A health study was conducted in three communities in the greater Montreal region; the first two were characterized by relatively high particulate and sulfur dioxide levels, respectively, and a third community without major industrial pollution. In each community, 300 men and women 45 to 64 yr of age were studied. Residents of the two more polluted communities exhibited a higher prevalence of respiratory symptoms and mean lung function evaluated by various tests was lower than in residents of the less polluted community. When intercity differences in age and smoking were accounted for, no statistically significant intercity differences in health status could be shown. Given the limitations of this study, the results provide no evidence to suggest that current Canadian standards for sulfur dioxide adequately protect human health as measured by the indices used in the study, for adults in the age range of 45 to 64 yr.
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.
After checking on the accuracy of work histories and estimating prevailing fibre concentrations by relevant time and place, all 244 deaths from lung cancer (ICD 162-164) in the Quebec mortality cohort were compared with internal controls matched for date of birth, mining area and smoking habit. Further studies of other causes of death and of lung cancer with controls unmatched for smoking are in progress. In the meantime, we consider that a useful estimate of lung cancer risks is given by the equation: RR = 1 + 0.00038 (+/- 0.00013) fibres/ ml.yr.
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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A review of 15,689 chest radiographs of Quebec chrysotile miners and millers, representing the latest film prior to November 1, 1966, for all such persons ever x-rayed, identified 206 men with pleural calcification. Of these, 198 had worked in the Thetford Mines area, 6 at Asbestos, and 2 at St. Remi de Tingwick; 2.5%, 0.08%, and 1% of the films from these areas, respectively. A series of case-control studies revealed that pleural calcification was concentrated in men employed at a small group of mines in Thetford Mines and occurred more often among miners and maintenance personnel than among millers. Calcification was not related to past history of illness or injury, place of residence, or employment in other industries. The distribution of pleural calcification in this Quebec industry suggests that it is related to some characteristic of airborne dust or mineral closely associated with the chrysotile that is encountered during mining in Thetford Mines but not in other mining areas. Possible minerals include mica, talc, and breunnerite.
To define the relationships between chrysotile exposure in fibre terms and death from specific cancers, and pneumoconiosis, all 11,379 persons born 1891-1920 who had worked in the asbestos mines and mills of Quebec for a month or more before 1967 were followed to the end of 1975. Among the 10,939 men, there had been 4,463 deaths, 634 from these causes. For each death, referents were randomly selected from among men in the cohort born in the same year as the case and known to have survived to a greater age. For each case and his referents, exposures accumulated up to nine years before the death of the case had been obtained as (million particles per cubic foot) x years. Fibre counts were estimated for each work-place so that all exposures could be expressed in (fibres/ml) x years. The ratio of the means for all 2,586 accumulated exposures was 3.46 (f/ml)/mpcf. Relative Risks (RR) were related to exposure by matched analysis. For pneumoconiosis and lung cancer, RR = 1 + b.(f/ml).y fitted well, with b estimated as 0.00647 and 0.00038, respectively. For cancers of upper and of lower G.I. tract, severe exposure was associated with elevated RRs, but rather unclearly. For other abdominal cancers, and laryngeal cancer, risks and exposure were not positively associated. The asbestos-smoking interaction in lung cancer was closer to multiplicative than to additive.