This paper draws together the mortality experience for a cohort of some 11000 male Quebec Chrysotile miners and millers, reported at intervals since 1971 and now again updated. Of the 10918 men in the complete cohort, 1138 were lost to view, almost all never traced after employment of only a month or two before 1935; the other 9780 men were traced into 1992. Of these, 8009 (82%) are known to have died: 657 from lung cancer, 38 from mesotheliona, 1205 from other malignant disease, 108 from pneumoconiosis and 561 from other non-malignant respiratory diseases (excluding tuberculosis). After early fluctuations. SMRs (all causes) against Quebec rates have been reasonably steady since about 1945. For men first employed in Asbestos, mine or factory, they were very much what might have been expected for a blue collar population without any hazardous exposure. SMRs in the Thetford Mines area were almost 8% higher, but in line with anecdotal evidence concerning socio-economic status. At exposures below 300 (million particles per cubic foot) x years, (mpcf.y), equivalent to roughly 1000 (fibres/ml) x years-or, say, 10 years in the 1940s at 80 (fibres/ml)-findings were as follows. There were no discernible associations of degree of exposure and SMRs, whether for all causes of death or for all the specific cancer sites examined. The average SMRs were 1.07 (all causes), and 1.16, 0.93, 1.03 and 1.21, respectively, for gastric, other abdominal, laryngeal and lung cancer. Men whose exposures were less then 300 mpcf.y suffered almost one-half of the 146 deaths from pneumoconiosis or mesothelioma; the elimination of these two causes would have reduced these men's SMR (all causes) from 1.07 to approximately 1.06. Thus it is concluded from the viewpoint of mortality that exposure in this industry to less than 300 mpcf.y has been essentially innocuous, although there was a small risk or pneumoconiosis or mesothelioma. Higher exposures have, however, led to excesses, increasing with degree of exposure, of mortality from all causes, and from lung cancer and stomach cancer, but such exposures, of at least 300 mpcf.y, are several orders of magnitude more severe than any that have been seen for many years. The effects of cigarette smoking were much more deleterious than those of dust exposure, not only for lung cancer (the SMR for smokers of 20+ cigarettes a day being 4.6 times higher than that for non-smokers), but also for stomach cancer (2.0 times higher), laryngeal cancer (2.9 times higher), and-most importantly-for all causes (1.6 times higher).
Comment In: Ann Occup Hyg. 1997 Jan;41(1):3-129072948
Comment In: Ann Occup Hyg. 2001 Jun;45(4):329-35; author reply 336-811414250
Primary prevention carried out today can reduce the disease incidence in the future decades. The present disease panorama is the consequence of past asbestos exposure mainly before the 1970s. The peak incidence of asbestos-induced diseases will be reached around 2010 in Finland. The number of asbestos-related premature deaths is at present annually about 150 which exceeds the figure of fatal work accidents. Asbestos-related cancer will increase still for 15-20 years and reach its maximum, about 300 cases, in 2010, and will start to decrease after that. More than 20,000 asbestos-exposed workers have participated in the medical screening and follow-up. The termination of exposure, antismoking campaigns, improved diagnostics and careful attention to compensation issues, as well as other potentials for prevention, were the central issue of the Asbestos Program of the Finnish Institute of Occupational Health. An important objective of research work is to improve early diagnostics, and thereby treatment prospects, in case of asbestos-induced cancers.
One prospective epidemiologic study of asbestos cement workers with radiological small opacities has been cited as a rationale for attributing excess lung cancer to asbestosis. This approach could have considerable practical value for disease attribution in an era of decreasing exposure. However, a recent International Agency for Research on Cancer review concludes that the mechanism of production of asbestos-related lung cancer are unknown. Asbestosis, therefore, cannot be a biologically effective dose marker of lung cancer susceptibility. Asbestosis nonetheless would be useful in identifying asbestos-attributable lung cancer cases if it could be proven an infallible exposure indicator. In this study, we tested this hypothesis in the chrysotile miners and millers of Quebec, Canada. We examined exposure histories, autopsy records, and lung fiber content for 111 Quebec chrysotile miners and millers. If the hypothesis of an asbestosis requirement for lung cancer attribution were accurate, we would expect as asbestosis diagnosis to separate those with lung cancer and high levels of exposure from those with lower levels of exposure in a specific and sensitive manner. This is the first such study in which historical job-based individual estimates based on environmental measurements, lung fiber content, exposure timing, and complete pathology records including autopsies were available for review. We found significant excesses of lung tremolite and chrysotile and estimated cumulative exposure in those with lung cancer and asbestosis compared to those with lung cancer without asbestosis. However, when the latter were directly compared on a case-by-case basis, there was a marked overlap between lung cancer cases with and without asbestosis regardless of the measure of exposure. Smoking habits did not differ between lung cancer cases with and without asbestosis. In regression models, smoking pack-years discriminated between those with the without lung cancer, regardless of asbestosis status. Most seriously, the pathologic diagnosis of asbestosis itself seemed arbitrary in many cases. We conclude that although the presence of pathologically diagnosed asbestosis is a useful marker of exposure, the absence of this disease must be regarded as one of many factors in determining individual exposure status and disease causation.
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The membrane filter (MF) method for evaluating asbestos fibre concentrations was introduced in the 1960s. Before that time the midget impinger (MI) was used in North America, while the long running (LRTP) and regular thermal precipitator (TP) were used in the U.K. All studies from which estimates of long-term health risks can be derived (i.e. those with individual cumulative lifetime exposure estimates) were based on the now obsolete methods. The reliability of converting these indices of exposure to MF equivalent concentrations was reviewed. It was concluded that no overall single factor could be derived for the Quebec mining and milling industry. However, it has been possible to derive conversion factors at the individual mill and work area level. Applying these in one Quebec mortality study analysis based on all jobs held by persons in the cohort gave an overall MF/MI ratio of 3.6. An examination of the confidence intervals surrounding the Quebec data, ratios derived for other chrysotile mines by other investigators, and measurements of fibre concentrations in the 1970s suggest that this was probably not unreasonable. Side-by-side and other measurements were used to convert MI concentrations in the U.S. textile industry to MF fibre concentrations. While conversions involve considerable uncertainty, independent measurements of fibres in the lung tissues of workers from the U.S. textile plant and Quebec mills show that in lungs the ratios of the concentrations of chrysotile to those of tremolite are quite consistent with the ratio of assessed exposures to these fibres in the two industries. There is an apparently higher risk of mesothelioma in one Quebec mining area (Thetford Mines) than in another (Asbestos). A high concentration of fibrous tremolite has been found in the lungs of workers in Thetford. A method of evaluating the extent to which mesothelioma risk in the chrysotile mining industry might be explained by tremolite exposures was proposed. The slope of the lung cancer dose-response relationship for the textile industry is approximately 50 times that for the mining and milling industry. Available data on the length distributions of fibres from Quebec mines and mills (up to 5% > 5 microns) and the Charleston textile plant (up to 21% > 5 microns) and some marginal indication of longer fibres in tissues from Charleston workers suggest that further work specifically addressing differences in the size distributions of long fibres in these industries is needed.
OBJECTIVES: The incidence of cancer among employees of a Norwegian asbestos-cement factory was studied in relation to duration of exposure and time since first exposure. The factory was active in 1942-1968. Most of the asbestos in use was chrysotile, but for technical reasons 8% amphiboles was added. METHODS: For the identification of cancer cases, a cohort of 541 male workers was linked to the Cancer Registry of Norway. The analysis was based on the comparison between the observed and expected number of cancer cases. Standardized incidence ratios (SIR) and 95% confidence intervals (95% CI) were estimated. Period of first employment, duration of employment, and time since first employment were used as indicators of exposure. Poisson regression analysis was used for the internal comparisons. RESULTS: The standardized incidence ratio was 52.5 (95% CI 31.1-83.0) for pleural mesothelioma, on the basis of 18 cases. The highest standardized incidence ratio was found for workers first employed in the earliest production period (SIR 99.0, 95% CI 51.3-173). No peritoneal mesothelioma was found. The standardized incidence ratio for lung cancer was 3.1 (95% CI 2.14.3), but no dose-response effect was observed. The ratio of mesothelioma to lung cancer cases was 1:2. CONCLUSIONS: This study showed a high incidence of mesothelioma and a high ratio of mesothelioma to lung cancer among asbestos-cement workers. The high incidence of mesothelioma was probably due to the fact that a relatively high proportion of amphiboles was used in the production process.