Mortality data from 9609 workers at two asbestos mining areas in Quebec were analyzed to assess the effects of the intensity and timing of exposure on lung cancer risk. Summary exposure measures based on differing assumption were computed for lung cancer cases and matched controls and were fitted to the data using conditional logistic regression. A non-linear relationship between intensity and risk fit both mining areas, but risk was greater at one area than the other. At the mine with lower risk, exposure occurring more than 30 years prior to death had little effect, while at the other mine risk did not vary with time since exposure and men starting employment before 1924 were at elevated risk. The results point to differences in dust composition at the two areas and illustrate the difficulties in estimating risk.
A respiratory survey was undertaken in chrysotile asbestos miners in British Columbia consisting of a questionnaire, spirometry, chest radiography, and physical examination. The tests were performed in 1977 and again in 1983. The population groups studied included 63 "exposed" (working in the plant more than nine years), 52 "controls" (working in the plant less than five years), and 38 residents of the village at the minesite. A subset of 39 was identified with high exposure (worked in the mill more than five years). Measured levels of environmental particulates were similar over the entire period of operation of the plant (1.4 to 14.0 million particles per cubic foot and 0.7-88.0 fibres/cc in the mill; 0.2 to 2.7 mpcf and 0.6 to 9.3 f/cc in the mine). The exposed groups were more likely to report cough and breathlessness than the two other groups and were also more likely to have abnormal FVC and chest x ray films (the latter not significant, p greater than 0.05) and to be more likely to have a combination of these abnormalities. There was no trend to progression in the combination of abnormalities associated with exposure on follow up. The heavily exposed group showed a significantly worse trend in FVC. This adverse trend was confined to those with initial abnormalities. Tobacco smoking did not increase the trend to progression in this group.
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Two cohorts of chrysotile miners and millers in Quebec were selected to study the extent to which chest radiographs taken while still employed predict mortality. The paper presents mainly findings in much the larger cohort, which consisted of 4559 men (two-thirds past workers) whose latest radiograph had been assessed by one of six experienced readers into what became the UICC/Cincinnati (U/C) classification; by the end of 1975 there had been 1543 deaths in this cohort. The findings were generally confirmed in the other cohort, comprising 988 current male workers, who had been examined in 1967-8 by questionnaires on respiratory symptoms and smoking and by lung function tests, and for whom all six readers had assessed their 1966 radiographs into the U/C classification; 130 men had died by the end of 1975. Men with any radiographic abnormality, heavy dust exposure, or a history of cigarette smoking had relative risks (RRs) of total mortality greater than unity. Death from pneumoconiosis was associated with small parenchymal opacities, usually irregular, of profusion l/l or more, and with heavy dust exposure but not with smoking. Most who died from lung cancer had smoked cigarettes, or had been heavily exposed to dust, or both. Small parenchymal opacities were present in most but not all the excess deaths due to lung cancer. Deaths from other malignant diseases showed no consistent dust or x-ray patterns. RRs of deaths from most other causes were raised for certain radiographic features. Failures in forecasting mortality were primarily due to deaths in which asbestos-related disease was not the primary cause but may have been a contributing factor. The main findings validated the U/C classification convincingly, particulary as the films had been taken as routine and were of modest quality. Despite objective rules for the reading and the fact that all six readers were contributing to the development of the classification, there was inevitably some observer variation. The importance of radiographic technique and the need for careful control of the reading is evident. Our results provide support for the use of the chest radiograph for surveillance of asbestos workers, and for environmental monitoring. Its protective value for individual workers, however, is limited to the extent that radiological progression continues after withdrawal from exposure, and by the carcinogenic risk associated with dust already retained.
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We report a further follow-up of a birth cohort of 11 379 workers exposed to chrysotile. The cohort consisted of 10 939 men and 440 women, born 1891-1920, who had worked for at least a month in the mines and mills of Asbestos and Thetford Mines in Quebec. For all subjects, length of service and estimates of accumulated dust exposure were obtained, with a smoking history for the vast majority. Three methods of analysis, two based on the "man-years" methods, the other a "case-and-multiple-controls" approach, gave results consistent with one another and with previous analyses. By the end of 1975, 4463 men and 84 women had died. Among men, the overall excess mortality, 1926-75 was 2% at Asbestos and 10% at Thetford Mines, much the dustier region. The women, mostly employed at Asbestos, had a standardised mortality ratio (SMR) all causes, 1936-75) of 0.90. Analysis of deaths 20 years or more after first employment showed that in men with short service (less than five years) there was no discernible correlation with dust exposure. Among men employed at least 20 years, there were clear excesses in those exposed to the heaviest dust concentrations. Reanalysis in terms of exposure to age 45 showed definite and consistent trends for SMRs for total mortality, for lung cancer, and for pneumoconiosis to be higher the heavier the exposure. The response to increasing dose was effectively linear for lung cancer and for pneumoconiosis. Lung cancer deaths occurred in non-smokers, and showed a greater increase of incidence with increasing exposure than did lung cancer in smokers, but there was insufficient evidence to distinguish between multiplicative and additive risk models. There were no excess deaths from laryngeal cancer, but a clear association with smoking. Ten men and one woman died from pleural mesothelioma. If the only subjects studied had been the 1904 men with at least 20 years' employment in the lower dust concentrations, averaging 6.6 million particles per cubic foot (or about 20 fibres/cc), excess mortality would not have been considered statistically significant, except for pneumoconiosis. The inability of such a large epidemiological survey to detect increased risk at what, today, are considered unacceptable dust concentrations, and the consequent importance of exposure-response models are therefore emphasised.
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Among 4463 deaths in a cohort of 10,939 men, born between 1891 and 1920, who had worked in the Quebec chrysotile mines and mills for at least a month, 244 were due to lung cancer. The interval from first asbestos exposure to death averaged 39.6 years; not unexpectedly, this interval was related to age at death and to age at first employment. However, the interval did not appear to be associated in any important way with other measures of exposure. All of the problems of interpretation pointed out by Enterline (1978) are acknowledged, and there is no guarantee of generalization to those exposed to asbestos in other circumstances. Nevertheless, among these 244 cases, there was no evidence to support the hypothesis that the latent period of asbestos-induced lung cancer depends on the dose.
Beginning in the 1930s, the Canadian asbestos industry created and advanced the idea that chrysotile asbestos is safer than asbestos of other fiber types.
We critically evaluate published and unpublished studies funded by the Quebec Asbestos Mining Association (QAMA) and performed by researchers at McGill University.
QAMA-funded researchers put forth several myths purporting that Quebec-mined chrysotile was harmless, and contended that the contamination of chrysotile with oils, tremolite, or crocidolite was the source of occupational health risk. In addition, QAMA-funded researchers manipulated data and used unsound sampling and analysis techniques to back up their contention that chrysotile was "essentially innocuous."
These studies were used to promote the marketing and sales of asbestos, and have had a substantial effect on policy and occupational health litigation. Asbestos manufacturing companies and the Canadian government continue to use them to promote the use of asbestos in Europe and in developing countries. Am. J. Ind. Med. 44:540-557, 2003.
There is a relationship between dust exposure, on the one hand, and serious disease and death, on the other, in chrysotile asbestos mine and mill workers of Quebec. Studies in current working populations indicate that prevalence of abnormality increases with increasing exposure. However, the relationship is weak and offers only a partial explanation of between-subject variability. In addition, there is no certain way to detect or predict change. Because of the relative nonspecificity of the health measurements examined and their poor relationship to exposure, control should be based on environmental monitoring, with biologic monitoring considered in a complementary role. This leaves the clinician with the dilemma of how best to advise the worker in whom questionable changes have been detected. At present, there appears little doubt that the decision must remain essentially clinical, based, on one hand, on all available information about the man, his job, and the plant or mine in which he works, from which an estimate of likely outcome must be made, and, on the other hand, on the social and human factors concerned, including the fact that removal from exposure does not necessarily prevent the appearance of abnormality.
Among a cohort of 544 men with at least 20 years of employment in chrysotile mining and milling at Thetford Mines, Canada, 16% of the deaths were from lung cancer and 15% from asbestosis. The excess over expected deaths from these causes account for 43 of 178 deaths in the group. The risk of death of asbestosis, at equal times fron onset of exposure, is very similar in miners and millers, factory workmen and insulators. The ratio of observed to expected deaths from lung cancer is similar in the miners and millers and factory workers, but higher in insulators. The risk of death of mesothelioma in miners and millers is decidedly less than the other two groups. The exact causes of the reduced risk in this category are not yet completely clarified.