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Toxicologyand Industrial Health, Vol. 7, No.112,1991 53 DANGEROUS AND OF PRODUCTS ACNADNCCEHRE-MCAICUASLINSGINPTRHOEPEORITLIES. -REFINING AND PETROCHEMICAL INDUSTRY: PART V ASBESTOS-CAUSED CANCERS AND EXPOSURE OF WORKERS IN THE OIL REFINING INDUSTRY - M. A. MEHLMAN UMDNJ Robert Wood Johnson Medical Group Environmental and Community Medicine 675 Hoes Lane Piscataway, NJ 08854 In the oil refining and petrochemical industries exposure to cancercausing asbestos particles, especially during equipment repair and maintenance, is very high. Up to 90% of workers in the oil refining industry had direct andlor indirectcontact with asbestos,and more than hurfof this contact occurred without the use of any kind ofprecaution, thus these workers are in high risk of developing lung cancer and mesothlioma, both fatal diseases. The hazards include: inadequate health and safety training for both company personnel and workers, failure to inform about the dangers and diseases (cancers)resulting from exposure to asbestos; excessive use of large numbers of untrained and uninformed contract workers;lack of use ofprotective equipment; and archaeological approaches and responses to repairing asbestos breaks and replacement of asbestos in oil refiningfucilities.For a better understanding of practices and policies in the oil refining industry,r@er to Rachel Scott's Muscle and Blood, in particirlar the chapter "Oil" (E.P. Dutton, New York, 1974), as well as to an editorial which appeared in the Oil and Gas Journal,April, 1968. INTRODUCTION Exposure to asbestos in the oil refining and petrochemical industries usually occurs by inhalation of asbestos fibers after the breakdown of man-made asbestos-containing products such as pipe insulation, ceilings, floor tiles, heat exchanges, diesel units, valves, gaskets, crude columns, and many other sources. Toxlcokgy and Indumtrkl Hoallh. Vol. 7, No. 1/2. pp. 63-71 Copyright 0 1QQ1 Prlncolon Sclrnliflc Publlmhlng Co., Inc. ISSN: 0740.2337 54 Mehlman While normally very low levels of asbestos are detected in ambient air samples, (approximately 3 to 3,000 fibers per cubic meter (f/m3) in rural outdoor air, asbestos fiber level during insulation and equipment maintenance work range between 15,000,000to 20,000,000 f/m3. The fiber level near, or at, oil refining plants have been found to be between 2,000,000 to 3,000,000f/m3 (Nicholson et al., 1982; Nicholson, 1976). The asbestosconcentration present in indoor air depends on how much asbestos insulation is present, and on the extent of the deterioration and crumbling of this material. Extremely high levels of asbestos in buildings that contained asbestos insulation have been reported up to 20,000,000 f/m3. Individuals who work with asbestos (maintenance personnel) or others who are present in the areas with deteriorating or crumbling asbestos are at significantly higher risk, regardless of exposure levels, of suffering from asbestos-related diseases, such as lung cancer and mesothelioma. ASBESTOS-CAUSED DISEASES Workers exposed to asbestos were found to have high risk of developing lung cancer and mesothelioma, both fatal diseases. There is now human evidence that breathing asbestos fibers can increase the risk of cancers of the stomach, intestines, esophagus, pancreas, kidney, and other possible sites (Table 1) (Selikoff et al., 1965, 1972). In addition to cancers, exposure to asbestos can cause a slow accumulation of scarring tissue in the lung and in the membrane surrounding the lung, resulting in difficulty in breathing and leading to the development of the potentially fatal disease, asbestosis. The systems associated with asbestos diseases are described in Table 2. TABLE 1 ASBESTOS-CAUSED CANCERS Lung Pleural Mesothelioma (Chest) Esophagus (Gullet) Stomach Colon Rectum Mouth and Throat Areas Lwnx Kidney pancreas Other sites, such as the Brain,etc. - Toxicology and Industrial Health, Vol. 7 ,No.112,1991 55 TABLE 2 SYMPTOMS ASSOCIATED WITH ASBESTOS DISEASES Asbestos Shortness of breath, cough, sputum, chest tightness, enlargement of ends of fingers and toes Lung Cancer Shortness of breach, chest pain or fullness, blood streaking, swellings anywhere (such as glands in the neck),clubbing of fingers and toes, unexplained cough and sputum, abdominal discomfort Pleural Mesothelioma Shortnessof breath, chest pain or fullness Peritoneal Mesothelioma Abdominal swelling or increase in girth, abdominal discomfort, bowel change,recent hernia Esophagus Difficulty in swallowing Stomach Indigestion, lack of appetite, nausea, vomiting, black stool HISTORICAL KNOWLEDGE ABOUT ASBESTOS DISEASE Knowledge of health hazards associated with asbestos dates from ancient history. Pliny, a Roman historian, reported that slaves working with asbestos became disabled (Hunter, 1969). Asbestos industries began on a commercial scale around 1860-1880, and by the turn-of-the-century lady inspectors of factories in Great Britain had made studies focussing on the dangers to humans from asbestos inhalation (Anderson, 1902; Castleman, 1984). In the early twentieth century, reports on the dangers of exposures began to appear in medical and scientific literature. In 1906 H.M. Murray described a case of pulmonary fibrosis in an asbestos worker who he first examined in 1899. The patient was thirty-three years old and the only survivor out of ten others working in the same facility. All others died at approximately thirty years of age. Many similar reports on asbestos injuries followed by W.E.Cooke (1924, 1927), H.M.Auriban (1906), L. Scarpa (1908), E.C.Collis (1910), F.L. Hoffman (1918), E.R.A. Merewether (1933), T Fahr (1914), H.K. Pancost (1917, 1918, 1925). S. McDonald (1927), T. Oliver (1927). G.G. Davis et al. (1934), R.G. Mills (1930), J.G. Burrow (1963), A.J. Lanza et al. (1935, 1939), I.J. Selikoff and D.H.K.Lee (1978), S.R. Gloyne (1933, 1953), and many others. In 1918 the U.S.Department of Labor published a report by F.L. Hoffman which described health hazards arising from the inhalation of dust in mining 56 Mehlman asbestos. Four years later the U.S.Bureau of Labor Standards (Bull. No. 806) published a guide to occupational hazards citing asbestos as one such hazard (Heiboff, 1932). Regulations and a guidebook on asbestos hazards were established in Marenl, England in 1932 and in the U.S.in'1933 (Bull. No. 41). Thus from review of the worldwide medical literature and other related information that was available to industry, it is concluded that since the late 1930s manufacturers of asbestos and manufacturers of asbestos-containing products have had sufficient knowledge to investigate the hazards associated with asbestos in its various uses. PHYSICAL AND CHEMICAL PROPERTIES OF ASBESTOS FIBERS Tables 3A and 3B summarize some of the chemical and physical properties of various kinds of asbestos: actinolite, amosite, anthophyllite, crocidolite, tremolite, and chrysotile. The chrysotile asbestos is generally known as white asbestos; amosite is known as brown asbestos, but may also be gray or greenish; crocidolite is known as blue asbestos but may also be lavender or green in color. All varieties are in solid forms, non-flammable, and have a melting point or decomposition temperature which varies from 600C for amosite to 104oOCfor tremolite. All the varieties of asbestos listed in Tables 3A and 3B are insoluble in water and organic solvents. Some asbestos can be dissolved in strong acid or base. Some researchers have contended that one of the most critical properties of asbestos is the absolute length of fiber present in various kinds of asbestos. However, the majority of researchers, including Stanton, have noted that while carcinogenicity is dependent on the length of fibers, it is even more dependent on the ratio of length to width. If the concentration of short fibers is high in an aerosol to which people are exposed, the cumulative contribution to carcinogenicity will most likely exceed that of the more carcinogenic longer fibers, which may be present but in a smaller quantity. In amosite, crocidolite, and chrysotile between 30 and 40% of the fibers are shorter than 1 pm, while 3 to 6% are shorter than 5 pm,and only 1 to 3% are shorter than 10 pm. Bittersohol(l97 1) and Bittersohl and Ose (1971) reported twenty-six cases of mesothelioma from 1967 to 1971 in the oil refining and petrochemical industries. Asbestos was used frequently in these industries and a high concentration of airborne dust containing fibers was present in the work environment. The studies examined 22 patients who worked in the chemical industry. One patient was the spouse of a chemical plant worker and had no Toxicology and Industrial Health, Vol. 7 ,No. 112,1991 57 Toxicology and Industrial Health, Vol. 7,No. 112. 1991 59 occupational exposure to asbestos. Sixteen workers had direct occupational exposure and nine had indirect exposure to asbestos. Chest X-rays were taken prior to development of mesothelioma, and in 17 out of 23 patients pleural thickening and pleural plagues were present. DISEASE CAUSED FROM ASBESTOS EXPOSURE IN HUMANS Tables 4A and 4B present documentation of deaths and cancers caused by various forms of asbestos in occupational settings and describe the f-yr/mL of exposure, exposure frequency, and duration of exposure. The occupational exposure that resulted in deaths from pneumoconiosis and asbestosis from chrysotile, amosite, and crocidolite ranged on average from 1 to 20 years. The f-yr/mL exposure was between 68 and 300. The injuries induced from 0.1 to 39 years of exposure from 20 to 75 f-yr/mL were asbestosis, fibrosis, abnormal X-ray,and decreased respiratory function. TABLE 4A. Diseases Caused From Exposure to Asbestos in Humans Speciee Exposure Frequency/ Duration Diseasea Reference nw of Asbestos CHRDNIC EXPOSURE Death 1. Human 105 (pneumoconiosis) 2. Human 6& (asbestosis) 3. Human 90(asbestosis) 4. Human 115(asbestosis) 5. Human 300 (asbestosis) 6. Human 90 (pneumoconiosis) 7. Human 100 (asbestosis) 8. Human Systemic 9. Human Less than 10yr 300 (asbestosis) 72 (asbestosis) 2 0 b (fibrosis) 50 (abnormal X-ray) 75 (decr. rem.function) Hughes et al., 1980, Dement et al., 1983 McDonald et al., I983 Peto et al., 1985 Nicholson et al.. 1979 McDonald et al., 1980 Finkelstein et al., I983 Henderson & Enterline, 1979 CH, RC,AM CH CH CH, CR CH CH CH, CR CH, CR, AM Berry et al., I979 Wollmer et al., 1987 I979 Irwig et al., I979 Enarson et al.. CH, C R AM CH CH, AM CH 60 Mehlman Tables 4A and4B also show that exposure to all forms of asbestos including tremolite, actinolite, amosite, crocidolite, and chrysotile results in lung cancers, mesothelioma, and gastrointestinal cancers. The f-yr/ml exposure ranges from 10 CEL to 450, and duration is from 1 to 20 years. Thus, it is possible to conclude that all forms of asbestos cause cancer and there is no known safe level of exposure. TABLE 4B. Diseases Caused From Exposure to Asbestos in Humans Exposure Species Frequency/ Duration Diseases Reference 5pe of Asbestos CHRDNICEXPOSURE (Continued) Systemic (Continued) 15. Human 14. Human Cancer lo+ yr (-UP) 0.1-39yr (=up) 26 (asbestosis) 17 (fibrosis) Roach et al., 1983 Green et al., 1986 CH CH, CR 15. Human More than 2- 450 CEL (lung cancer, Less than 10 yr mesothelioma) Weill et al., 1979 CH, CR, AM (-up) l6. Human Less than 2 yr 10 CEL (luna cancer. GI Newhouse and Berry, CR, CH, AM (occUP) cancer m&thelioma) I979 17. Human 20+ yr 3 0 CdL (lung cancer, Nicholson, et al. CH (=up) mesothelioma) 1979 18. HUlllan 1-20yr 90CEL (lungcancer) Amandus and TR,AC (=up) Wheeler 1987 19. Human 1-20 yr 50 CEL (lung cancer, McDonlaid, et a]. CH (OCCUP) mesothelioma) 1983 20. Human 3.8 yr 50 CEL (lung cancer, Hughes, et al. CH, CR, Ah4 (aver. occup) mesothelioma) 1987 21. Human Less than 5 yr 72 CEL (lung cancer. Peto, et al. CH, CR (=up) mesotheiioka) 1985 22. Human ND BO CEL (lung cancer, GI Enterline et al. CH, CR, AM 23. Human (=up) Less than 9 yr c4a4nCceErLm(luesnogthcealnicoemr,a) 1987 Finkelstein, et al. CH, CR (-up) mesothelioma) 1983 24. Human 1-20 yr 180 CEL (lung cancer) McDonald, et a1 CH (occup) 1984 25. Human 10-30 yr 14 CEL (lung cancer) Dement, et al., CH 26. Human (occup) 3-51 yr 180CEL (lung cancer, 1983 Henderson and CH mesothe1ioma) Enterline, et al., (OCCUP) 1979 27. Human 1-20 yr 45 CEL (lung cancer) McDonald, et al, CH, AM, CR (OCCUR) 1982 Jllis value converted to a corresponding exposure of 3,400,000fim" for 20 years. This value converted to a corresponding exposure of 1,000,000 fim:'for 20 years. LOAEL lowest observed adverse effect level; NOAEL .no observed adverse effect level; f/yr/ mL fiber-years per milliliter; yr year; CH I chrysotile; CR . crocidolite; aver. 1 average; AM . amostie; occup . occupational; Eiesp . respiratory; decr. 1 decreased; CEL . cancer effect level; GI gastrointestinal; TR . tremolite; AC . actinolite; ND . no data. Toxicology and Indusrrial Healrh, Vol. 7 ,No. 112, 1991 61 DISEASES OF PETROCHEMICAL AND OIL REFINING INDUSTRY WORKERS The high risk of lung cancer and mesothelioma in the oil refining and petroleum industries is of major concern for maintenance workers of all categories. A number of studies have shown that exposure to low-level asbestos (in areas adjacent to industrial facilities and in family household exposure of workers) can result in significant risk of developing mesothelioma (Selikoff, 1977; Newhouse & Thompson, 1965; Haries et al., 1972; Wagner et al., 1960). R. Lilis et al. (1980) examined maintenance workers (welders, carpenters, electricians, pipefitters, and others) from the oil refining and petrochemical industries. 137 workers from oil refining and 185 from the petrochemical industry were classified by age distribution and by duration since onset of work (in years). In the petrochemical workers, irregular opacities indicating parenchymal intestine fibrosis, pleural thickening, and calcification (with or without thickening), and a high prevalence of chest X-ray abnormalities were found in workers with 30 or more years of occupational exposure. In oil refining workers, the studies revealed irregular opacities, indicating intestine pulmonary fibrosis in 23% of the cases; and radiological abnormalities of the pleura were found in 25% of patients, a rather significant number. Dyspnea on exertion was highly prevaierit in the workers. The risk of developing lung cancer and mesothelioma in this occupational setting also is high. The examination of oil refinery workers such as boilermakers, carpenters, crane operators, distillation workers, electricians, filter plant operators, forklift operators, inspection workers, labor persons, stupping checkers, and welders, who do not directly handle asbestos but rather were subject to indirect asbestos exposure, found that even this "bystander" exposure resulted in risks of cancer comparable to workers directly exposed to asbestos in other industries and occupations. STUDIES OF ASBESTOS EXPOSURE IN OIL REFINING INDUSTRY Method In 1990, a questionnaire on the uses, disposal, and handling of asbestos was prepared and mailed to Oil Chemical and Atomic Workers local unions representing the following corporations: Mobil Oil, Chevron USA, Shell, TOSCO, ARCO, Texaco, Fletcher Oil, Golden Eagle Refining, Golden West Refining, Lacy Oil, Beacon Oil, Witco, Sunland Refining, Union Oil, Sond Refining, U.S. Oil and Refining, AMOCO, Genex, Exxon, Phillips, Pennzoil Refining, Bloomfield Refining, Ashland, Cities Service, Quaker State, Columbia Gas, MAPCO, Citgo Petroleum, Fina Oil & Chemical, Crown Central, Kerr-McGee, Gulf, British Petroleum, Sun, and others. 62 Mehlman The questionnaire asked the following questions: When was asbestos used, and on what equipment? How much contact did workers have with the asbestos during installation, repair, or removal, and what type of protective equipment was used, if any? Also, the types of products containing asbestos in each facility were identifed. Analysis For Asbestos Bulk samples (approximately 400)were taken from one refinery (over a period of several years) and analyzed for their asbestos content. Several established laboratories with considerable experience in asbestos analysis carried out polarized microscope analyses in accordance with NIOSH and EPA prescribed methods. ASBESTOS USE IN THE U.S. Based upon the above-mentioned questionnaire, it was shown that significant amounts of asbestos-containing products were used in the oil refining and petrochemical industries in the United States from 1900-1990. In 1965, 721 tons of asbestos were used in these industries. The primary uses of asbestos were in asbestos-cementpiping, electrical insulation, packing, and gaskets. By 1988, total asbestos use decreased ten-fold, to 71 tons. This very significant decrease occurred across the board in all primary areas of asbestos use where workers were most exposed to asbestosfiber dust. PRODUCTION WORKERS Table 5 shows the annual average number of production workers in the U.S. petroleum refining industry from 1947 to 1977, and reveals a gradual decrease in number of workers over the three decades. However, this decrease may be deceptive as it does not reflect the more recent oil industry hiring practices; it does not include contract employers whose numbers have increased greatly since 1947 and may have exceeded salaried workers. TABLE 5 Production Workers in Petroleum Refining (U.S.) YEAR NUMBER OF WORKERS (ANNUAL,AVERAGE) 1947 146,000 1952 144,000 1957 132,000 1962 lOl,Ooo 1%7 89,600 1972 92,400 1977 99,000 Toxicology and Industrial Health. Vol. 7,No. 112, 1991 63 RESULTS OF SURVEY OF U.S. OIL REFINING AND PETROLEUM INDUSTRIES In a 1990 survey of the oil refining industry in the U.S., asbestos was found to be used in boilers, buildings, compressors, crude columns, drums, FCC-CAT Crackers, furnaces, gaskets, wall boards, valves, pipings, heat exchanges, roofs, storage tanks, towers, tile, turbines, and other areas. Figures 1, 2, 3, and 4 show photographs or various areas within a typical refinery and illustrate numerous asbestos breaks to which humans are exposed. Analysis of asbestos samples show that approximately 40% of the product used in the refinery was chrysotile, 30% was amosite, and 30% was a combination of chrysotile and amosite. This survey also established that up to 90% of workers in the oil refining industry had direct or indirect contact with asbestos, and that more than half of the time (57%). no precautions of any kind were used by individuals working with asbestos. These findings are consistent with findings that a large percentage of workers in oil refining industry showed significant radiological changes due to exposure to asbestos. ACKNOWLEDGEMENT I would like to thank the following individuals for their generous assistance with various aspects of this research. Professor Irving J. Selikoff and Professor William Nicholson of Mount Sinai School of Medicine; Sylvia Krekel, Jean Urand, and Anthony Mazzochi of the Oil, Chemical and Atomic Workers, International Union, AFL-CIO, at Denver, Colorado; Dennis Stephano of Oil, Chemical and Atomic Workers Union, Local 8-234, members of the safety committees of local unions of OCAW in numerous states, representing oil refineries and petrochemical plants; Tom Brown of Workplace Health Fund, Washington, DC; and Professor Burton Davidson, Department of Chemical Engineering, Rutgers University, New Jersey. FICVRE la. Crude unit showing massivc columns. All t a n colorpd pipes are asbestos. There are numeruus asbestos breaks. FIGCRE 1b. 1):esel unit shoNing numerous asbestos breaks Toxicology and Industrial Health, Vol. 7 ,No. 112, 1991 65 FIGURE 2a. Crude vacuum still (desalter unit) showing asbestos breaks. R G U R E 2b. Boiler house. All asbestos with large number of breaks. Toxicology and Inditsttial Health, ilol. 7, N o . 112, 1991 67 FIGURE 4a. Part of catalytic cracker showing asbtstm exposed pipes (area 4). FIGURE I b . E x p ~ pd~ p eshowing asbestos bwak 68 Mehlman REFERENCES ANDERSON, A.M. (1902). "Historical Sketch of the Development of Legislation for Injurious and Dangerous Industries in England." Dangerous Trades (T. Oliver, Ed.) p. 25. Dutton, New York. Also in Goldberg, R.W. (193 1). Occupational Diseases. p. 13. Columbia University Press, New York. AURIBAULT, M. (1906). "Note sur 1'Hygieneet la Securite des Ouvriers dans la Filatures et Tissages dAmiante." Bull Insp. Trav.Paris. 14:120-132. BERRY, G, GILSON, J.C., HOLMES, S., LEWINSOHN, H.C., and ROACH, S.A. (1979). "Asbestosis: A study of dose-responserelationships in an asbestos textile factory.'' Br. J . Ind. Med. 36:98-112. BITTERSOHL, VON G. (197 1). "Epidemiologische Untersuchungen uber Krebser-krankungen in der Chemischen Industrie." Arch. Geschwulstforsch. 38: 198-209. BITTERSOHL, VON G. and OSE, H. (1971). "Zur Epiderniologie des Pleuramesothelioma." 2.ges. Hyg. 17:861-864. BURROW, J.G. (1963). AMA: Voice of American Medicine. pp. 52-52. Johns Hopkins Press, Baltimore. CASTLEMAN, B.I. (1984). Asbestos: Medical and Legal Aspects. Law & Business, Inc., Harcourt Brace Jovanovich, New York & Washington, D.C. COLLIS, E.C. (1911). "Dusty Processes.'' Annual Report of the Chief Inspector of Factories and Workshopsfor the Year 1910. p. 188. H.M. Stationery Ofc., London. COOKE, W.E. (1924). "Fibrosis of the Lungs Due to the Inhalation of Asbestos Dust." Br. Med. J . 2:147. COOKE,W.E. (1927). "Pulmonary Asbestosis." Br. Med. J. 2: 1024-1025. DAVIS, G.G., SALMONSEN, E.M., and EARLYWINE, J.L. (1934). The Pneumo-konioses (Silicosis)Bibliography and Laws - Volume 1, pp. 153, 166, 182-183,208-210, 213. Industrial Medicine, Inc., Chicago. DEMENT, J.M., HARRIS, R.L., SYMONS, M.J., and SHY, C.M. (1983). "Exposures and Mortality Among Chrysotile Asbestos Workers. Part 11: Mortality." Am. J. Ind. Med. 4:42 1-433. ENARSON, D.A., EMBREE, V., MACLEAN, L., and CRZYBOWSKI, S. (1988). "Respiratory Health in Asbestos Miners,in British Columbia: A Longitudinal Study." Br. J. Ind. Med. 45459-463. ENTERLINE, P.E., HARTLEY, J., and HENDERSON, V. (1987). "Asbestos and Cancer: A Cohort Followed Up to Death." Br. J. Ind. Med. 44: 396-401. FAHR, T. (1914). "Demonstrationen: Praparate und Microphotogrammes von einen Falle von Pneumokoniose." Muenchener.Med. Woch. 11:625. FINKELSTEIN, M. (1986). "Pulmonary Function in Asbestos Cement Workers: A Dose-Response Study." Br. J.Ind. Med. 43:406-413. FINKELSTEIN, M. (1983). "Mortality Among Long-Term Employees of an Ontario Asbestos-Cement Factory." Br. J. Ind. Med. 40: 138-144. Toxicology and Industrial Health, Vol. 7 ,No. 112, 1991 69 GLOYNE, S.R. (1933). "The Morbid Anatomy and Histology of Asbestosis.*' Tubercle 15: 445-451,493-497, 550-558. GLOYNE, S.R. (1935). Abstract of the Preceding Article, Bull. Hyg. 10: 219-220. Reprinted in Pneumoconiosis Abstracts I: 143 (1953). GREEN, F.H., HARLEY, R., VALLYATHAN, V. et al. "Pulmonary Fibrosis and Asbestos Exposure in Chrysotile Asbestos Textile Workers: Preliminary Results." In: Accomplishments in Orzcology. The Biological Effects of Chrysotile. Vol. 1, No. 2, 59-68. HARRIES, P.G., MACKENZIE, F., SHEERS, G., KEMP, J.H., OLIVER, T.P. and WRIGHT, D.S. (1972). "Radiological Survey of Men Exposed to Asbestos in Naval Dockyards." Br. J. Znd. Med. 29: 274-279. HENDERSON, V.L.,and ENTERLINE, P.E. (1979). "Asbestos Exposure: Factors Associated with Excess Cancer and Respiratory Disease Mortality." Ann. NY Acud. Sci. 330: 117-126. HOFFMAN, F.L. (1918). "Mortality From Respiratory Diseases in the Dusty Trades (Inorganic Dusts)." Washington, D.C.: U.S. Bur. Labor Statistics Bull. NO. 231, p. 172-180. HUGHES, J. and WEILL, H. (1980). "Lung Cancer Risk Associated with Manufacture of Asbestos-Cement Products." IARC Sci. Publ. 30:627-635. HUGHES, J., WEILL, H. HAMMAD, Y.Y. (1987). "Mortality of Workers Employed in Two Asbestos Cement Manufacturing Plants.**Br. J. Ind. Med. 44: 161-174. HUNTER, D. (1969). The Diseuses of Occupatiorzs. 4th Ed., p. 1009, Little, Brown & Co., Boston. IRWIG,L.M., DU TOIT, R.S., SLUIS-CREMER, G.K.,et al. (1979). "Risk of Asbestosis in Crocidolite and Amosite Mines in South Africa.', Ann. NY Acad. Sci. 330: 35-52. LANZA, A.J. and VANE, R.J. (1939). "Industrial dusts and the Mortality from Pulmonary Disease.,' Am. Rev. Tuberc. 39:419-438. LANZA, A.J., MCCONNELL, W.J., and FEHNEL, J.W. (1935). "Effects of the Inhalation of Asbestos Dust on the Lungs of Asbestos Workers.,' P&I. Health Rep. 5O:l-12. LILIS, R., DAUM, S., ANDERSON, H. ANDREWS, G. and SELIKOFF, I.J. (1980). "Asbestosis Among Maintenance Workers in the Chemical Industry and Oil Refinery Workers.,' In: Biological Eflects of Mineral Fibers. International Agency for Research on Cancer (IARC). MCDONALD, J.C., LIDDELL, D.F., GIBBS, G.W., ESSYEN, G.E., and MCDONALD, A.D. (1980). "Dust Exposure and Mortality in Chrysotile Mining, 1910-75."Br. J. Ind. Med. 37:ll-24. MCDONALD, A.D., FRY, J.S., WOOLLEY, A.J., and MCDONALD, J.C. "Dust Exposure and Mortality in an American Factory Using Chrysotile, Amosite, and Crocidolite in Mainly Textile Manufacture.', Br. J.Znd. Med. 39:368-374. MCDONALD, A.D., FRY, J.S., WODLEY, A.J., et al. (1983). "Dust Exposure and Mortality in an American Chrysotile Textile Plant." Br. J.I nd. Med. 41:151-157. 70 Mehlman MCDONALD, S. (1927). "History of Pulmonary Asbestosis." Br.Med.J. 2: 1025-1026. MEREWETHER, E.R.A. "A Memorandumon Asbestosis." Tubercle. MEREWETHER, E.R.A. and PRICE, C.W. (1930). "Reporton the Efiects of Asbestos Dust on the Lungs and Dust Suppression in the Asbestos Industry." H.M. Stationery Ofc. MEREWETHER, E.R.A. (1930). "The Occurrence of Pulmonary Fibrosis and Other Pulmonary Infections in Asbestos Workers." J. Indust. Hyg 12:198- 222,239-257. MILLS, R.G. (1930). "Pulmonary Asbestosis: Report of a Case." Minnesota Med. 13:495-499. MURRAY, H.M. (1907). Departmental Committee on Compensation for Industrial Diseases Minutes of Evidence. Appendices and Index. pp. 127- 128. Wyman and Sons, London. NEWHOUSE, M.L.,BERRY G. (1979). "Patterns of Mortality in Asbestos Factory Worker in London." Ann. NY Acud. Sci. 33053-60. NEWHOUSE, M.L. and THOMPSON, H.(1965)."Mesothlioma of Pleura and Peritoneum Following Exposure to Asbestos in the London Area." Br. J. Ind. Med. 22:261-269. NICHOLSON, W.J. PERKEL, G., and SELIKOFF, I.J. (1982). "Occupational Exposure to Asbestos: Population at Risk and Projected Mortality - 1980-2030."Am. J . Ind. Med. 3:259-311. NICHOLSON, W.J., SELIKOFF, I.J., SEIDMAN, H., et al. (1979). "Long- Term Mortality Experiene of Chrysotile Miners and Millers in Thetford, Quebec." Ann. NY Acud. Sci. 330:1 1-21. OLIVER, T.(1927). "Clinical Aspects of Pulmonary Asbestosis." Br. Med. J. 2: 1026-1027. OLIVER, T. (1927). "Pulmonary Asbestosis in its Clinical Aspects.'' J . Indust. Hyg. 9:483-485. PANCOAST, H.K., MILLER, T.G.,and LANDIS, H.M. (1917). "A Roentgenologic Study of the Effects of Dust Inhalation Upon the Lungs." Trans. Assoc. Amer. Phys. 32:97-108. PANCOAST, H.K., MILLER, T.G.,and LANDIS, H.M. (1918). "A Roentgenologic Study of the Effects of Dust Inhalation Upon the Lung." Republished. Amer. J . Roent. 5:129-138. PANCOAST, H.K. and PENDERGRASS, E.P. (1925). "A Review of Our Present Knowledge of Pneumocomiosis, Based Upon Roentgenologic I Studies, with Notes on the Pathology of the Condition." American J. Roent. 14:381-423. I PETRO, J., DOLL, R., HERMON, C., et al. (1985). "Relationship of Mortality to Measures of Environmental Asbestos Pollution in an Asbestos Textile Factory." Ann. Occup. H y g . 29:305-355. ROACH, S.A., HOLMES, S., BEVERLY, W.A.H., et al. (1983). "British Occupational Hygiene Society Report from the Committee on Asbestos: A Study of the Health Experience in Two U.K. Asbestos Factories." Ann. I Occup. Hyg. 27:358. Toxicology and Industrial Health, Vol. 7 ,No. 112,1991 71 SCARPA, L. (1908). "Industria dell'Amiantoe Tuberculosi." Proc. Int. Med. Congr. 18th 358. SELIKOFF, I.J. (1977). "Cancer Risk of Asbestos Exposure." In: Origins in Human Cancer (H.H. Hiatt, Watson, J.D., and Winsten, J.A., 4 s . ) . pp. 1765-1784. Cold Spring Harbor Laboratory, New York. SELIKOFF, I.J. and LEE, D.H.K. (1978). Asbestos arid Disease. p. 23. Academic Press, New York. WAGNER, J.C., SLEGGS, C., and MARCHAND, P. (1960). "Diffuse Pleural Mesothelioma and Asbestos Exposure in the North Western Cape Province." Br. J. Ind. Med. 17:260-271. WAGNER, J.C. (1980). "Biological Effects of Mineral Fibers." Vol. 2, Lyon (IARC Scientific Publication No. 30). WEILL, H.,HUGHES,J., WAGGENSPACK, C. (1979). "Influence of Dose and Fiber Type on Respiratory Malignancy Risk in Asbestos Cement Manufacturing." Am. Rev.Respir. Dix. 120:345-354. WOLLMER, P., ERIKSSON, L., JONSON, B., et al. (1987). "Relation Between Lung Function, Exercise capacity, and Exposure to Asbestos Cement." Br. J. Ind. Med. 44542-549.