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
A cohort of some 11,000 men born 1891-1920 and employed for at least one month in the chrysotile mines and mills of Quebec, was established in 1966 and has been followed ever since. Of the 5351 men surviving into 1976, only 16 could not be traced; 2508 were still alive in 1989, and 2827 had died; by the end of 1992 a further 698 were known to have died, giving an overall mortality of almost 80%. This paper presents the results of analysis of mortality for the period 1976 to 1988 inclusive, obtained by the subject-years method, with Quebec mortality for reference. In many respects the standardised mortality ratios (SMRs) 20 years or more after first employment were similar to those for the period 1951-75--namely, all causes 1.07 (1951-75, 1.09); heart disease 1.02 (1.04); cerebrovascular disease 1.06 (1.07); external causes 1.17 (1.17). The SMR for lung cancer, however, rose from 1.25 to 1.39 and deaths from mesothelioma increased from eight (10 before review) to 25; deaths from respiratory tuberculosis fell from 57 to five. Among men whose exposure by age 55 was at least 300 million particles per cubic foot x years (mpcf.y), the SMR (all causes) was elevated in the two main mining regions, Asbestos and Thetford Mines, and for the small factory in Asbestos; so were the SMRs for lung cancer, ischaemic heart disease, cerebrovascular disease, and respiratory disease other than pneumoconiosis. Except for lung cancer, however, there was little convincing evidence of gradients over four classes of exposure, divided at 30, 100, and 300 mpcf.y. Over seven narrower categories of exposure up to 300 mpcf.y the SMR for lung cancer fluctuated around 1.27 with no indication of trend, but increased steeply above that level. Mortality form pneumoconiosis was strongly related to exposure, and the trend for mesothelioma was not dissimilar. Mortality generally was related systematically to cigarette smoking habit, recorded in life from 99% of survivors into 1976; smokers of 20 or more cigarettes a day had the highest SMRs not only for lung cancer but also for all causes, cancer of the stomach, pancreas, and larynx, and ischaemic heart disease. For lung cancer SMRs increased fivefold with smoking, but the increase with dust exposure was comparatively slight for non-smokers, lower again for ex-smokers, and negligible for smokers of at least 20 cigarettes a day; thus the asbestos-smoking interaction was less than multiplicative. Of the 33 deaths from mesothelioma in the cohort to date, 28 were in miners and millers and five were in employees of a small asbestos products factory where commercial amphiboles had also been used. Preliminary analysis also suggest that the risk of mesothelioma was higher in the mines and mills at Thetford Mines than in those at Asbestos. More detailed studies of these differences and of exposure-response relations for lung cancer are under way.
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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.
It has been suspected for many years that amphibole fibres in the tremolite series, a low level contaminant of chrysotile asbestos, may contribute disproportionately to the incidence of mesothelioma and perhaps other exposure-related cancers. A cohort of some 11,000 Quebec chrysotile workers, 80% of whom have now died, provided the opportunity to examine this hypothesis further. An analysis was made of deaths from mesothelioma (21), cancers of the lung (262), larynx (15), stomach (99), and colon and rectum (76), in men employed by the largest company in Thetford Mines, with closely matched referents. Risks were estimated by logistic regression for these five cancers in two groups of mines--five mines located centrally and ten mines located peripherally; tremolite contamination had been demonstrated to be some four times higher in the former than in the latter. Odds ratios for work in the central mines were raised substantially and significantly for mesothelioma and lung cancer, but not for the gastric, intestinal or laryngeal cancer sites. In the peripheral mines, there was little or no evidence of increased risk for any of the five cancers. The hypothesis that, because of the difference in distribution of fibrous tremolite, cancer risks in the central area would be greater than in the periphery was thus substantiated. That the explanation may lie in the greater biopersistence of amphibole fibres than chrysotile is important in framing policies for the use and control of asbestos and is directly relevant to the selection of man-made mineral fibre substitutes.
All cases of mumps meningoencephalitis diagnosed at our institution during the past 15 years were reviewed. There were 24 cases, 16 between 1973 and 1977, 3 between 1978 and 1985 and 5 in 1986 to 1988. Four of the recent cases occurred 19 to 26 days after receipt of a new mumps vaccine (Urabe Am 9 strain) released in Canada in 1986. The remaining 20 cases were clustered in winter and spring. The average age was 6.2 years and the ratio of males to females was 5:1. Clinical presentations were fever (90%), vomiting (90%), meningismus (70%), headache (65%), parotitis (50%) and seizures (30%). The mean cerebrospinal fluid white blood cell count was 513/mm3 (lymphocyte predominance); 55% of patients had a cerebrospinal fluid protein level of greater than 0.4 g/liter, and the cerebrospinal fluid:blood glucose ratio was greater than 0.4 in all. Two patients had adverse sequelae. The clinical and laboratory features of these cases were not significantly different from the vaccine-associated cases.
A large cohort of men born between 1891 and 1920 and employed for at least a month in the chrysotile producing industry of Quebec has been under study since 1966. These men were followed from first employment (the earliest in 1904) to 1992, by which time over 8000 had died, 657 from lung cancer. The current study is of 488 cases of lung cancer formerly employed at three places, viz. a major complex, here called Company 3, in the region of Thetford Mines (243 cases), the mine and mill in the town of Asbestos (206) and a small asbestos-products factory in the same town (39). For each case, four referents were sought by random selection from among survivors to a greater age, after matching on place of employment, age of starting work, smoking habit and date of birth. This process was highly successful, although six cases had less than four referents. For each man (the 488 cases with 1941 referents) and for each calendar year of employment, we obtained the fraction of the year worked at various levels of intensity, assessed in 13 'dust categories' of mpcf (million particles per cubic foot). We then calculated how many years each man spent at these various levels; these years, adjusted for the length of the working week (66 h until 1937; 48 h 1938-1949; and 40 h 1950-1985), were accumulated up to ten years before the death of the case. The men were classified according as they were non- or ex-smokers, or smokers, of cigarettes. For each man at Company 3 and one referent for each, his years of work in a central area of five mines and in a peripheral area of ten mines were differentiated; contamination of the chrysotile by fibrous tremolite was known to be much greater in the central than in the peripheral area. Case-referent comparisons, within place of employment, were made by conditional logistic regression. As anticipated from earlier subject-years analyses, lung cancer risks were found to be negligible for years worked in dust categories 1 and 2 (averaging 0.5 and 2 mpcf), regardless of place; as the upper limit of category 1 is considerably higher than permitted nowadays, the lung cancer risk from exposure to chrysotile at permitted levels can be taken as extremely small. Patterns of exposure-response for higher categories were irregular. At Company 3, some risks appeared elevated for years spent in the higher dust categories: 3-4, 5-7, 8-10 and 11-13, with averages around 9, 20, 36 and 92 mpcf, respectively. For categories 3-4 and 8-10, the odds ratios were high for some or all work in the central area, but minimal for years spent in the peripheral area only. Odds ratios were fairly low for cigarette smokers who worked in categories 5-7 and also for years spent in the highest categories (11-13). At the mine and mill in Asbestos, all risks were low except for years worked by non- and ex-smokers in categories 7-13 (ca. 40 mpcf). There were no increased risks at the factory. It was known from the subject-years analyses that most of the excess had occurred at Company 3, but it is now clear that for all practical purposes it was confined to the central area there, probably due largely to fibrous tremolite and in dust conditions of at least dust category 3. The average of this category was 7 mpcf or very roughly 24 fibres/ml, about two orders of magnitude higher than today's hygiene standards.
Comment In: Ann Occup Hyg. 2001 Jun;45(4):327-9; author reply 336-811414249
Comment In: Ann Occup Hyg. 2001 Jun;45(4):329-35; author reply 336-811414250