Document xz9BGG3b2j4MOB4Zk7Zng95zE

STOOI1851 TRANSACTIONS of the 32nd ANNUAL MEETING of INDUSTRIAL HYGIENE FOUNDATION OF AMERICA, INC TRANSACTIONS BULLETIN No. 41 Management and Scientific Conferences OCTOBER 10 - It, 1967 CHATHAM CENTER PITTSBURGH, PENNSYLVANIA I "c ** DOW 06063 i S T 0 0 I1852 K "cif / 2. ^ l/ao 1 < ASBESTOS BODIES AND BI0EFFECT5-A JOHN M. G. DAVIS, Ph.O. Deportment of Pothology, University of Cambridge, United Kingdom ftesearch Biophysicist, Asbestosis Research Council of Greet Britain ROBERT T. P. daTREVILLE, M.D. Managing Director, Industrial Hygiene foundation PAUL GROSS, M.D. Director, Research laboratory. Industrial Hygiane foundation DETECTIVE STQgY (if?) As an introduction to this Detective Story. I should U** to point out that no on* disputes the im portance of placing on "trial" material! suspected of producing haaard to health in order that adverse moeffects of such exposures as may oceur in man1# working and living environments may not escape notice but be detected and controlled by appropriate and effective means, common to good industrial nvgiene practice. This paper is an outline of the history of the asbestos body from its first discovery through a period when it was considered of little clinical significance to the present day when it holds the central position in what some people suggest could be one of the greatest industrial medical problems of the age. First, let me outline some of the terms that are going to be used in the course of this presentation: 1. Asbestos -- This is a general term that covers a number of fibrous minerals of which feu* ;'?< are of commercial importance. These are crocidoUte or blue aebeetos from South Africa; amoeite ,.-h ts red in color and is alto mined chiefly in South Africa:' chrysotile which is white and occurs in ~..ny countries of the world, and aathopholite which is also white and is mined mainly in Europe. The pertanee of this will become apparent when we discuss the finding of asbestos bodies in the lungs of the -rtar population in the North American continent. 2. Asbestosis --This is a type of lung fibrosis that oceura in workers exposed to large amounts *aoetos dust. It may or may not be associated with recognisable clinical disease during life, and is pr.uuccd by all types of asbestos. 3. Bronchial carcinoma -- This is the layman's lung cancer that we know is associated with heavy smoking and has also been found to occur frequently in workers exposed to large amounts of a*~.estos dust. Again, this tumor appears to be associated with all asbestos types. 4 Mesothelioma --This is a very rare tumor that developa from cells lining the chest and ab dominal cavities. These tumors so far appear to be associated with exposure to only one type of asbestos. . crocidolvte which as has been noted is blue and is mined chiefly in South Africa. Asbestosis was first recognised as an induatrial disease at the turn of the century, but at the time, the bodies were not noticed. Later in 1914, Fahr and Feigel* discovered "strange crystals" in lung sections from a case of asbestosis. Later, Cooke* in 1924, reported "curious bodies" from ssbestosis cases but because of their beaded structure, he thought they might be fungi. Stewart and Haddow3 m .'ijo believed that the bodies were associated with the disease and coined the term ssbestosis bodies .-fid this term was used for some time until it became noticed that large numbers of bodies could be -'ur.d in the lungs of asbestos workers without the presence of very much pathological change. Gloyne* in 1932 demonstrated that each body consisted of an asbestos fiber as a core with some .:-.nc material around it and it was suggested that this coating might have the function of protecting the . - ie,, front the harmful effects of the mineral. This led to the term asbestos bodies being substituted *-nesto*is bodies and there the situation remained until quite recently. The bodies, it was thought. < urred in relation to asbestos and were regarded as diagnostic of exposure to this dust but not indication of disease. ?ht situation was only changed by the report of Wagner9 in 14o that the rare pleural tumor, the - " was in South Africa associated with exposure to blue asbestos or rrocidolite tn the ui.ra r,-as Th<- association of ordinary bronchial carcinomas with exposure to asbestos dust h.,.j . . r. recognize*:, but it has recently been shewn that this is related to high dust dosages m as'.rstu: >.'Hers nd careful environmental control has almost eliminated this tumor an a problem tn factonec -f: reported, on the other hand, that many of bin imh.-s never '.u,rkn! m the mines, hut h-*d . .i\ .. ir. the, it- e-.j; areas, and indeed, may only have lived n afi*,* lei .. year or twt.. often *> eii. ii.- also howed that the time lag between last < \p>.'*ur>- -n<: tumor format.on was aiwty. ii.t-n DOW 06064 * a / 00 -H o o CO T.ms discovery presented entirely new problems. While asbestosis and bronchial carcinomS1 were obviously connected with severe dust exposure, these were solely problems for the asbestos CO industry; but if a very small amount of dust could cause a mesothelioma, might not asbestos-products be a hazard to the whole population? Since the presence of asbestos bodies in the lungs was considered the best way of demonstrating asbestos exposure, it w*as logical to examine the lungs of normal members of the populatioa for the presence of these bodies and the first report on one of these studies eras published by Thompson* in 196 j. He found 26 percent of autopsy eases in Capetown contained what appeared to be asbestos bodies. Since then, several other studies have been completed including one by Cauna* Totten, and Gross'^ ui 1965 which reported that 46 percent of autopsies in the Pittsburgh area contained bodies. These results led to the sugggstion in some circles that although less than 600 cases of mesotheliomas have so far been, reported in the medical literature of the whole world, the increase in asbestos consumption in recent years might produce a great epidemic of these tumors in the future. These reports have in fact received great publicity in the press and have led some people to suggest thst the use of asbestos should be banned altogether. This very year an article appeared in Prevention Magazine8 suggesting that it might be unsafe to visit Expo *67 because of the risk of contami nation by asbeatos in the air based on Or. William M. Thurlbeck'e' findings. This asbestos scare has. however, ignored some of the published faets on mesotheliomas and new information suggests that others cannot be taken at their face value. First, asbestos is not s siegle mineral. Wagner reported quite distinctly that his mesothelioma eases were associated with the erocidolite areas and he found so cases associated with either ameeite or chryeotile. la other countries attempts to demonstrate that exposure to dusts other than crocidolite could produce mesotheliomas have $o far been almost completely unsuccessful. The mesothelioma problem ia therefore not.as far as we can see at the moment, one that involves the whole asbestos industry, but only users of erocidolite and. fortunately, this mineral represents a relatively small proportion of total world asbestos consumption. As regards the dosage required, we must examine the conditions in the South African mining areas from which Wagner obtained his eases. In these mining areas it is common practice to surface roads with the waste rock from asbestos mining and the rest of this material is deposited in dumps. Wsgner states that some of his esses played among these dumps as children and others no doubt drove along the roads with car windows wide open. These cases, therefore, although they may have had a very low ex posure by industrial standards, probably inhaled far more dust than could evar be met by members of a normal urban population. Finally, we must reconsider the evidence for the exposure of the normal urban population to as bestos dust, and thia means re-examining the position of the asbestos body in this problem. These bodies were for many years believed to be formed only around asbestos fibers* but recently evidence has ac cumulated that the deposition of a similar coating can occur around a number of materials, and studies have been undertaken in the Mellon Instituted 1 * and in the United Kingdom** In an endeavor to find out just how many materials will produce asbestos-like bodies, and also to attempt to discover the chemical processes involved. In order to discuss this work, it ia aeeeasary to summarise what ia Inown about the structure and chemistry of genuine asbestos bodies. Gloyae in 1932 had demonstrated that the body coating contained iron*and Beger** in 1933 had shown that protein material was also involved. The pretence of iron in the capsule haa led to Perl's stain being used as an aid in finding these bodies. The capsule stains dense blue and is more easily seen in tissues than the natural brown color. When we first examined the structure of asbestos bodies in the electron microscope, we found that the coating was made up of email dense granules about 60 A* in dia meter. Similar granules had previously been reported in a number of tissues and it had been assumed that they represented either ferritin or haemosiderin. Since this tied in well with the known iron protein nature of the capsule, it was suggested thst the asbestos body eoating was made up of one of these chemi cals. As regards the anatomy of the bodies, it was found that although sometimes only one dense layer of coating material was present, in other cases the coating consisted of a number of different layers of varying thickness and density. Occasionally the outermoet layer was made up not of granules but fine filaments about 60 A* in diametsr which we now believe to represent calcium deposits. For the experimental production of bodies with non-asbestos materials, two techniques were used q In Pittsburgh.hameters were injected intrstracheally with the duet, while in Cambridge we used intra- C 06065 fibber and elastia. la both injection sites all the a a foreign materials produced bodiaa which with tha light microscope appeared vary similar to aabaatoa bodiaa. That ia to aay thay war* golden brown ia uaatainad sections aad war# oftan aagmaatad. Parl'a ataia ahowad that tha coatiag contained iron in commoo with aabaatoa bodiaa. For thia raaaoa Dr. Paul Croaa la Pittaburgh auggaatad tha tartn "ferruginous" body and auggaatad that thia gaaaral tarm ahould ba used for all bodiaa iouad ia humaa lunga at laaat until tha mineral involved waa poaitivaly identified.la Cambridge wa have been attempting to examine theaa bodiea with the alactroa microaeope to aaa how thair fiaa atructura comparaa with gaauina aabaatoa '* bodiaa aad have acme iataraatiag raaulta. although tha difficultiea of euttiag thin aactiona of tiaaue con taining glaaa fiber or aluminum ailicata have ao far precluded getting photographa of tha quality that wa did with genuine aabaatoa bodiaa. ^ However. U ia clear that whatever tha foreign material that stimulatec tha production of a "ferruginous*' body, tha coating consists of small danaa granules approximately 60 A* in diameter. Tha coating is usually in tha form of a single layer, but ia some cases, as with aabaatoa. a layering affect caa ba aaaa. Thia layering is especially noticeable with elaetia bodiaa. In the case of this material, however, the process involved ia slightly different siace the graaular material ia deposited iaaide the large elastia fibers aad not around the outside. This appears to be some form of impregaatioa that starts at one point aad works inwards until the whole elastia fiber is impregnated. The situation at present ia then that we must not assume that "ferruginous" bo'dies aeea ia the lungs of the normal population are asbestos bodiea uatil their mineral core has been definitely recognised. Almost the only method of identifying these small particles accurately is by electron diffraction and thia involves a very great deal of work in manipulating the small bodies onto an eltctron microaeope grid. However, in Dr. Gross' laboratory, a study of these structures has commenced which we hope will give an indication of what percentage of humaa "ferruginous" bodies are caused by asbestos. SUMMARY Asbestos has been related to certain bioeffects which appear specific and are dose related. These effects include asbestosis which will occur in almost all exposed persons if sufficiently high exposures are maintained for long enough periods. In addition, some individuals so exposed develop bronchial car cinomas. Industrial hygiene practices have been very effective ia controlling both these forms of occu pational disease. There has bees recogaitioa for many years that workers exposed to asbestos dust develop "asbestos bodies. " First observed in individuals who had asbestosis they were called "asbestosis bodies" but when it became evident that they frequently occurred in the absence of this disease, the name was changed to asbestos bodies. The current furor over asbestos bodies results from two developments which recently appeared in the professional literature and were widely reported in the news media with varying degrees of sensa tionalism. This has resulted in considerable public apprehension on an international scale. These developments were:firstly,Wagner's study of mesothelioma eases associated with crocidolite asbestos exposure often non-oceupational in nature, and secondly, Thompson's conclusions that asbestos is a significant urban air pollutant based on his findings that over 26 percent of urban dwellers can be shown to have asbestos-like bodies in their lungs. Because of this, some individuals have expressed the opinion that asbestos should oc withdrawn from many of its uses. e.g. . in brake linings. However, the basic assumption that asbcstos-like bodies can only be produced from asbestos has proved incorrect and this casts considerable doubt on the theory th*t has been the chief basis'of the asbestos "scare. " 81 DOW 06066 S T 0 0 I1854 lST 0 0 1855 N REFERENCES 1. Fahr and Feigel (in reference by Gloyne. SR.. "Asbestos", International Labor Office Occupation and Health Supplement. Jan. 1938) 2. Cooke. W. E.. Brit. Med. J.. p. 147 (July 26. 1924) 3. Stewart and Haddow. Brit. Med. J..2: 580 - 581 (1929) 4. Glome. S-R. . Lancet 1: 1351 (1932)" 5. Wa|ner. J. C. . Proceedings of the Pneumoconiosis Conference. Johannesburg (1959): A.J.Orenetem. Editor. J.lt A. Churchill Ltd.. London. England 6. Thompeon. J. G. et at. South African Med. J. .37: 77 (1963) 7. Cauna. D.. Totten. R. S. and Groee, P., J. Amer. Med. Aaan. 192: 371-373 (1965) 8. ''Expo '67: Superb. But la It Safe? ", Prevention MagsslasTlJuly 1967) 9. Aojilvel. L. and Thurlbeck. W. M. . Can, Med. Aaan, J. 95: 1179*1112(1966) 10. Groea. P.. Cralley. L. J. and dcTreville, R.T.P. .Amer. Ind. Hn. Aaan, J.' 28: 541-542. (Nov.-Dee. 1967) 11. Grote. P. et al. "Pulmonary Ferruginoua Bodice: (1) Their Development in Reaponee to Filamentous Dusta; (2) A Method of laolating and Concentrating Them."(To he published in Archives of Pathology) 12. Davis. J.M.G.. Annals of the New York Acad. Scl. 132: 98-111.(Dec. 31 1965) 13. Beger, Virchow^s Archives.290: 280-353 (1933) 84 DOW 06067