine there were 72 particles per cc. of air, of which about one-third were under bn. and a microphotograph of this specimen shows very little dust and particu larly no fibers: this good result is believed to be due to the effective exhaust ven tilation. The long fiber cotton which comes mostly from America and Egypt scarcely reaches the lungs as the fibers are caught in the mucous membrane of the upper air passages. The short fiber cotton which comes from the East Indies and the small mineral particles are easily drawn into the lungs and there may give rise to disease. The author refers to the latest inter national literature on the subject of these diseases and particularly to several English authors. Among the diseases mentioned are simple bronchitis, strippers' asthma, chronic bronchitis, silicotic dyspnea, weav ers' cough, and tuberculosis. The author investigated the health of 34 workers who had worked in the industry over 10 years. These were examined clini cally and by X-rays and in 19 nothing ab normal was found; in 7 there was tuber culosis, but in none of these was there a family history of tuberculosis, and the remainder had bronchitis or difficulty of breathing. In no case were any changes found in the lungs resembling pneumo coniosis or pneumonomycosis.--A. J. C. I ndustrial D usts--P ulmonary T ubercu losis and Pneumoconiosis. K. W. Jitlen. Med. Lavoro, Feb. 1, 1933, vol. 34, pp. 48-80. Dusting experiments were made with a variety of industrial dusts using rabbits as experimental animals. The injurious effects of high silica dusts is emphasized.--L. T. F. DUST, SMOKE, F] S, AND VAPORS: THEIR DETERMINATION AND ELIMINATION City Air P ollution and Its Control. H. B. Metter. Aerologist, Feb., and Mar., 1933, vol. 9. In two articles the author gives a good informative resum of the air pollution problem for the lay reader, including con trol of combustion, physiologic and economic effects of pollution, and regulatory recom mendations. Possible dangers to health are rather broadly covered with embodiment of intangible results difficult of proof. Practical scientific control has outstripped ordinance requirements which should be extended to control of combustion, dust, and sulfur acids, each of which is amenable to improvement. Raising requirements will stimulate betterment in design of automatic fuel feed devices; practical dust separation equipment is on the market; and even the status of pollution by sulfur acids, which presents just now the greatest technical difficulties, may be improved by regulations stipulating as low a sulfur con tent as feasible in the fuel sold, since it is possibleto separate part of the sulfur in the coal as mined. Small apartments and homes are factors slighted in the consideration of control.--C. L. Pool. 102 T H E JOURNAL OF IN D U S T R IA L H Y G IE N E [xv, no. 6 (e) The hyaline nodules increase in size Silica, in the Organism and Siliceous by extension at their periphery. Coales Particles in Blood. L. Lematte and E. cence of adjacent nodules takes place and Kahane. Abstr. as follows from Compt, brings about involvement of further areas rend., 193S, vol. 196, pp. 676-678, in Chem. of the lung. (The conditions described Abstr., May BO, 19SS, vol. B7, p. 0,79. under (c), (d), and (e) constitute the dis A form of gelatinous silica from lung ease silicosis.) tissue, soluble in nitropercbloric aoid, is Macroscopically the changes observed in called "silica of constitution." Compact silicosis are: (a) In the early stage. A mineral particles less attacked by the acid variable number of palpable, pearly-white may come from respiratory dust. 0.3 to nodules up to 2 or 3 mm. in diameter on the 0.7 mg. silicate per gram of dry fibrin comes pleural surface of the lung. On section, the from the blood; this amount is much less cut surface of the lung is studded with pig than the content reported by other authors. mented foci, widely scattered, a moderate A deposit of silica particles of the second proportion of which are only palpable. The variety, too small to be weighed, regularly tracheo-bronchial lymph nodes may be accompanies the other. slightly enlarged and deeply pigmented, and may exhibit foci of fibrous induration. T he S ilicic Acid C ontent o r Lungs in (b) Later stages. The fibrotic nodules Pneumoconiosis. Christian Hackmann. are increased in number, size, and density, Abstr. as follows from Beitr. path. Anat., and coalescence of these may be found. 1938, vol. 90, pp. 6B3-6B6, in Chem. Abstr., The portions of the lung between the fibrotic May 10,1938, vol. 37, p. BB07. nodules may be emphysematous. The The amount of silica present in normal tracheo-bronchial lymph nodes are smaller lungs is very small during childhood but in size than those seen in the early stage and tends to become greater with increasing age. are fibrosed. In marked silicosis, injuries to the tissues The presence of tuberculous infection are usually observed when the silica content usually modified the pathological appear exceeds I per cent, of the weight of the dried ance. Special attention was drawn to the lung tissue, higher values being associated three following types: with greater degrees of injury. (a) In which the picture of silicosis above described may be little, if at all, modified, R eview of Silicosis. P art II. Adelaide but in which only a biological test can R. Smith. N. Y. Stale Dept. Labor, Indus- demonstrate the presence of B. tuberculosis. trial Bulletin, Apr., 1933, vol. IB, pp. 90-9B. (b) In which the coexistence of silicosis Factors in the development of silicosis are and typical tuberculosis lesions is easily the type and percentage of silica or silicate recognizable. in dust, the presence of other substances (c) In which the presence of tuberculosis which may complicate the physiological is easily recognizable, but the existence of reactions, the size of particles and degree silicosis is more difficult to determine. of dustiness, and the length of exposure. For compensation purposes, any stage of Breathing of dust containing free silica in silicosis that is complicated with active the cyrstalline or quartz form is most tuberculosis should be considered as causing injurious, magnesium silicate is serious in serious and permanent impairment and producing " usbestosis," and other silicates e equivalent to third stage silicosis. cause milder disease. The usual damage In order to claim compensation for silico from a high silica content appeared to be sis, the claimant must have had the equiva nullified where clay was present in the dust, lent of 2 years' aggregate employment in but in other coses the presence of alkali was an occupation or occupations involving thought to increase the severity. exposure to a silica dust hazard in the State Only particles less than 10 microns in size in which the claim is filed, unless the claim are likely to enter the lungs, but most ant was subjected to a prior physical exami process dust encountered runs smaller. nation authorized by the employer and at Much of the dust is invisible in the micro-' th at time was not found to have silicosis. --E. P. Pendergrass. scope, and even atmospheres rid of visible dust may cause silicosis. In jobs of moder- Sept., 19SS] ABST ate dustiness 20 to 50 million particles per cubic foot of air are found, but the many factors make it hard to say what exposure is safe. With granite dust of 35 per cent, free silica, 10 million per cubic foot are apparently safe. Studies and figures abroad and here exem plify the ubiquity and seriousness of silico sis and concomitant tuberculosis, e.g. in mining and quarrying in Great Britain and the colonies, Germany and Italy; amongst grinders, sand blasters, foundry molders, and pottery workers in Germany; and amongst stone masons in Holland. The American figures for similar trades are astounding when first clearly comprehended, and pertinent summaries enlighten the effects on th e lungs of spray coating, abra sives, cement, rock drilling, diatomaceous earth, slate milling, and talc mining occu pations.--C. L. Pool. Coal Miner's Lu n g : A P reliminabt Ac count o r th e C hemical Analysis and P athology of th e L ungs o r C oal M iners in N ew S outh Wales. C. Badham and II. Taylor. Med. Jour. Austra lia, April 39th, 193$. Details are given of the occupational his tory and post-mortem findings in 31 cases, of which 19 had been coal miners, 6 metal liferous miners, 1 a m etal polisher, 1 an ore miller, 2 had no dust exposure, and 2 died from tuberculosis. The special meth ods used for determining the content in the lungs of silica and silicates, and of coally matter, are described. The opinion is expressed th a t different dusts set up dif ferent types of fibrosis in the lungs. Th essential features of coal miner'aslung are upper lobe consolidation, fibrotjff nodules, non-tuberculous cavitation, ana coal dust accumulation. This condition renders miners more vulnerable to respiratory dis eases, such as bronchitis and pneumonia; in advanced cases cardiac disease with cir culatory failure is aggravated. But it is doubtful whether tuberculosis can be aggra vated or caused by a coal dust which has a high carbonaceous content. Compensation should be based upon disability which may be absent in cases with well marked radiographic fibrosis; disability can only be determined by clinical methods.--E. L. C. Sept., 1933] ABSTRACTS 103 ate dustiness 20 to 50 million particles per cubic foot of air are found, but the many factors make it hard to say what exposure is safe. With granite dust of 35 per cent, free silica, 10 million per cubic foot are apparently safe. Studies and figures abroad and here exem plify the ubiquity and seriousness of silico sis and concomitant tuberculosis, e.g. in mining and quarrying in Great Britain and the colonies, Germany and Italy; amongst grinders, sand blasters, foundry molders, and pottery workers in Germany; and amongst stone masons in Holland. The American figures for similar trades are astounding when first clearly comprehended, and pertinent summaries enlighten the effects on the lungs of spray coating, abra sives, cement, rock drilling, diatomaceous earth, slate milling, and talc mining occu pations.--C. L. Pool. Coal Miner's Lung: A P reliminary Ac count of the C hemical Analysis and P athology of the Lungs of Coal Miners in New South Wales. C. Badham and H. Taylor. Med. Jour. Austra lia, April $9lh, 19SS. Details are given of the occupational his tory and post-mortem findings in 31 cases, of which 19 had been coal miners, 6 metal liferous miners, 1 a metal polisher, 1 an ore miller, 2 had no dust exposure, and 2 died from tuberculosis. The special meth ods used for determining the content in the lungs of silica and silicates, and of coally matter, are described. The opinion is expressed that different dusts set up dif ferent types of fibrosis in the lungs. Th essential features of coal minerVlung are upper lobe consolidation, fibrotp nodules, non-tuberculous cavitation, and coal dust accumulation. This condition renders miners more vulnerable to respiratory dis eases, such as bronchitis and pneumonia; in advanced cases cardiac disease with cir culatory failure is aggravated. But it is doubtful whether tuberculosis can be aggra vated or caused by a coal dust which has a high carbonaceous content. Compensation should be based upon disability which may be absent in cases with well marked radiographic. fibrosis; disability can only be determined by clinical methods.--E. L. C. I nfra-red P hotomicrographs of the AsbestosisLung. S.R.Gloyne. Tuber cle, Feb., 19SS, vol. IB, p. $08. The article describes a preliminary at tempt to employ infra-red photography in the study of inhaled particulate matter. " The photomicrographs reproduced (in the article) are taken on Ilford infra-red plates, using a `pointolite' lamp for illumination and the infra-Ted filter. A 1/12 in. oil immersion lens was used in all cases.'' Focusing could not be carried out with the filter in place. "In each case a control photograph was first taken of identically the same field with an Ilford fine grain ordinary plate" and with this same focus a second exposure was then made on an infra red plate. "The exposure of the latter was, however, 15 to 20 seconds longer." A series of comparative photographs of asbestosis bodies indicates that in infra-red plates the detail is somewhat more pro nounced, some of the bodies invisible in ordinary light are clearly discernible and the black pigment frequently seen in asbes tosis does not register. However the author admits that these differences may be due to the fact that the infra-red filter alters the focus.--Leroy U . Gardner. T he E ffect of Cement D ust upon Work ers. A. E. Russell. Abst. asfollowsfrom Am. Jour. Med. Sci., 1938, vol. 185, p. 330, in Can. Med. Ass. Jour., June, 1933, vol. $8, p. 687. The purpose of this investigation was primarily to measure in terms of physical condition and disabling sickness, the effects upon the workers of exposure ito known quantities of cement dust. The study was conducted throughout a period of nearly three years. The workers were examined twice during this period and where indicated special examinations and x-rays were made. If an employee remained away from work on account of illness the exact nature of the illness was ascertained. In the mill where the investigation was conducted the air contained from 22 to.63 million particles per cubic foot of air. These particles were not larger than 10 microns. -Chemical analysis showed that cement contains about 62 per cent, lime and 22 per cent silica. Other constituents 126 TH E JOURNAL OF INDUSTRIAL HYGIENE [xv, no. 6 diarrhea and abdominal cramps in 1925; the result of treatm ent makes the diagnosis in 1926 be complained of mental confusion, of multiple sclerosis unlikely. That the incoordination, pain in the back, weakness convulsions were in the nature of tetany of the legs and twitchings of the arms. seems to be borne out by their appearance Examined in April, 1927, he displayed pal* while the patient was on a low calcium diet, lor, a lead line on the gums, exaggerated by spectacular improvement following equal reflexes and lead in both urine and treatment with calcium and by the exist feces. The blood pressure was 120 systolic ence of the Chvostek and Trousseau, phe and 80 diastolic, and never exceeded 130 nomena. The second spell occurred in the systolic at any time during the illness. The course of a diarrheal disease when the hemoglobin in April, 1927, was 85 per cent., gastro-intestinal tra c t was unable to ab and there were no stipple cells. sorb injected calcium. Treatment during the first 4 days con sisted of the administration of 4 cc. of syrup of hydriodic acid every 3 hours; during this phase of the treatment the output of lead in the excreta increased. Mobilization was P revention of Lead P oisoning in Indus try. G. H. Gehrmann. Am. Jour. Pub. Health, July, 1989, vol. 98, pp. 687-899. attempted on the fifth day, calcium lactate 1 gm. and 1 quart of milk (each twice a day) being given. In a month the lead line had disappeared, and lead disappeared from the urine and feces. In Jan., 1928, the patient was sufficiently improved to permit de-lead Lead P oisoning in a G lass B ead C olor ing Works. F. W. Bickerl. Abate, from Zentralbl.f. Gewerbehyg., 1989, vol. 19, pp, 911-919, in Bull. Hyg., June, 1988, vol. 8, p. 400. ing. This was done by giving 1 gm. of Colored gloss beads are a t present pre ammonium chloride every hour and by pared by introducing the color, mixed with requiring of the patient a calcium-poor white lead, inside the bead by an instrument diet. Included in the dietary were meat, resembling a pipette with a fine drawn-out liver, potato, rice, fruit and all milk-free' point. Women who do this work a t home foods; forbidden were milk, eggs, and green warm the nozzle of the introducer between vegetables. Early in March, the patient their lips after every two or three beads. reported that he had never felt better in An expert woman can do five gross of beads his life; but on March 11, 1928, he experi in one hour, and so brings to her mouth enced a series of tetany-like convulsions, the color containing white lead 200 to 300 with periods of pronounced cyanosis and times an hour. Five women affected with marked apnea; each seizure began with lead poisoning were found. Although the twitching of the muscles of the right eye teeth in all had been well cared for, all pre and spread to the entire body. Chvostek's and Trousseau's signs were elicited between attacks. Following the intravenous ad ministration of 60 gm. of calcium chloride, sented a distinct blue line, as well as small bluish patches on the mucous membrane inside the cheeks on a level with the lower teeth. Numerous basophilic punctate red the patient experienced relief. During blood corpuscles were found and there was the next 6 months he was well, but in the hematoporphyrinuria. The women com fall of 1928 he began to become worse. plained of pains in the limbs, especially in Headaches, confusion, and right hemiano- the calf muscles, and headache with loss of pia appeared. In Dec., 1928, a second series appetite. When the cause of the illness was of convulsions occurred; they were similar recognized the use of white lead was stopped in type and in response to treatment to the and titanium dioxide used in its place. earlier seizures. The patient gained very slowly, his mental state remaining confused, Investigation of Lead Content in the and he died in Nov., 1929, of acute broncho T artar and S aliva of Workers in the pneumonia. Lead Industry. J . Schmidt. Zeniralbl. The case is almost certainly one of lead encephalopathy; the chemical components of the blood and urine rule out uremia, while f. Gewerbehyg., May-June, 1983, N. S. vol. 10, pp. 101- 104. - Lead determinations were made on the Hov., 1938) ABSTRA tartar and saliva of a number of workers in oi the lead industry, a group of people suffer- A ing from lead poisoning, and on a rabbit and turtle which had been given lead poi- I zoning artificially. A control lead deter mination was carried out as a check on the method of analysis. The results show that there is no relation between the symptoms of lead poisoning and the lead content in the tartar, and th a t the lead content of the p tartar can therefore not be used as means o of diagnosis. There is furthermore no tela- t tion between the "lead line" and lead con- , tent of the tartar. In no instance was any 1 lead found in the saliva. i The author concludes th a t lead deter- 1< mination of the saliva or ta rtar as a method < / DUST HAZARDS AND T he M orbid Anatomy and H istology of Asbestosis. S . R. Gloyne. Tubercle, July, 1988, pp. 448-461. Asbestos dust differs greatly in structure and chemical composition. Occupational conditions in mines, quarries, and factories, so vary the exposure to dust that some workers experience massive, rapid doses, ; while others have only slow and gradual exposure to small doses. Operatives range . from strongmen to weakling girls, whose pul- i monary tissue is not identical. Other dis eases may confuse the pathological picture. Peculiar long needle-shaped particles char acterise asbestos dust; the resulting fibrosis is diffuse, silicotic nodules being absent. The changing conditions lead to unusual forms of asbestosis. In the pleura the dis ease is marked by the obliterative nature of the process. The naked eye appearance of a lung is characterised b jj dense blueblack areas corresponding to Vie secondary , lobules, surrounded by thick bands of inter lobular connective tissue, generally with a reddened background of terminal broncho- ` pneumonia in the less affected portions of the lung. Signs of disease in other organs are few. An excellent colored plate exhibits the naked eye appearance.--E . L. C. / T he M orbid Anatomy and H istology of Asbestosis. S . R. Gloyne. Tubercle, Aug., 1983, pp. 498-497. This article is a further contribution by Nov.,`l933] ABSTRACTS 127 tartar and saliva of a number of workers in the lead industry, a group of people suffer* ing from lead poisoning, and on a rabbit and turtle which had been given lead poi soning artificially. A control lead deter mination was carried out as a check on the method of analysis. The results show that there is no relation between the symptoms of lead poisoning and the lead content in the tartar, and that the lead content of the tartar can therefore not be used as means of diagnosis. There is furthermore no rela tion between the "lead line" and lead con tent of the tartar. In no instance was any lead found in the saliva. The author concludes that lead deter mination of the saliva or tartar as a method of diagnosing lead poisoning is aimless.-- A. D. B. Lead in the Crbro-spinal Fluid after Lead P oisoning. M. Kasahara and K. Arimichi. Abstr. at follows from Z. get. exp. Med., 1932, vol. 81, pp. 698-897, in Physiol. Abstr., Aug., 1933, vol. 18, p. 370. Dogs and goats were used and the lead given per os. The cerebro-spinal fluid was obtained by suboccipital puncture and the lead estimated by Nakaseko's method. A goat of 15 kilo weight receiving 270 g. lead acetate in 10 days showed 0.95 g. lead in 10* cc. fluid. In dogs the fluid was col lected from 5 poisoned animals and 0.28 g. of lead per 10* cc. of fluid found. DUST HAZARDS AND TH EIR EFFECTS T he M orbid Anatomt and H istoloot of Asbestosis. S. R. Gloyne. Tubercle, July, 1933, pp. 445-451. Asbestos dust differs greatly in structure and chemical composition. Occupational conditions in mines, quarries, and factories, so vary the exposure to dust that some workers experience massive, rapid doses, while others have only slow and gradual exposure to small doses. Operatives range from strongmen to weakling girls, whose pul monary tissue is not identical. Other dis eases may confuse the pathological picture. Peculiar long needle-shaped particles char acterise asbestos dust; the resulting fibrosis is diffuse, silicotic nodules being absent. The changing conditions lead to unusual forms of asbestosis. In the pleura the dis ease is marked by the obliterative nature of the process. The naked eye appearance of a lung is characterised bjfi dense blueblack areas corresponding to t'ie secondary lobules, surrounded by thick bands of inter lobular connective tissue, generally with a reddened background of terminal broncho pneumonia in the less affected portions of the lung. Signs of disease in other organs are few. An excellent colored plate exhibits the naked eye appearance.--E. L. C. T he M orbid Anatomt and H ibtologt of Asbestosis. S. R. Gloyne. Tubercle, Aug., 1933, pp. 493-497. This article is a further contribution by the above author and deals with the asbes tos fibre and the tissue reaction it provokes. The asbestosis lung shows five kinds of par ticles: (a) carbon pigment common to all town-dwellers; (b) amorphous brown pig ment, presumably blood; (c) sharp jagged particles, probably carbonaceous; (d) the asbestos fibre, and (e) the asbestos body. Asbestos fibres may also be found in the upper respiratory tract. The tissue reac tion is three-fold: (a) thickening of the fibre by deposition of organic iron-contain ing material to form the asbestosis body; (b) cellular changes, of which the chief are accumulations of large phagocytic dust cells and asbestosis giant cells; and (c) the fibro sis common to all forms of pneumoconiosis. The asbestosis giant cell is not a cell in the true sense, as is the tuberculosis giant cell. I t is a minute collection of phagocytes, fused together, and is an attem pt on the part of the tissues to protect themselves against an irritant which cannot be lysed or absorbed. A characteristic immobiliza tion, with long persistence, of phagocytes occurs, expecially of the asbestosis giant cell. The subject is to be continued.-- E. L. C. T he M orbid Anatomt and H istoloot of Asbestosis. S . R. Gloyne. Tubercle, Sept., 1933, pp. 550-558. This article 1b th e last of a series by the same author dealing with asbestosis; it is 128 THE JOURNAL OF INDUSTRIAL HYGIENE [xv, no. 6 concerned with microscopic appearances. The characteristic of the asbestosis lung is the holding up of the dust fibres at the distal end of the respiratory bronchioles and in the alveolar ducts, with a cellular reaction of large mononuclear phagocytes and the occurrence of asbestosis giant cells. Later the lymphatics and adjacent air sacs are blocked with the dust and phagocytes. Finally, an increase of connective tissue follows round the bronchioles, alveolar sacs, capillaries, and venules, in the inter lobular septa and beneath the pleura, com pletely obliterating all lung configuration. The characteristics of asbestosis are its diffusencss, its tendency to affect the lower lobes and set up pleural adhesions, the pres ence of asbestosis bodies, and concomi tant tuberculosis and bronchopneumonia.-- E. L. C. R apid D evelopment from Latent to Severe Silicosis. Friedrich Scheidemandel. Zischr. f. Tuberk., 1933, vol. 67, pp. 341-346. A case report is given of a man who had worked as a stone cutter for 29 years and who became ill in 1929, with pulmonary symptoms of cough, dyspnea, and weight loss which lead to roentgen examination. From this a diagnosis of bilateral tuberculo sis was made. No evidence of pneumoco niosis was seen. Repeat films were made and not until July, 1931 was definite evi dence of pneumoconiosis seen. The man died in April, 1932and a post mortem exami nation was made in June, 1932 at the re quest of the Union to which the man be longed. Microscopic evidence of silicosis was found. I t is concluded that there was so-called latent, unrecognized pneumo coniosis present at the first examination and that this progressed rapidly under the stim ulation of the tuberculous infection. The German law regarding the compensa bility of dust diseases is briefly discussed. The clinical signs of dyspnea and impaired circulation combined with unmistakable roentgen evidence of pneumoconiosis are necessary for this occupational disease to be considered worthy of compensation. I t is only when tuberculosis is combined with pneumoconiosis that the former is com pensable. The author believed the law is a bit too rigid in its terminology as there are cases where silicosis is present in sufficient degree to cause symptoms but not to result in definite roentgen changes. Mention is made of the chemical effect of silica in the alkaline body fluids; also the experimental proof that silicosis favors the development and progress of a tuberculous infection. The necessity for autopsy exam ination for the conclusive diagnosis of sili cosis in certain cases is noted. Reproductions of four roentgenograms are given.--E. P. Pendergrass. Etiology of S ilicosis. A. J. Lama. Jour. Am. Med. Assn., August 19, 1933, vol. 101, p. 683. This paper reviews briefly the known facts, discusses the recent Pichcr studies, enumerates some of the common causes of silicosis, and concludes with the following: " Silicosis is a widely spread occupational disease and its peculiar relationship to tuberculosis, the difficulties of diagnosis, and the extreme difficulty associated with efforts for prevention and control, all com bine to make it a disease of major impor tance. For this reason, I desire to empha size most strongly the necessity for the pre cise recording of the patient's occupation, both by physicians ana hospitals, especially in cases which present pulmonary symp toms. Not merely the patient's present but also his previous occupations should be ascertained. Recent investigations and studies have revealed various types of pneumoconiosis which tend to confuse further both diagnosis and prognosis. This makes imperative an accurate marshalling of all the etiologic factors in the consideration of any case in which the inhalation of silica dust is con cerned." T he C linical Manifestations of Sili cosis. R. R. Sayers. Jour. Am. Med. Assn., August 19,1933, vol. 101, p. 680. As the author points out, this paper is essentially a review of the three papers recently published by him with Meriwether, Lanza, and Adams.--P. D. Silicon D ioxide Content of Lungs in H ealth and D isease. IF. D. McNally. Jour. Am. Med. Assn., August, 1933, vol. 101, p. 684. This is a review with numerous references followed by tabulations of analytical data Nov., t9SS] A from the author's autopsy material. V his analytical procedure may be questr he shows th at silicosis can be unfail proven by analyses of the lungs a t aut< He suggests 1.13 mg. of silica per grr dried lung as the normal. Specimens nitely silicotic contained varying am< up to 26 mg. per gram of dried lung.-- Mineral Matter in Lonqs. W . E . C Brit. Med. Jour., Sep. 9, 1933, p. 49* A method is given for preparing material so as to detect its mineral coi The tissue is digested for 2 or 3 days trypsin; then the turbid fluid is centri and examined. Next the remaining and lung are reincubated for 24 hour; acidified; then the fluid is centrifug. before and examined. Finally the de; in the centrifuge tubes aVe .mixed strong sulfuric acid and potassium bi m ate and boiled; then the tube is c fuged and the deposit examined as b The first deposit contains carbonaceou other mineral particles; the second cor in addition carbonaceous and "c> m atter; the final deposit contains ; insoluble silicates, diatoms, etc., free organic and "coaly" matter.--E. L. C T he Silica Content of Lungs. . Sladden. Lancet, Ju ly IB, 1933, 193-195. Facts are presented gatlfered from p logical and chemical investigation < lungs from colliers, stone-masons, pc and others who were exposed to indr dusts. No effort is made to distil! between silica and silicate in analyzin dried lung substance. The records divided into six groups uncording 1 silica content of the lung;*his group found to agree with the aniounts of fi' present in the lungs; the higher is th centage of silica, the greater is the an, of fibrosis. Coal-dust alone, apart silica, was not found to cause serious sis. The conclusion is stated th at the silica content exceeds 1.0 per ce< the dried lung substance, fibrosis, ci contributory towards death, is u. present; quantities below this an while not negligible, are seldom asso with deaths attributable to pulmonai Nov., 1933] ABSTRACTS 129. from the author's autopsy material. While his analytical procedure may be questioned, he shows that silicosis can be unfailingly proven by analyses of the lungs at autopsy. He suggests 1.13 mg. of silica per gram of dried lung as the normal. Specimens defi nitely silicotic contained varying amounts up to 26 mg. per gram of dried lung.--P. D. Mineral Matter in Lunos. IP. E. Cooke. Bril. Med. Jour., Sep. 9, 193S, p. $96. A method is given for preparing lung material so as to detect its mineral content. The tissue is digested for 2 or 3 days with trypsin; then the turbid fluid is centrifuged and examined. Next the remaining fluid and lung are reincuhated for 24 hours and acidified; then the fluid is centrifuged as before and examined. Finally the deposits in the centrifuge tubes aVe .mixed with strong sulfuric acid and potassium bichro mate and boiled; then the tube is centri fuged and the deposit examined as before. The first deposit contains carbonaceous and other mineral particles; the second contains in addition carbonaceous and "coaly" m atter; the final deposit contains silica, insoluble silicates, diatoms, etc., free from organic and "coaly" matter.--E. L. C. T he Silica Content op Lunos. A. F. Sladden. Lancet, July 16, 19SS, pp. its-m. Facts are presented gathered from patho logical and chemical investigation of 60 lungs from colliers, stone-masons, potters, and others who were exposed to industrial dusts. No effort is made to distinguish between silica and silicate in analyzing the dried lung substance. The records are divided into six groups uncording to the silica content of the lung;*his grouping is found to agree with the amounts of fibrosis present in the lungs; the higher is the per centage of silica, the greater is the amount of fibrosis. Coal-dust alone, apart from silica, was not found to cause serious fibro sis. The conclusion is stated that when the silica content exceeds 1.0 per cent, of the dried lung substance, fibrosis, clearly contributory towards death, is usually present; quantities below this amount, while not negligible, are seldom associated with deaths attributable to pulmonary dia- ease, except when tuberculosis has inter vened; when the silica content exceeds 1.6 per cent., severe fibrosis, sufficient in itself to lead to death, is invariably present. Such severe fibrosis so damages the pul monary drainage system that the accumu lation of further dust inhaled is rapidly accelerated, thus greatly increasing the danger to life.--E. L. C. Silicotic Lungs: T he M inerals T het Contain. W. R. Jone. Jour, llyg., Aug., 19SS, pp. 307-369. This article is one of considerable interest.' It is written by a geologist after examining the petrology of rocks, the dust of which has been blamed for causing silicosis, and the mineral residues of 29 silicotic lungs. The author gives reasons for concluding that pulmonary fibrosis, due to dust, is not in the main caused by quartz, or free silica, but by a mineral, sericite, a hydrated sili cate of aluminium and potassium, also known as "secondary white mica." This mineral is present in minute fibres and scales in all rocks and materials incrimi nated as originating silicosis; i t is also found in the residues and the lung tissue. No quartz-bearing rocks are known to start silicosis, except those containing in abun dance fibrous aggregates of such silicate minerals as sericite and sillimanite; asbestos also is a fibrous silicate. Rocks containing a relatively small percentage of quartz, but much of these fibrous silicate minerals, have been recognized as causing silicosis. No opinion is expressed as to whether these minerals act merely as mechanical irritants, or induce chemical changes, in instigating the growth of fibrous tissue in the lungs. There are good petrological illustrations.-- E. L.C. Silicates and Silicatosis. C. P . McCord. Indust. Med., July, 1933, vol. 6, pp. $-16. "A discussion of the origin and effects of dusts containing little or no free silica." This is a review, with extensive quotations and citations from the literature. T he E ffects of C olloidal Silica on E xperimental T uberculosis in Guinea-pigs. S . L. Cummins and C. Weatherall. Jour. Hyg., Aug., 1933, pp. - 696-306.