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
To evaluate the importance of exposure to ambient air pollution for lung cancer risk, we conducted a case-control study in the vicinity of a nonferrous metal smelter. The smelter started operations in 1930 and had very high emissions during the early decades, particularly of arsenic and SO(2). Among subjects deceased 1961-1990 in the municipality where the smelter is located and who had not worked at the smelter, 209 male and 107 female lung cancer cases were identified and matched by sex and year of birth to 518 and 209 controls, respectively. Information on smoking habits, occupations and residences was collected by questionnaire to next-of-kin and from registry data. Living close to the smelter was associated with a relative risk (RR) for lung cancer of 1.38 [95% confidence interval (CI) 0.89-2.14] among men, adjusted for smoking and occupational exposures. No clear difference in risk was detected for men deceased 1961-1979 compared to men deceased 1980-1990 (RR point estimates 1.42 and 1.29, respectively). There appeared to be an increased risk especially for men exposed in the beginning of the operations (RR = 1.51, 95% CI 0.90-2.54), in particular combined with exposure duration shorter than 20 years (RR = 2.52, 95% CI 0.89-7.11). For women, however, no overall increased risk for lung cancer was observed. Although not significant, our findings thus indicated an increased risk of lung cancer among men living close to the nonferrous smelter. This increase appeared to concern primarily men exposed during the early years of operations, when emissions were very high.
Alcohol intake has consistently been associated with increased breast cancer incidence in epidemiological studies. However, the relation between alcohol and survival after breast cancer diagnosis is less clear.
We investigated whether alcohol intake was associated with survival among 3146 women diagnosed with invasive breast cancer in the Swedish Mammography Cohort. Alcohol consumption was estimated using a food frequency questionnaire. Cox proportional hazard models were used to calculate hazard ratios (HRs) and 95% confidence intervals (95% CIs).
From 1987 to 2008 there were 385 breast cancer-specific deaths and 860 total deaths. No significant association was observed between alcohol intake and breast cancer-specific survival. Women who consumed 10 g per day (corresponding to approximately 0.75 to 1 drinks) or more of alcohol had an adjusted HR (95% CI) of breast cancer-specific death of 1.36 (0.82-2.26;p(trend)=0.47) compared with non-drinkers. A significant inverse association was observed between alcohol and non-breast cancer deaths. Those who consumed 3.4-9.9 g per day of alcohol had a 33% lower risk of death compared with non-drinkers (95% CI 0.50-0.90;p(trend)=0.04).
Our findings suggest that alcohol intake up to approximately one small drink per day does not negatively impact breast cancer-specific survival and a half drink per day is associated with a decreased risk of mortality from other causes.
Cites: Cancer Causes Control. 2002 Aug;13(6):543-912195644
Cites: JAMA. 2001 Nov 7;286(17):2143-5111694156
Cites: Int J Cancer. 1991 Oct 21;49(4):526-301917153
Cites: Nutr Cancer. 1993;20(2):167-778233982
Cites: N Engl J Med. 1995 May 11;332(19):1245-507708067
Cites: Cancer. 1995 Jul 15;76(2):275-838625103
Cites: JAMA. 1998 Feb 18;279(7):535-409480365
Cites: Breast Cancer Res Treat. 1998 Sep;51(1):17-289877026
Cites: Breast Cancer Res Treat. 1999 Feb;53(3):241-5310369070
Cites: Cancer. 1999 Sep 1;86(5):826-3510463982
Cites: Alcohol. 2005 Apr;35(3):213-2516054983
Cites: J Natl Cancer Inst. 2005 Nov 2;97(21):1601-816264180
Ambient air concentrations of asbestos fibres were measured during the period 20 June to 12 August, 1980 at three locations; Danville, Asbestos and Wottenville in the eastern townships of Quebec. Measurements were made with low-volume samplers and measurement periods ranged from 3 to 13 days. Fibre counts were made by means of electron microscopy. Our results indicate that overall fibre concentrations are related to atmospheric stability and to the direction of the prevailing wind with respect to the source of emission. Fibre concentrations are then related to total dust content of the ambient air for the town of Asbestos. Spatial variations of mortality are in turn related to the variations in the concentration of ambient air dust particles.
The analysis of 321 necropsies made in Clinical Infections Hospital N 2 from 1991 to 2001 showed a significant increase in the number of deaths of HIV-infection beginning from 1996. The highest mortality (40%) was registered among males aged 25-34 years. The deceased had a wide spectrum of opportunistic diseases (infections and tumors). The deceased with AIDS most frequently had cytomegaloviral infections (19%), tuberculosis (14%), Kaposi's sarcoma (10%), bacterial pneumonias (8%), toxoplasmosis (7%). A late stage of AIDS was characterized by generalized opportunistic diseases, the presence of several severe infectious diseases and more frequent neoplasms.
Mortality and workers' compensation patterns were studied among 1,064 Ontario asbestos insulation workers. A proportional mortality analysis of 153 asbestos worker deaths found increased mortality from malignant diseases (65 deaths observed; 35.1 expected), cancers of the lungs and pleura (32 deaths observed; 11.5 expected), peritoneal mesothelioma (4 deaths), and respiratory diseases (14 deaths observed; 7.9 expected). Despite the publicity given to asbestos-associated diseases, dependents of many men potentially eligible for workers compensation awards have not received pensions because claims were not filed. These findings suggest that much occupationally related disease is not being recognized in Ontario.
Tobacco and low socioeconomic status have been acknowledged as potential risk factors for upper aero-digestive tract (UADT) cancers in North America. In context of reducing adult male smoking prevalence (by over 50%), in the past few decades in Canada, this study tried to document changes in smoking-attributable UADT cancer mortality rates, among Canadian males of different social strata, between 1986 and 2001.
The contribution of smoking to UADT cancer mortality was estimated indirectly by using lung cancer mortality as an indicator of the accumulated mortality from smoking in a population. This method was applied to UADT cancer death rates of 35-69 year old socially stratified males. Data, stratified by neighborhood income quintile, could be obtained from Statistics Canada, for four census years, 1986, 1991, 1996, and 2001.
A total of 2704 male deaths were analyzed. Between 1986 and 2001, UADT cancer deaths reduced by 30% (32 to 22 per 100,000) but the proportion of these deaths attributable to smoking reduced much more, by 41% (22 to 13 per 100,000). In the span of fifteen years, absolute social inequality (measured by rate difference between the highest and the lowest stratum) in smoking-attributable male UADT cancer mortality in Canada reduced by 47% and relative social inequality (measured by rate ratios) reduced by 9%.
The present analyses reveal that between 1986 and 2001, smoking-attributable UADT cancer mortality rates among adult males (35-69 years) in Canada reduced in all social strata and the social inequalities in these rates have narrowed. Analysis of more current data will be of interest to confirm these trends.
Cites: Cancer. 2000 Apr 1;88(7):1728-3810738233
Cites: Br J Cancer. 2011 Dec 6;105 Suppl 2:S6-S1322158323
Cites: Am J Epidemiol. 2002 Jul 1;156(1):11-2112076884
Cites: Br J Cancer. 2002 Jul 1;87(1):43-812085254
Cites: Cancer Causes Control. 2003 Nov;14(9):897-90614682447