Document LK9Kw3mzLw4w1Rk4DdM74xZJQ

PLAINTIFF'S EXHIBIT SA-51S Asbestos: a status report William J. Nicholson, PhD, and Philip J. Londrigan, MD The Mount Sinai Medical Center, . City University ofHew York, New York, NY, USA Current Issues In Public Health 1996,2:118-123 in buildings in the United States and Europe, it is of vital importance that this debate be brought to a swift conclusion. This review considers epidemiologic studies of the health effects of asbestos in populations exposed to commercial chrysotile and to mixtures of chrysotile and other forms of asbestos. We show that evidence for the human carcinogenicity of chrysotile asbestos is incontrovertible. We suggest that efforts to describe chrysotile asbestos as "safe" are false, self-serving, and commercially motivated. Asbestos is a term given to a group of minerals that crystallize in a fibrous habitat. Four minerals have commercial importance--chrysotile, amosite, crocidolite, and anthophyllite. Of these, chrysotile is the most important, accounting for more than 95% of current world production. The various minerals dif fer chemically and structurally, but all readily sepa rate into extremely fine fibers, most of which are thinner than 1 pm in diameter. As such, they can easily become airborne during manufacturing processes using asbestos or by abrasion or distur bance of asbestos-containing materials. Their thin ness also allows them to be readily inspired and car ried into the lower regions of the human lung, where they can become lodged and cause bodilydamage. The modem history of asbestos disease dates from the turn of the century', when two cases of asbestocic lung scarring were briefly described in asbestos tex tile workers. The pulmonary disease resulting from such scarring was well described in subsequent pub lications and the term asbestosis was applied to it in 1924. An association of bronchogenic carcinoma with asbestos was first suggested in the 1930s. Mesothelioma, a malignancy of the lining of the chest or abdomen, was clearly associated with asbestos in I960, Asbestos has been declared a proven human carcinogen by the US Environmental Protection Agency, the International Agency for Research on Cancer, and the World Health Organization. Despite publication over the past four decades of a voluminous literature on the causal association between asbestos and disease in different populatioas, and despite extensive experimental demonstra tion of the carcinogenicity' of all forms of asbestos in laboratory animals, there currently exists an extensive and often acrimonious debate concerning the car cinogenicity of chrysotile asbestos. Because of the continuing extensive sale and use of asbestos in South and Central America, Asia, and Africa and the continued widespread presence of asbestos materials THE SPECTRUM OF ASBESTOS DISEASES A seminal study that established much of our current knowledge of the spectrum of asbestos diseases was conducted by Selikoff and Seidman [1] (Table 1). It followed 17,800 heavily exposed asbestos insulation workers for 20 years and dearly demonstrated the wide range of malignancies caused by asbestos. Of these malignant diseases, bronchogenic carcinoma and mesothelioma were the two most important, accounting for more than 90% of the increased can cer risk in this population. Nearly 24% of the deaths in this group of workers were due to bronchogenic carcinoma and 9% to mesothelioma. Lesser degrees of excess cancer mortality' were seen at other sites including the esophagus, stomach, colon and rectum, larynx, pharynx and buccal cavity, gall bladder and bile ducts, and kidney. Overall, among insulators whose asbestos exposure began prior to 1968, 30.9% of deaths were excess cancer deaths resulting from one of the above malignancies; additionally another 8.6% of deaths in this population were due to asbestosis. Although the mortality experience of this unusual group is extraordinary, the insulators were not alone either in their exposure to asbestos or in their risk of asbestos-associated cancer. In 1982 our group made estimates of the expected mortality in the United States from past occupational exposures to asbestos (2). Considering labor turnover since 1940, it was esti mated that approximately 700 asbestos-related deaths occur each year among workers directly installing or removing insulation. Additionally, a much larger pop ulation of construction workers was also exposed to asbestos, albeit to lower levels. Because of the much greater number of construction workers, many more asbestos-related deaths are taking place among them. Thus it was estimated that approximately 7000 deaths are occurring each year in current or former shipyard and construction workers and in W'orkers exposed to asbestos through maintaining insulation materials in plants and powerhouses. We estimated that the total kill in the United States from the asbestos epidemic will exceed 200,000 deaths. 118 1996 RAPID SCIENCE PUBLISHERS ISSN 1076-7762 120 Public health disciplines and themes Table 2. Risks of lung cancer and mesothelioma in workers exposed to various asbestos minerals Asbestos exposure and location Type of asbestos Textile manufar.tur- 100% Chrysotile* ing (South Carolina) Textile manufactur- 98% Chrysotile ing (Rochdale, UK) 2% Crocidolite Textile manufactur- 98% Chrysotile ing (Pennsyivania) 1% Crocidolite 1 % Amosite Amosite insulation 100% Amosite manufacturing (New Jersey) Insulation applica- 60% Chrysotile* lion (United States) 40% Amosite* Asbestos products 80% Chrysotile* (United States) 15% Amosite* 5% Crocidolite* Asbestos cement 89% Chrysotile* products manufac- 10% Crocidolite* turing (Louisiana and 1 % Amosite* Ontario) Crocidolite mining 100% Crocidolite Chrysotile mining 100% Chrysotile Percentage increase in lung cancer for a 1 -y exposure to 1 f/cm3 of asbestos* 2.6 1 1.4 4.3 ' 0.8 0.5 1.8 1 0.1 Details of the calculation of these unit exposure risks are described by the Environmental Protection Agency [31. Chrysotile as mined in Canada is contaminated by a small amount of tremolite (generally less than 1 %). This contaminant is carried over into fiber used in different industries. The percent ages in the column refer to the percentage of commercially sold fiber, including the contamination. ' The percentages of the various fibers used in the plants studied were not given. The estimates are based on published product compositions. _ exposure to 1 fiber/mL. These risks are not statisti cally different from one another and cannot be attributed to the small use of commercial 'amptrbole asbestos in two of the textile plants. Indeed, the highest lung cancer risk was found in 'the textile plant that used no commercial amphiboles. Among the remaining nonmining studies, the per centage increase in lung cancer for each year of exposure to 1 fiber/mL ranged from 0.5% to more than 4%, irrespective of the type of fibers used in the production process. The only exceptions were two studies of friction product manufacturing and one of asbestos cement production. In each of these three studies, severe uncertainties limit the validity of the lower risks reported. All remaining risks, involving substantial amphibole exposure, are similar to those of predominantly chrysotile exposures, Within the sta tistical uncertainties of the data. Even a pure crocidolite exposure in mining demonstrated an increased risk of only 1% for each year of exposure to 1 fiber/mL [41. Although studies of chrysotile mining and milling demonstrate an excess risk of lung cancer, the risk is more than 10 times lower than that seen in studies of asbestos production workers exposed only to chrysotile or to 97% to 98% chrysotile. The origin of this lower risk in the miners is not fully understood. Part of the difference may reflect the different fiber size distributions between the mining and milling operations and the textile plants and other produc tion facilities. Fibers are presumably clumped togeth er and are larger in mining and milling but more fragmented and smaller in the user industries. In summary, the available data on workers employed in the production of asbestos products strongly indi cate a chrysotile lung cancer risk similar to those seen in workers exposed to amosite and crocidolite asbestos. The best estimate of lifetime lung cancer risk for worker exposure to chrysotile in the using industries (as opposed to the mining and milling industries), is an increase of 1% in risk for each, year of exposure to 1 fiber/mL (Kj. = 0.01). Higher fiber exposure circumstances or longer periods of expo sure would give directly proportional higher risks. lit certain textile operations, the unit exposure risk appears to be as much as three times higher than this lower limit. No data are available to indicate the pres ence of a threshold below which there is no risk from exposure to any asbestos mineral. MALIGNANT MESOTHELIOMA The risk of mesothelioma by asbestos fiber type can be analyzed in several ways. First, because the risk of lung cancer is very similar across ail exposures to all fiber types, excluding mining and milling of chrysotile, one can use the excess number of lung cancers as a measure of cumulative fiber exposure. With comparable follow-up periods, the ratio of the number of mesotheliomas to excess lung cancer is a Table 3. Ratio of mesothelioma to adjusted excess lung cancer according to type of asbestos exposure** Type of exposure Studies, n Mesothelioma/excess lung cancer Pleural cases All cases Chrysotile Predominantly chrysotile Amosite Predominantly crocidolite Anthophyllite Talc (tremolite) Mixed exposures 8 6 2 6 1 2 16 0.13 0.24 0.13 0.47 0 0 0.19 0.14 0.48 0.22 0.61 0 0.08 0.4 *From Environmental Protection Agency [3J. Adjusted to the US male cancer rates in 1970. 122 Public health disciplines and themes Table 4. Risks of mesothelioma in workers exposed to various asbestos minerals" Asbestos exposure and location Type of asbestos Risk coefficient Textile production (Rochdale, UK) insulation workers (United States) Factory workers (Paterson, NJ) Miners and millers Cement workers (Ontario, Canada) Chrysotile 1 xlO-o Chrysotile and amosito Amosite l.Sx10-e 3.2 x 10-3 Crocidolite 13.4x10-8 Chrysotile and croci- 12x10-8 dolite The listed risk coefficients correspond to the values KL in the relation, !M = KL x f x [(T -10)1 - (T - D - i0)51, where 1M is the mesothelioma mortality rate, f is the average fiber concentration in f/mL, 7" is the time since start of exposure, and D is the duration of exposure. fifth that observed. Data points represent an average of 15 years for the first point and an average over 10 years for the remaining three. The principal finding is that the time course of mesothelioma risk is totally incompatible with an exposure pattern that begins only in the late 1930s. Indeed, the 95%.confidence limits on three of the four data points do not intercept the expected distrib ution for amosite exposure. Barring unknown expo sures to amphiboles prior to 1935, the data present strong evidence that chrysotile is the substantial, indeed the dominant contributor to the mesothelioma risk experienced by this group of insulation workers. The study by Selikoff et at. [51 of the entire union membership of US and Canadian insulators also strongly indicates the existence of a chrysotiie mesothelioma risk. Follow-up for this study began in 1967, 30 years after the earliest incorporation of amosite by insulation manufacturers into their prod ucts. However, the risk of mesothelioma rises steeply with time from first exposure for at least 50 years. Were only amosite contributing to risk, this pattern would not be expected. One can also estimate risk of mesothelioma due to chrysotile through direct calculations in mixedexposure circumstances (Table 4.) These analyses show that risk of mesothelioma/fiber exposure, as measured by KM, is virtually the same for exposures to 97% chrysotiie + 3 % crocidolite, 60 % chrysotile + 40 % amosite, and 100 % amosite. The value of KVi from the study of Canadian cement workers is higher than the chrysotile-amosite exposures, as was a value of KL in the same group of workers. As noted previ ously, there may be substantial errors in the exposure estimates of this study. The value for a pure crocido lite exposure, as calculated by de Klerk and Armstrong [6] for the mining population of Australia, is about 10 times greater. As with the values of KL in Tabic 1, Km is not definite because of uncertainties of exposures in the early exposure years of the groups under study and from uncertainties of small numbers. Indeed, from a consideration of the ratios of mesothelioma to excess lung cancer, the mesothe lioma potency of crocidolite would appear to be only two to four times greater than chrysotile or amosite mesothelioma potency. Nevertheless, in contrast to the analysis of crocidolite lung cancer risk compared with other fibers, the data do indicate a greater mesothelioma potency for crocidolite. CONCLUSIONS The case is strong that chrysotile is a potent causative factor for both lung cancer and malignant mesothelioma among exposed workers. Data to support this case derive from more than 40 studies of different fiber exposure circumstances. Chrysotile is shown to be a powerful carcinogen when the time course of risk is considered in mixed fiber exposures. Chrysotile is shown also to be a potent human carcinogen in direct calcula tions of risk. All available data suggest that chrysotile dominates the risk in those circum stances in which it is the principal fiber used. The risk of chrysotile in producing mesothelioma is similar to that of amosite on a per fiber exposure basis. Cnx'idolite would appear to have a potential four to 10 times greater to produce mesothelioma for equal exposure than chrysotile. Chrysotile is a proven human carcinogen. Assertions that it is safe and claims that it can be used safely in developing nations are contrary to fact and extremely dangerous. William J. Nicholson, PhD, and Philip J. Landrigan, MD, Mount Sinai School of Medicine, City University of New York, 1 Gustave levy Place, New York, NY, 10029, VSA.