Document 99D6GDy7dxy9X3xwpYGjnvMDV

. ` . * ' ASBESTOSIS ' . - RXTQST OF TWO USXS * x * . HAROLD L. STEWART, MJ5- CARL J. BUCHER. 1LD. Ajn ' ERNEST H. COLEMAN. M_D. wusxuitu . : ' s . iijl! - ''v' Asbestos u such was known to PUay. Charlemagne is said to have' possessed a table doth made of it. which was deaased by passing through lire. The mineral deposits of asbestos are found in Canada, Italy.. Africa and Rhodesia. It is a silicate occurring in minerals is combine- cion with iron, copper, calcium or magnesium. It occurs in the form of libers which an be woven. In addition, finer pacddes are used is the manufacture of sheeting, tiles, asbestos millboard and paper. The increasing need for brake linings for motor cars, fireproof curtains,, insulations, mattresses and steam packings has expanded the spinning industry considerably. The use of the dust in cement and plaster Tor the erection of fireproof buildings has increased the danger of inhalation in the most hazardous form of the industry. Its expansion from 500 tons in 1880 to 330.000 tons in 1925 and the fact that methods of manu facture have been introduced, for utilizing the fine dust for new purposes- hare contributed to the beginning appearance of a pneumokoniosis due to inhalation of asbestos dust,1 known as pulmonary asbestosis. : In 1906, Montague Murray * presented evidence before the Depart mental Committee on Compensation tor Industrial Diseases, that be had had under his care in 1900 a worker employed in an asbestos factory who developed respiratory symptoms and died. At the autopsy* extensive pulmonary fibrosis was found, which Murray attributed to inhalation of asbestos dust. . . In 1924. eighteen years later, Cooke * reported a similar case com plicated by pulmonary tuberculosis. He was the first to describe the * Submitted for publication. July 17. 1931. * * From the Department of Pathology, Jefferson Medical College and Hospital, aided by a grant from the Martin Research Fuad 1. Mcrrtrether. E. R. A.: J. Indus*. Hyg. 12:198. 1930. 2. Murray. Montague: Departmental Committee on Compensation for Indus- tj1 Diseases. Mimttcs of Evidence. Appendices and Index. 1907. Cd. 3496. p. 127; Re. n 1907. Cd. 3495, p. 14. >. Cooke. \V. .: Brit. M. J. 2:147. 1924 ; 2:1(124, 1927. ' . '.yag , :a*AT sj , .. - - |m*^5m3* ' *. - V 916 ARCHIVES Of PATHOLOGY Oar second case confirms previous observations that the asbestoss bodies have a tendency to disappear in a caseous area. We have also shown that in such an area following an add-fast stain (25 per cent nitric add) the bodies do sot stain so well for iron and have a less definite morphology, but are sdQ recognizable as such, so that if these are present in the sputum in any case, they should be recognized on a routine smear eves after it has been treated with add. The finding, of tsberde baefli in the sputum in the second case on two different occasions, plus the gross and microscopic features charac teristic of tuberculosis, is sufficient to establish such a diagnosis. It is significant, however, that many more specimens of sputums were exam ined far add-fast badUi in which none were found, and that no one noted the asbestosis bodies in the sputum, although these were not being looked for specifically. An important additional finding in case 2 was that of asbestosis bodies at the spleen. Although we have diligently searched the literature, mention of such a finding, to our imowiedge, never previously has been made. Whether these bodies get there by the blood stream as emboli or whether they are earned there by phagocytic cells, we are not pre pared to say and have no evidence on which to base a conduaton. The fact that they are in that organ, irrespective of how they got there, seems to be significant. * It is interesting that neither in case 1 nor in case 2 (despite the marked pulmonary fibrosis and the thickening of the smaller pulmonary arteries) was there any dilatation or hypertrophy of the heart an either side. . StnilLUtY Two eases of pulmonary asbestosis are reported. In the first case, the symptoms were rdaxfvdy unimportant. In the second case, the dis ease was concomitant with tuberculosis and, with it, was the cause of death. The sunilanty between some of the features of tuberculosis in childhood and tuberculosis complicated by asbestosis is suggested. In asbestosis the lung is not the only organ invaded by asbestosis bodies. As we have shown, the spleen and the lymph nodes may harbor large asbestosis bodies. From the histones there appears to be a further need for study along the fines of prevention of this disease. --zrr?: V '*: - - - -- -- * ' '' `" ass*yas n> - V '^tfCW/rs? OF'PATHOLOGY "conioa bodies'" ia the lain; now known u "asbestosis bodies," ^i] IJcT^csid * worked out the hfctciogie features. The latter bettered dta* ~bc ijiiHes were portions of asbestos in process of alterarioa'and aJisorp non jy hydrolysis, with the passing of silica into a colloidal state .and ' -sum a gel. Stewart and Stewart and Haddow * showed that ties* nodia could be found in the juices expressed from affected lung* ail<j esuli. be found in the sputum by digesting it with equal quantities yt* ' aauilirgda. Lynch and Smith.4 working without knowledge of ;ui> oemenscated these bodies by digesting sputum with 10 per cent .sociiam .rydisdde. GloyaeT proved by means of dark-ground Ulunanatiou, that^?V whet tbs golden-yellow asbestosis body was dissolved in eaneentsated snlphxric add. it had a central core consisting of a minute a*hmn:si *' . T^easbestos 5ha itself under dark-ground ulunuaation hartbe appor.^,. aaeeot a sharp piece of wire. Fibers measuring 200 mlcrous^eau'ptas^ v. dne irecBcdvc mechanism of the upper respiratory tract aad%ster the - long. ` `` v- . thi*dnM V *v the *sple* eM9n . ' .* T&e be ig an intea ' sei4*"! ^ ^ tosis.o*w ^ipuoiedj " i * V#J. % nr-'ofga^a.- **?o*t of cases Ga 1.--/ a white mu. catered the Jetfenoo Mcdseal 'Tftiifi Hnspi&j ma Jem i. 1931, a the service of Dr. Edward Xlopp. He complained erf headache, - aiwfranimt distention and eructation of add and pa ` A' iiarnniii of Salerseaa m made. A chrteeysteewmr u performed. * Peritaaaa rfm'fi ipeil V : sad ae patient died. The history disclosed cerain facts relative m asbmmait Tie jidat had worked is a ipioaer m aa asbestos mill for mm yean. Aitte^T 3* asmwpbere was not very dusty, he ware stiver dost ia Ws For s* years following such employment, be worked aa a laborers Doting tim' past rre years, he had morning cough with moderate expeeumboct Thera was so tmerr o hemoptysis or paia in the cheR. He had some dyspnea md ardiac * ' zMiptaaoc. Physiol examination was unimportant with the exceptios that he tod . an amhysematoas type of chest. The iaporBnt rotten lfwirrwiniu wet - anghxr acrcased peribronchial markings throothost both lungs and sane akwe cgpoio id both root areas. The cardiac shadow appemd to be aarmai The - Ksoxmr was not examined. . .. . . Az the poirmnruui examination, the heart appeared normaL The* left tme weigjwi 270 Go. and the tight 339 Gm. They were bluish gray, practically free . from sdbmions and crepitant throughout On section, no grots pathologic teoe rraa asoorm.nhle. Microscopically, there was a moderate grade of emphysema. ' 4. McDonald. Brit if. J. 2: IMS, 1927. limwarr. M. J.: Brit it J. 2:i09. 192d; 2:531, 1939. Stewart if. Jtud aat>w. .4l.5 C; J. Path. A 3act. 31:172, 1929. 6. Lyrsh- K. it. and Smith. W. .A: J. A. if. A. H:(x59. 1990. 7. Gvsyne. S. R.: Tubercle IP:MX 1929. . , 5, 'AV4 W. and GJoyw*. S. Jt: Lancet i: -US. 1930. ' iirrniurVfl '' a ^y.^taaaed beaiii&r13? : ctftinaon a ' e;irlng;'>aab*sst ''`''was.aTypM Sne prot 'f vessels an t*..cnlosis of ^^g.-'Eariy * Jn.ifae major ' i asbestosis in ' -** mdependenth t Cast 2.-7 worked In so precaati `duties were loss of wei: in hi* span portion of 9. Gear .f ' . ` .` v--* '* A STEWART ET AI~--ASBESTOSES 911 uf the alveolar walls were slightly thickened. A few typical ashestosis bodies tfere jeen in the alveolar wails. There were scattered snail collections oi brown tod hlackish dust, free and within phagocytic ceils, in fibrosed areas. Much oi th* dost and all ot the ashestosis bodies stained positively for iron.. The liver and dtv spleen were not pigmented. ' Tlie question of the relation of pulmonary asbestosis to tuberculosis is in interesting one. The fact that they are frequently associated is sr'iied. Whether tuberculosis becomes implanted on pulmonary asbes tos* or whether the occupational disease lights up a quiescent lesion is a mooted question.1 It is true that when tuberculosis occurs, it is liable to le of an anomalous type. Gardner and Cummings * exposed series oi guinea-pigs to attenuated tubercle bacilli and to an atmosphere laden with asbestos dust and attenuated cuberde hadlit, They found, in the first instance, that normal guinea-pigs receiving the strain of attenuated raberde bacilli showed tubercles in the lung and in the tracheobronchial Ivnqih nodes comparable to the primary complex in man. The lesions caseated and healed by resolution. Spread of the infection with macro scopic disease in other viscera was rare. On exposing guinea-pigs to attenuated tubercle bacilli and to asbestos dust. 3Z2 per cent of one group oi animals showed some evidence of spreading tuberculosis. New disease began as a local extension from primary tubercles and metastasiacd to areas where dust reaction had occurred. The tendency to healing by fibrosis was marked. Macroscopic disease in the spleen was common and occurred occasionally in the liver. In another group receiv ing asJwvtos and attenuated tubercle badlli, the localization of tubercles was atypical. Many badlli were seen napped in fod of dust reaction. Some produced local tuberdes; others immediately entered dilated lymph vessels and were carried to the tracheobronchial lymph nodes. Tuber culosis of these nodes sometimes occurred without involvement of the lung. Early disease of the spleen and of hepatic lymph nodes occurred is the majority of cases. The combined action ot tubercle badlli and asbestosis in the lung produced more fibrosis than did either agent acting isdejwndentiy. - C\*c 1--.1. J. aged 5i entered a hospital m December. 1928. In 1921,* 1m eerkeri in an wivitn* factory for a period- ae abowt mm months. In this factory. precaution* were taken against inhalation ot asbestos dost. Exactly what his dude* were was tmr*ihie to determine. On admission, he complained ot fatigue, lots <ti weirht and a 5Jightlr productive cough. Tubercle bacilli were demonstrable is hts <putum at that time. On roentgen examination, a cavity m the right upper ponk-:: << the che-t and a.fine stippling in the lower portions of the lower lung ' artiner. I.. W.. and Cummings. D. E.: J. Indust. Hyg. 18:63. 1931. t I m st- Wi ill * it N:* * $5 . ri-"v> mS> .'A * 912' ;.* ARLHtVRS OF PATHOLOGY , ft *field* suggesting pneumokomosis were found. There wu improvemem; the patiot' was discharged sod September, 1930. he continued under was admitted to observation as an ambulatory patient the Jefferson Hospital tor Diseases' of. fe tbn - fi' Qint, in the service of Dr. B. Gordom He complained oi the same symptoms'** before. Physical examinations remkd the following salient facts: He was aarfe*. edly emaciated. The chest was emphysenatoes in type Expansion was TM--*i iimited. particularly in the right upper portion, where there was -lagging.. Over the apex ot the right Itmg. physical si*ns indiatire of a cavity were pmimr Ow the rawimUe both hap. expansion was limned; tactile fromtta was ibereased: breath sounds were roughened and lomewhat eaggerated. and there were ~nmurium sonered rales. The area of cardiac dnlncss was within aormai limits; the heart sounds were distant; there was a mitral murmur at tfae apcc. Tbs ihrlomui appeared to be normal. There were dabbing oi the fingers and earring ot the nails: the skin was slightly cyanotic. The patios left the hospital in March, 1931. against medical advice, somewhat improved, but be returned a taoofa later with exacerbation oi all his ijuiptuim and an acsts respiratory infectiom SEb coarse was progressively dowaumrd;. .bronchopowimnnii developed, and be died. April 2. 193L At no time daring his stty in Jefferson Hospital were tabcrtM bacilli found in his spatmm There were a moderate secondary anemia, a sltgbe ' elevation oi nonprotein aitroges^ and negative results from Kahn and Wasssrmaim tes& On roentgen examumtioo, Sept. 20.' 1931, there was multiple small mritatiom ' in the right upper lobe, and the interlobar plesa below it was much tfrirfrunuL la the tower lobe, right, and in the middle and lower lobes. left there was aa increase in the markings dm resembled a dost change. The heart appeared normal. , ; y .; At the postmortem the hart weighed 280 Go. and measured 12 by 3 by 6 an. The myocardium was mottled red and yellow, and appeared soft * and dnlL There were many arm, gray, translucent aoduies on the free gargins of the mitral valve leaflets. The corooarm were thickened and tortuous;.-and com mined atheromatous plaques. The parietal pleura on both sides "was dhddy studded with small, discrete, gray, pinhead-sued aoduies, firm in consistency. Sion* 1st ones were present, but much leu frequently, on die visceral pleura Over tfaa ' bases of both lungs, firm fibrous adhesions completely obliterated the pksal c ides. Between the bases of the hags and tbe diaphragm, these adhesions mi converted into a thick, tough, yellow, homogeneous substance having tbe appear- anee of hyaline cartilage. Tbe right lung weighed 960 Go. and tbe ldt 330 Gm. The consistency of both lungs was much inceiecd over tbe *yynali The bases were particularly firm and tough, and dark brown. The upper half of the right upper lobe was excavated by a large mulrilocuar cavity. The wall of this did aot differ in density fmm that os the adjacent log tissue, giving tfae Impression that the cavity had formed so rapidly that a limiting fibrous wall was not thrown out. The cavity measured 6 cat. across, and through tt coursed many thrombosed blood vessels. It had a foul, fetid odor as of gangrene. Throughout tbs remainder of trite lung there were patchy areas elevated slightly above the cat surface, gray and red. moist, and measuring about 1 an. in diameter. In the left hmg, is addition to what has already been dscribcd for it. were two round nodules, similar m appearance, one in the upper union of the lower lobe and one in tbe lower portion of tbe upper lobe on the outer aspect near tbe pleura The one in' the lower lobe was slightly larger, measuring 4 cm. is dismeter. It ent with increased resistance and on section wa* composed ot thick, dense srands of fibrous tissue, iotcrmtsgM with gray, cheesy material. The regional lymph node draining- -tins area ms similar to this nndule There were no cavities in this lung. In many fresh amenta ewntned fmm these caswn areas, no tuberde bacilli were found. . -".{`^floroscopMafly. "* * . CBetpoaedT offefttbriwiff^eBs* 'y`reaftmarebla awa.'y 3|kny *^-osoosts was pracriealbM^bsm; .; w^oett fbrned' tuberdas. _ ? ; -Th* mvlaUs ia tbe Eriwtys ':>v_ by scan^-of fibnier'tymsa.': pli were, unmineri'frftmbt 'i*. fses^ tbe large eavit^ ja *thwt -i a***>-..<*;? *L <**** ^ * ?, -* Fig. I* (cast 2).--A small bi > . ^asbcstqus bodies." Tbs fine t * distinctly'seen; X 408. - . ^ faction aecrosts. very little pot * Holt hyperemia and a thin, new blasts. *1 "The principal lesson of the 1 * tbe lower lobes. In many piaez others, the alveoli had bean car were inflamed, and there were * ccntage of the arteries were ti srtidng feature m the lungs'-w - (jut numbers in the fibrosed'ai spaixology I STEWART ET AL.--ASHESTOSJS 9U There was improvement; tiw psriim u aa ambulatory,patient. :1a efferson Hospital fa; Disoaea o the He complained of th* sans j"n*-V^ u- #* following salient' facts*-.He was mark*' jkiiuiuui in type Expansion was; orach where there was lagging;-, i^rer . oi a cavity were premiL. Over*' limited; tactile fremitas was -increased; esesgieruted, and there were --^ waswithm normal lbnitii; thevhaart . rarmur at the apes.T3ie*abdomen, glnbbing;. <j. the fingers/' and-<sjyp*rf --The pattern left- thei hospital *(a* iflipjuved*.-bw ha retarded* month and an acute respiratory, affeetfat .JQs - rh^ewiiiiiijiiia <JerekJp|ed*.aad'he,:dit _ r" '5n Jefferson Hospital were, rabersieV Wkrata secondary1 aaenna\ slight-'v v* resuft* irom Kahn ind .Wauernswn*:. &f31, there was nndfiple sraaKedeitaspP ' &r plcnra bdow it wet ;fftqel'. thjtVri1^-' * C MC. aadrlpwer Iobes*vfat,'*' 4v* a. hta VcI hanged. `S_he, ..... {test w^ghed ^SO-Gm, Mi'tgMm'A.'ft graded red and yettow, aqd.- apfiearsd'. toft - fttsyuhjcaat todays'd&nfceAte anrr^' *? were ffnekened faff tandbes; aodgfa* f$sai pieura-oa bodr sidia/..-)U> faddy vdwudd flcAilss. fomfa-gPBauthaCy.. 'Sir**-** tigatsool 9{*nr fecarapfetcy/oblitcrhc^' the /pieural,*w ' y $5* adhesion* '***' |mef*n*pae*bttstatieffJhrring the appear* ' ` 9.^a wtf.Urffat 830 <** Elover tbeodmaj. TJidbhi**' i*3>* <S>ppr&dlfaC<to>$'right iTtty.'Jfte walfiaf tfafr,dii*Jfa-' ifrSwdns wallow ita ifntrira o*6 ^ t'lt* eoaraui raanydfiroiiibusul bkod gdngmsw .Throughbuf tymamits ?* > idafigatly *bot tbreaC stafaeL'3greyr***^ bk'duenW.~!:<htk.lt tong, in. addffl** \jt vwesfcftwo. roiniQiodnle*,^aumlar***-* (gflpf^Mtoand or* is th*'iwifcjwrti`*,l gihj'^eata?: ob^'W tht'lWsr. J<**> )JtamL|uATt da wifafaeruased rraisuflcav* ^ ----- iiutiuiiW^La' . this Ja' W *4(^1 ifl't&s ^ra^:{artBaiAl^&ja^se^^ > Microscopically, the parietal pieora was sttxkkd with toberdes. Thee were ' (tstposed of epithelioid cel1*, a few lymphocytes, giant ceil* and fibroos tissue in ctfsidcnble ^t^j***. ilany were hyalinized to a cusstdesaMe extent. Caseatiuo aeffosis was pracheaily absent. They were oi the prote;uve type, with a tew wdl famed tubercles. -. Tim aodaies in the left lung were large, caseous areas, divided op into lobulea by-mads oi fibrous t**w*. Sections from them and from the tubercles in the pleara were eaauznned for tubercle bacilli, but none were found. la seasons taken from the large cavity in the upper lobe of the right lung there were tresh liqua* o4 _ ,v Fig. 1 (cue 2).--A bronchiole completely filled whit cellular exudate and _ *nhsinaii bodies." The fiat segmentation aad the duhhed end in some on be ** dudaedy seta; X *. .fadoe necrosis, very little polymorphonudcar aad 1. nmhui:.m> cefl infiltration, kittle hypstemia aad a this, newly formed layer com^*d chiefir ot young fibro* .'blasu. . The principal lesion of the lungs was a diffuse fibrosis, parricuJariy marked in to lower Mw, In many places, the alveolar walls were markedly thickened: in .retwis, th* alveoli had been completely replaced by fibrous tissue. Many bronchi ' "Wet* inflamed, and there were many areas of pneumonia present. A high per* vetage of the arteries were the seat oi aa obliterative endarteritis. Tlie most r.WJdBf feature in the Istgs was the Hishotosis bodies." They were present in - ' cnat amnben in the fibrosed areas, m wmr alveolar wall* and *pnres and in the . tX . . j.'. tC f.' !5 ' - * - ^ i" i SB; U Si(dgSSre >. * . 5 .>.f *..914 ARCHIV'ES OF smaller bmnchial branches. Particles of then ware fragn>ted and were fmq'jn*- _ v phagocytic ceils. Mainly mttrplMNmriear lenkucytes they lay luma and p^yhlasts in small dutters wtth.ceileesoas <t poly- T*: / * aiwut them.'often complete* `occluding.a *\f . Vr f-t.*'.9". that fas dae^r.pi^n^rf'- snail bmchk>l* or an alveolar duct. They manured roughly from 10. tfc micron* and were tnkka I*uwil They had a variety of appearances. but.* cbgr-' ^jr*-**^Ktefc gi^r m i. airtrrfetie mnrpiailvey* Tltey were seen often as a seriee of regular disks-'vejy * * much as are red Mood cdls in rouleaux formation. Frequently.a senes'of disk* ' ended in a club form on mte or on both ends. Sometimes they-were, seen as long delicate filament* ending in clubbed ends; or again as short dubbed forms, single oe double. suggesting a dumbbell. Occasionally, single, paired or eoeeal tame la dtaitsi wen* found r even purelike aggregations. They were present in the juice: T r- femnfta'oidi&t r.., ;vf. gad.Hie mete a <queeicd from the lungs. They did not stain with hmnaxoxylia^osm or Oram's stain. They did. however, give the Prussian btua reaoioa-.for iron'in varying, teaibte TO it degrees of intensity, in dm main ratbir pinnounnad ~ In tba caseous nihsirnlim areas in the left lung, these asbestotts bodies were fewer in namber than'in the TpS adjacent long tissae. A few were normal, bat many were pale *wuh ^ .. '; . /{fm crne^Tost $$fiS3S 1vJr'"' teetfkaae. . tba . ^;-esQ2xtejI'^ctDr .*% ^ ft8***8 deve* ``-vfarther yoBuiutafc rV Fig. 2 (cue 2).--Splen. An asbestosis body is lying in the center of the Held. One end is dabbed; the other pointed; X 400. . . *. . *. *. a #* *. outline. When these caseous areas had bean stained for preutan blue rewidoo following the staining of them for sad-fast bacteria (cartel fuchiin saturated solo- tion 95 per cent alcohol, decotoriaarion with 25 per cent nitric sod. Loader's methylene bine), the asbaetosia bodies stained a pale green 'instead of a dbhncr blue, and their morphology was less regular/tec they could sdU. be maoggited. fn addition to the asbestosis bodies there was considerable goJden-brewn-aad'biacfc granular pigmeiu present m phagocytic cells. Much of this gave the iron reaction. In the spleen, the redcaio-endotbalial cells were loaded with a fine, amorphous golden-brown and sometimes blackish dost. Some of this dost was eemceilular. A few large, typical asbestosis bodies were found Pncdslly every hepatic cell contained a few granules of a golden-yellow pigment . Many of the Kopder*ed!s contained considerable quantities of light golden-yellow and bladash granules of piement About the portal radicles it was common to sera few ceils loaded with pigment In the mucosa of the stomach there wet many' phagocytic ceils Sled with fine, golden-brown pigment granules. In the ladney, many, cells were sera in the capillaries of the giomentii which wee filled with coarse granules of a -brown and blackish pigment The lymph node draining the caaeou area m * . .`.'.7 . . '-v j . ;a , T* *** f^'cv^-.'dnrc tnB^fVtl-e '?^'Sinf5 tft become nor tiesiit fx ,V' Sww moiring . itraies dm tbes] ^\a short ggpoiote masks m ore v 4>- *r T3ie narted,. -is . sbetmBB'the base , ` findmf.of rajndh -/ v ~he presence of sl We bore hem y V r'tfae-audhmg <* -Vmdes and nafaexe tfu> form of leak learn, trrihmg ^asbestos tahaiaao in a pextooa * " ' ^question as tb ui A , t*Xxm the mdesner < paeans to ns. this u the asbestosc *. -*/ 916 ARCHIVES OF PATHOLOGY Our second case confirms previous observations that the asbestosis bodies have a tendency to disappear in a caseous area. We have also shown that in such an area following an add-fast stain (25 per cent nitric add) the bodies do not stain so well for iron and have a less definite morphology* bat are stiH recognizable as such, so that if these are present in the sputum in any case, they should be recognized on a routine smear even after it has been treated with add. The finding, of tnberde badHi in the sputum in the second case on two different occasions, plus the gross and microscopic features charac teristic of tuberculosis, is sufficient to establish such a diagnosis. It is significant, however, that many more specimens of sputum^ were exam ined for add-fast badHi in which none were found, and that no ooe noted the asbestosis bodies in the sputum, although these were not being looked far specifically. An important additional finding in case 2 was that of asbestosis bodies in the spleen. Although we have diligently searched the literature, mention of such a finding, to our Imowledge, never previously has been made. Whether these bodies get there by the blood stream as emboli or whether they are earned there by phagocytic cells, we are not pre pared to say and have no evidence on which to base a conclusion. The fact that they are in that organ, irrespective of how they got there, seems to be significant, ' It is interesting that ndtber in case 1 nor in case 2 (despite the marked pulmonary fibrosis and the thickening of the smaller puhnonary arteries) was there any dilatation or hypertrophy of the heart an either side. . . StniZlAMY Two cases of pulmonary asbestosis are reported. In the first case, the symptoms were relatively unimportant. In the second case, the dis ease was concomitant with tuberculosis and, with it, was the cause of death. The similarity between some of the features of tuberculosis in childhood and tuberaxlosis complicated by asbestosis is suggested. In asbestosis the lung is not the only organ invaded by asbestosis bodies. As we have shown, the spleen and the lymph nodes mar harbor Urge asbestosis bodies. From the histones there appears to be a further need for studs along the fines of prevention of this disease. w \