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111. COMMUNITY EFFECTS OF NONOCCUPATIONAL ENVIRONMENTAL ASBESTOS EXPOSURE

Irving J. Selikoff, M.D., F.A.P.H.A., and E. Cuyler Hammond, Sc.D., F.A.P.H.A.

Introduction largely unidentified at present and of unstudied biological importance. THERE has long been curiosity concern- ing community exposure to pneumo- coniosis-producing dusts, partly because Environmental Asbestos Disease the assumed "spill-over" from primary It may be profitable to review studies industrial sources might be expected to of one pneumoconiotic dust, asbestos, in yield information concerning effects of the light of these suggestions. The pos- minimal exposure and partly because sibility of community asbestos disease community studies were needed to give has been known almost as long as base-line data against which to evaluate itself. In 1927, shortly after findings in groups of miners living in republication of the case report which these communities.1' 2 Nevertheless, it gave the its name,8 Had- was not until the serious consequences dow9 reported finding asbestos bodies in of neighborhood beryllium disease were the of a person living close by an clarified3'4 that the important potential asbestos factory. Other neighborhood of community exposure to pneumo- cases of asbestos disease have been re- coniotic dusts was widely recognized. ported since.10-12 Bobileva, et al.,13 re- In the recent past, there has been ported experiences suggesting impaired growing interest in this problem, rang- health in children living downwind of ing from the health effects on children an asbestos plant in the Soviet Union. of cement and similar industrial dusts The import of such scattered observa- in Rumania5 and neighborhood bys- tions was muffled, however, until the re- sinosis in ,0 to environmental pneu- ports of three germinal studies, within moconiosis adjacent to the Rajasthan a short time of each other: Kiviluoto desert.7 We may anticipate that such (1960)14; Wagner, Sleggs, and March- interest will increase for a number of and (1960)15; and Thomson, Kaschula, reasons. First, because of growing con- and MacDonald (1963) .16 In each, a cern over in general and pathological "marker," considered al- particulate air pollution in particular; most pathognomonic for asbestos expo- second, because of the appreciation that sure, was unexpectedly found in groups the biological activity of known pneumo- in the general population not known to coniotic dusts is not limited to heavily be industrially exposed to asbestos. exposed workmen, but may affect others indirectly exposed in the community; Stigmata of Environmental Asbestos and, lastly, because study of community Exposure effects of pneumoconiotic dusts may sug- Pleural Calcification - Scattered in- gest methodology and technics suitable stances of calcification of the pleura, for the investigation of other environ- particularly the parietal pleura, were ob- mental factors, including inhaled dusts served in asbestos workers during the

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1930s and 1940s, but their significance another common pleural complication of as a roentgenologic sign of asbestos ex- asbestos exposure but, when diffuse, posure was not appreciated until the re- need not have the same diagnostic sig- port of Jacob and Bohlig in 1955, in nificance as calcification. However, such which such calcification was described may occur in more or less dis- in approximately 5 per cent of 343 Dres- crete plaques, and Kiviluoto has called den asbestos workers.'7 Investigations attention to these as additional pleural since then have demonstrated the ex- stigmata of asbestos exposure.20 traordinary frequency of this finding Pleural - of among asbestos workers and have em- the pleural surface in association with phasized a cardinal feature-that it is asbestosis have been known for over rarely seen in less than 20 years from 30 years. Weiss suggested an etiologic onset of exposure (Table 1) .18 relationship in 1953,21 but such pro- Kiviluoto discovered 499 instances of posals faced the difficulty of infrequency such calcification during a community of reported cases and the absence of epi- x-ray survey among 6,312 adults in the demiological studies to suggest that these Kuusjarvi commune in . Struck were other than chance associations. by this, and the absence of any such cases Wagner's report changed this. He in- among 7,101 adults in the neighboring vestigated 33 cases of diffuse pleural Ilomantsi commune, he astutely ob- mesothelioma in the North Western Cape served that the first commune contained Province of (an asbestos- an asbestos mine and postulated that the producing area) and in 32 cases demon- people with calcification (farmers, strated at least suggestive evidence of housewives) had been subject to endemic potential asbestos contact, usually non- environmental asbestos exposure.'4 His occupational, as, for example, residence countrymen, Laamanen, Noro and in an asbestos area.15 Since this report, Raunio, subsequently reported air diagnosis of pleural mesothelioma has studies showing asbestos dust at dist- been a signal to seek previous asbestos ances up to 50 km from the mines, in- exposure. cluding deposits ranging from 1.52 gm/ Asbestos Bodies in General Popula- 100 m2/month 4 km away to 34.6 gm/ tion-Asbestos when in the , 100 m2/month at 0.5 km.19 have the capacity of becoming charac- Pleural Plaques-Pleural fibrosis is teristically coated; these fibers form

Table 1-Time of onset of radiologically evident pleural calcification among 1,117 asbestos insulation workers

Years from Chest roentgenogram onset of % calci- Grade of calcification exposure No. normal fication 1 2 3 40+ 121 42.1 57.9 37 20 13 30-39 194 65.4 34.5 46 15 6 20-29 77 89.6 10.4 8 0 0 10-19 379 98.9 1.1 5 0 0 0-9 346 100.0 0.0 0 0 0

Total 1,117 96 35 19

SEPTEMBER. 1968 1 659 asbestos bodies which, when seen, can studies of Newhouse and Thompson.28 hardly fail to attract attention. This was Investigating 76 at Lon- so even before asbestos disease was don Hospital, they found 31 occurred known (Marchand, 1906).22 Thomson in asbestos workers. Of the remaining took advantage of this phenomenon to 45, 20 occurred in individuals living demonstrate the frequency of inhalation within half a mile of an asbestos fac- of asbestos by the general public. He tory or in the household of an asbestos examined smears of lung bases in 500 worker. Similar findings were reported consecutive autopsies in Cape Town, and by Elmes and Wade in Belfast.29 Thom- in 26.4 per cent found asbestos bodies.16 son's observations have also been con- While asbestos bodies do not have the firmed: 25 per cent to 50 per cent of same significance as calcification or adults coming to autopsy in Pittsburgh,30 mesothelioma (disease may be absent Finland,31 Miami,32 Montreal,33 New and no conclusion concerning time of in- York,34 and Belfast,35 are now found to halation can be drawn), Thomson's ob- have asbestos bodies in their lungs. servations have been very important in demonstrating the frequency of commu- nity exposure to asbestos at present in Table 2-Observed and expected number many areas of the world. Simultaneously of deaths among 370 asbestos insula- these observations raise the serious ques- tion workers during the 52-month tion whether inhalation of presumably period from January 1, 1963, through April 30, 1967. Expected numbers are small amounts carries a concomitant based upon United States mortality risk of widespread community asbestos data disregarding the smoking habits disease. of the subjects. Recent Epidemiological Observed Expected Investigations Cause of death deaths deaths Stimulated by the above observations, studies of environmental asbestos dis- Total, all causes 94 47.5 ease have been extended. First, the re- Total (all sites) 49 8.6 lationship of mesothelioma to asbestos Cancer of lung, pleura, has been clarified. Peritoneal meso- bronchus, and trachea 27 2.3 thelioma has also been shown to be as- Bronchogenic sociated; Enticknap and Smither23 found carcinoma 24 * Pleural 9 such tumors in 52 consecutive autop- mesothelioma sies in one asbestos factory. Large col- 3 t lections of asbestos-associated meso- 7 t theliomas have been published.24-26 The Cancer of stomach 3 0.6 significant incidence of asbestos-related Cancer of colon mesothelioma has now been demon- and rectum 5 1.2 strated in our laboratory. In a prospec- Cancer of all other tive 52-month study of 370 experienced sites combined 7 4.5 asbestos insulation workers, from Jan- Asbestosis 15 0 uary 1, 1963, to April 30, 1967 (sur- Heart and circulatory vivors of a larger group of 632 fol- disease, including lowed 1943-1962), there were 94 deaths. stroke 22 28.5 Ten were due to mesothelioma, three to All other causes of death 8 10.4 pleural and seven to peritoneal27 * United States data not available, but figure should (Table 2). be only slightly less than 2.3. t United States data not available, but these are rare Perhaps more germane have been the causes of death in the general population.

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Problems and Perspectives comitantly we are investigating occupa- tional and other characteristics. Prelim- The foregoing overview indicates that inary data suggest that unrecognized at least one pneumoconiotic dust, asbes- occupational sources may add to, and tos, may be widely disseminated into override, general community asbestos the general community from industry exposure (Table 3). sources or end-product use; that such 2. The existence of wide potential for dissemination may produce detectable direct or indirect occupational exposure disease; and that methods to study the has not been considered sufficient, question can be designed. It would be nevertheless, to explain the frequent oc- misleading, however, to suggest that the currence of asbestos bodies in the lungs situation has been clarified, even con- of people coming to post mortem in cerning asbestos, and totally inaccurate urban communities. It should imme- concerning other pneumoconiotic dusts. mediately be said that neither Thomson The following questions, for example, in his original communication nor other require study and explanation: investigators since undertook to prove 1. Epidemiologic studies are concerned that the "asbestos bodies" found by with the "general public." But insofar as them were actually the result of inha- pneumoconiotic dusts are concerned, lation of asbestos fibers and were not, how "general" is the public? E. L. Col- indeed, the result of tissue reaction to lis many years ago described pneumo- some other mineral yielding an coniosis in dock workers after inhaling end-product which had the appearance coal dust ;36 their counterparts, 50 years of those bodies characteristically seen in later, were truck drivers who inhaled large numbers in an asbestos worker's asbestos at a construction site. When we lungs. Studies to clarify this aspect of consider that in some countries 5 per the problem are in progress. cent of the employed population works While there is no doubt concerning the in the asbestos-rich construction indus- frequency of what appear to be asbestos try, we may appreciate that indirect oc- bodies in autopsied lungs, the signifi- cupational exposure may constitute a cance of this observation is not currently significant proportion of "community clear. Discovery of asbestos bodies in exposure," to be supplemented by con- routine post-mortem studies is simply siderable unrecognized occupational as- evidence at best that at some time as- bestos exposure. The latter would in- clude the occasional use of asbestos ma- Table 3-Asbestos bodies in the lungs terials by workmen not usually con- of a sample of persons in the general sidered prone to asbestos exposure; such population at autopsy in New York uses would include a carpenter sawing City, 1966. Preliminary analysis by asbestos building board, a plumber using occupational categories. asbestos rovings for joints, and an elec- With trician stripping asbestos-covered wire asbestos and cable. With over 3,000 uses for Sex and No. of bodies asbestos, now currently known,37 oppor- occupation subjects No. % tunities for indirect and otherwise un- recognized occupational exposures may Men be frequent. Blue collar workers 197 120 60 We are now studying asbestos bodies White collar workers 111 45 41 in the lungs at autopsy in several thou- Women: Housewives 47 14 30 sand consecutive deaths in three general hospitals in , and con- Total 355 179 50

SEPTEMBER, 1968 1661 bestos fibers have been inhaled, with- cruited from the farming population) in out indicating when such inhalation oc- a nearby asbestos mine. The mine could curred. It has long been known that hardly have been the only source, since asbestos bodies can be formed in human it had been open for less than two lungs in two or three months, or per- decades (latent period). Examination of haps less.38 Disease could be anticipated the soils worked by the affected farmers only as a result of inhalation that had demonstrated asbestos minerals to be occurred a considerable time before.39 present; even the stone fences were made On the other hand, it is likely that most of outcroppings of mineral. asbestos now being discovered post mor- Such must be categorized tem in persons who have not been in- as the result of intimate exposure under dustrially exposed has been of recent unique conditions, among certain agri- deposition, since there was previously cultural workmen and their families, much less asbestos about to pollute the rather than what may be called general air. For example, annual world produc- asbestos air pollution. tion of asbestos was 500 tons in 1890, Much more study of asbestos air pol- 200,000 tons in 1920, 500,000 tons in lution is required-its extent, sources, 1930, compared with 4,000,000 tons per range, persistence-as a background for year at present. appropriate epidemiological investiga- 3. Asbestos air pollution -General tions concerned with its disease potential. community air pollution by asbestos 4. Mesothelioma - Asbestos workers microparticles may occur from indus- frequently die of mesothelioma, and trial sources or from disintegration or other cases are often found to have had use of asbestos products. Under certain close environmental contact.15'28'35'42'43 circumstances, as noted, it is probable But is there any disease potential as the that asbestos disease may occur. But it result of general asbestos air pollution? is by no means proved that such gen- So far, there seem to be few mesotheli- eral asbestos air pollution, presumably oma deaths in the general population. A with only small numbers of fibers in- review of 31,652 consecutive deaths, haled, results in widespread disease. among over 1,048,183 people in the gen- Cases of pleural calcification among eral public (1959-1962), revealed only Kiviluoto's farmers may not be evidence 3 cases of mesothelioma.44 Moreover, is of asbestos air pollution from the local asbestos the only pneumoconiotic cause mine and mill, a facile explanation. This of mesothelioma? Wagner produced ex- explanation is not available, for exam- perimental mesothelial tumors with silica ple, for Hromek's finding of 273 in- as well as with asbestos,45 as did Hueper stances of similar pleural calcification with polyurethane.48 during a survey of 9,871 persons in an 5. The statistical and epidemiological agricultural area of Czechoslovakia with difficulties in evaluating the community no asbestos mine or other known ex- effect of an environmental agent, in a posure.40 disease process with multiple potential An alternative explanation can be de- causes, is seen with . This is rived from the recent experiences of the most common tumor among asbestos Zolov, Bourilkov, and Babadjov.41 These insulation workers at this time; one in investigators found instances of pleural five deaths is caused by this .47 calcification among farmers (largely With this lead, asbestos bodies are tobacco) in the Avren region of being sought by a number of investiga- (5.6 per cent of males and 2.8 per cent tors among random cases of lung cancer of females examined), in about the same in the general population to find a pos- percentage as among the workmen (re- sible link to asbestos. But how allow for

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Table 4-Observed and expected number of deaths due to bronchogenic carcinoma among 370 asbestos insulation workers during the 52-month period from January 1, 1963, through April 30, 1967, by smoking habits Workers Observed Expected Smoking habits observed* deaths deaths Never smoked regularly 48 0 0.05 History of pipe, cigar smoking only 39 0 0.13 History of regular cigarette smokingt 283 24 2.98 Total 370 24 3.16

* All with more than 20 years from onset of exposure. t Includes cigarette smokers who also smoked pipe or cigars. the effect of cigarette smoking which ber, age and smoking habits taken into overwhelms the asbestos effect? Thus, of account (Table 4). the 370 asbestos workers referred to 6. In demonstrating pathogenetic and above, all with more than 20 years since etiological relationships, chronic disease onset of exposure, followed prospectively epidemiology has frequently faced the for 52 months (January 1, 1963 to April difficulty of a long period of clinical 30, 1967), 87 did not cigarettes. latency. Asbestos disease is another None of these men died of lung cancer. example. We have recently been able to On the other hand, 283 had a history define the range of such latency for one of cigarette smoking; 24 died of lung group of workmen exposed to asbestos cancer or eight times the expected num- asbestos insulation workers. Table 5

Table 5-Years from onset of asbestos exposure to death of 113 workers who died of bronchogenic carcinoma, mesothelioma, or asbestosis. Years onset of Pleural exposure Bronchogenic meso- Peritoneal to death Total carcinoma thelioma mesothelioma Asbestosis 20-24 3 3 - - - 25-29 9 8 - - I 30-34 25 17 3 2 3 35-39 30 16 3 4 7 40-44 17 11 - 2 4 45-49 20 9 - 2 9 50-54 5 4 - - 1 55-59 4 1 - 1 2 Total 113 69 6 11 27

NOTE: 14 of the 17 mesotheliomas were well established as such. In three the histological diagnosis was less firmly established.

SEPTEMBER. 1968 1 663 Table 6-Age at time of death of 113 asbestos workers who died of bronchogenic carcinoma, mesothelioma or asbestosis. Pleural Age Bronchogenic meso- Peritoneal at death Total carcinoma thelioma mesothelioma Asbestosis 35-39 1 1 - - 4044 1 1 - - 45-49 1 1 - - 50-54 16 9 3 3 1 55-59 24 15 2 2 5 60-64 21 11 1 3 6 65-69 22 16 - 1 5 70-74 10 6 - - 4 75-79 14 6 - 2 6 80-84 3 3 - - - Total 113 69 6 11 27 shows the number of years from first of exposure will teach us little of the po- asbestos exposure to time of death of tential of asbestos exposure, and will 113 consecutive deaths due to asbestos- serve only to dilute pertinent observa- related diseases (bronchogenic carci- tions. Moreover, investigations should noma, pleural mesothelioma, peritoneal aim to follow exposed individuals as mesothelioma and asbestosis). None of long as possible, since risk does not the 113 men died in less than 20 years stop at retirement age or with cessation from onset of exposure, and 101 (89 of occupational exposure. per cent) of them did not die until 30 Data from studies which do not en- or more years had elapsed since onset compass such periods of observation may of exposure. Table 6 shows these same be difficult to interpret.48 In one recent 113 men classified by age at time of study, limited to review of social security death. Only three of the men died under records of individuals working in as- the age of 50 while 49 of them died bestos factories between 1948 and 1951. after age 65. although 21,755 records were examined, In epidemiological studies designed to a considerable portion represented men ascertain potential asbestos disease, par- who could not have reached 20 years ticularly neoplasia, it is obviously neces- from first employment at the end of the sary to consider such latency and, in the period of observation. Compounding case of joint exposure to two agents, this difficulty was the fact that over 90 latency of both must be considered. In per cent were under the age 55 in 1950, practical terms, populations studied and therefore relatively few had reached should contain as many individuals as even age 65 at the end of f -e study pe- possible, with more than 20 years from riod. For those who had reached age 65, onset of exposure. Asbestos exposure no data were recorded concerning their rarely causes disease in less than 20 fate after that age. Conclusions drawn years from onset; inclusion of young- from such data can only be guardedly sters or others with inadequate duration accepted.

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The answer to these and other equally amianto e nella popolazione. Rass. Med. Indust. 29:375-379 (Sept.-Oct.), 1960. intricate problems will require original 12. Petrovic, L. J. Asbestosis in . Higijena 11: efforts. While 166-175, 1959. approaches and diligent 13. Bobileva, A. T.; Bukhantseva, R. M.; Lovtsova, S. animal studies outside the laboratory E.; and Sadilova, Ml. S. The Amount of Dust in Residential Districts of Asbeat and Its Effect on the may be interesting [Webster (1963) Children's Health. Hig. 23:9-12, 1958. studied wild baboons and rats to demon- 14. Kiviluoto, R. Pleural Calcification as a Roentgeno- logic Sign of Non-Occupational Endemic Antho- strate asbestos in the environs of an phyllite-Asbestosis. Acta radiol. 194 (Suppl. 1). asbestos mine49 and we have been study- 1960. 15. Wagner, J. C.; Sleggs, C. A.; and Marchand, P. ing wild rats trapped in urban and rural Diffuse Pleural Mesothelioma and Asbestos Exposure in North Western Cape Province. Brit. J. Indlust. areas], no reliable conclusions will be Med. 17:260, 1960. available without appropriate epidemio- 16. Thomson, J. G.; Kaschula, R. 0. C.; and MacDonald, R. R. Asbestos as a Modern Urban . South logical studies of well-defined cohorts. African M. J. 27:77, 1963. This especially applies to human popu- 17. Jacob, G., and Bohlig, H. Roentgenological Com- plications in Pulmonary Asbestosis. Fortschr. Geb. lations with graduated degrees of expo- Rontgenstrahlen 83:515, 1955. sure, including groups with indirect oc- 18. Selikoff, I. J. The Occurrence of Pleural Calcifica- tion Among Asbestos Insulation Workers. Ann. New cupational and endemic environmental York Acad. Sc. 132:351, 1965. 19. Laamanen, A.; Noro, L.; and Raunio, V. Observa- exposure. tion on Atmospheric Air Pollution Caused by As noted, these will have to be investi- Asbestos. Ibid. 132:240, 1965. 20. Kiviluoto, R. Pleural Plaques and Asbestos: Further gated with a long latent period in mind. Observations on Endemic and Other Nonoccuipational Various disciplines will have to be en- Asbestosis. Ibid. 132:235, 1965. 21. Weiss, A. Pleurakrebs bei lungenasbestose, in vivo listed-pathologists, clinicians, epidemi- morpholgisch gesichert. Medizinische, 1953, p. 93. ologists, basic scientists, and many 22. Marchand, F. Ueber eigentuinliche pigmentkristalle in den lungen. Verhandl. Deutscht Gesell. 17:223-228, others-but the results will warrant the 1906. 23. Enticknap. J. B., and Smither, W. J. Peritoneal efforts. Indeed, they may lead to a new Tumors in Asbestosis. Brit. J. Indiist. Med. 21:20. dimension of the word "pneumoconiosis" 1964. 24. McCaughey, W. T. E.: Wade, 0. L.; and Elmes. which, after all, is only 100 years old.50 T. C. Exposure to Asbestos Dust and Diffuse Pleural Mesotheliomas. (Correspondence.) Brit. M. J. 2: REFERENCES 1937. 1962. 25. Leichner, F. Primary NMesothelioma of Peritoneum 1. Enterline, P. Mortality Rates Among Coal Miners. in a Case of Asbestosis. Arch. Gewerbepath 13: A.J.P.H. 54,5 :758-768 (May), 1964. 382. 1954. 2. Stocks, P. On the Death Rates from Cancer of the 26. Web-ster. T. Mesotheliomatous Tumors in South Stomach and Respiratory Diseases in 1949-53 Among Africa. Pathlology and Exnerimental . Ann. Coal Miners and Other Male Residents in Counties N'ew York Aca(l. Se. 132:623, 1965. of and Wales. Brit. J. Cancer 16,4:592-598 27. Selikoff, T. J.: HIammond. F. C.: and Chitrg. J. (Dec.), 1962. Asbestos Fxpostire. Smoking an(d Neoplasia. J.A.M.A. 3. Eisenbud, M.; Wanta, R. C.; Sunstan, C.; Stead- 204:106, 1968. man, L. T.; Harris, W. B.; and Wolf, B. S. Non- 28. Newbouise, M. ._ anti Thiompson, H. Mesotbelioma Occupational . J. Indust. Hyg. 31:282-294, of Pleuira and Peritoneuim Following Exposure to 1949. Asbestos in the Area. Brit J. Indtsst. Med. 4. Chesner, C. Chronic Pulmonary Granulomatosis in 22:261. 1965. Residents of Community Near Beryllium Plant: 29. Elmes, P. C.. andI Wadle. 0. L. Relationship Be- Three Autopsied Cases. Ann. Int. Med. 32:1028, tween Exposttre to Asbestos and Pleuiral Malignancy 1950. in Belfast. Ann. New York Acad. Sc. 132:549-557, 5. Lupu, N., and Velikan, K. Pneumoconiosis in ]965. Children of Industrial Cities, with SiO2 Air Pollu- 30. Cauna, D.; Totten. R. S.; and Gross, P. Asbestos tion. Gig. i Sanit. 10-13 (Dec.), 1958. Bodies in Human Lungs at Autopsy. J.A.M.A. 192: 6. Batawi, M. A. El, and Hussein, M. Endemic .371. 1965. in an Egyptian Village. Brit. J. Indust. 31. MIeurman. I,. Asbestos Bodies and Pletural Plaques Med. 21:231-234, 1964. in a Finnish Series of Autopsy Cases. Acta path. et 7. Goyal, A. R. Pneumoconiosis in the Non-Industrial microbiol. scandlinav. 111,1 (Su,pp.), 1966. Popuilation of Rajasthan. J. Indian M. A. 30,3: 32. Thomson, J. G., and Graves, W. MI. Asbestos as 79-82, 1958. an Urban Air Contaminant. Arch. Path. 81:458, 8. Cooke, W. E. Pulmonary Asbestosis. Brit. M. J. 2: 1966. 1024, 1927. 33. 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SEPTEMBER, 1968 1 665 36. Collis, E. L., and Gilchrist, J. C. Effects of Dust Schalet, N. Mesothelioma and Its Association with Upon Coal Trimmers. J. Indust. Hyg. 10:101, 1928. Asbestosis. J.A.M.A. 201:587, 1967. 37. Rosato, V. Asbestos. Its Industrial Applications. New 44. Selikoff, I. J.; Churg, J.; and Hammond, E. C. York, N. Y.: Reinhold, 1959, p. 478. Relation Between Exposure to Asbestos and Meso- 38. Simson, F. W., and Strachan, A. S. Asbestosis thelioma. New England J. Med. 272:560, 1965. Bodies in the Sputum: A Study of Specimens from 45. Wagner, J. C. Experimental Production of Mesothelial Fifty Workers in an Asbestos Mill. J. Path. & Tumours of the Pleura by Implantation of Dusts in Bact. 34:1, 1931. Laboratory Animals. Nature 196,4850:180-181 (Oct. 39. Selikoff, I. J.; Bader, R. A.; Bader, M. E.; Churg, 13), 1962. J.; and Hammond, E. C. Asbestosis and Neoplasia. 46. Hueper, W. C. Cancer Induction by Polyurethane, Am. J. Med. 42:487, 1967. and Polysilicone Plastics. J. Nat. Cancer Inst. 33: 40. Hromek, J. The Mass Incidence of Characteristical 1005-1027, 1964. Pleural Changes in Citizens of the Western Part of 47. Selikoff, I. J.; Churg, J.; and Hammond, E. C. the Former Jihlava Region. Rozhl. v Tuberk. 22: Asbestos Exposure and Neoplasia. J.A.M.A. 188:22, 405, 1962. 1964. 41. Zolov, C.; Bourilkov, T.; and Babadjov, L. Pleural 48. Enterline, P. E., and Kendrick, M. A. Asbestos- Asbestosis in Agricultural Workers. Environ. Res. Dust Exposures at Various Levels and Mortality. 1 :287, 1967. Arch. Environ. Health 15:181, 1967. 42. Lieben, J., and Pistawka, H. Mesothelioma and 49. Webster, I. Asbestosis in Non-Experimental Animals Asbestos Exposure. Arch. Environ. Health 14:559, in South Africa. Nature 197:506 (Feb. 2), 1963. 1967. 50. Zenker, F. A. Ueher staubinhalationskrankheiten der 43. Borow, M.; Conston, A.; Livornese, L. L.; and lungen. Deutsche Arch. Klin. Med. 2:116, 1867.

Dr. Selikoff is Professor of Environmental Medicine, Mount Sinai School of Medicine of the City University of New York (Fifth Avenue and 100th Street), New York, N. Y. 10029. Dr. Hammond is Vice-President for Epidemiology and Statistics, American Cancer Society (219 East 42nd Street), New York, N. Y. 10017 This paper was presented before a Joint Session of the Epidemiology, Engi- neering and Sanitation, Maternal and Child Health, Occupational Health, and Radiological Health Sections of the American Association at the Ninety-Fifth Annual Meeting in Miami Beach, Fla., October 25, 1967. This study was supported in part by USPHS Grant No. UI-00440.

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