A case-control study of male-female differences in cigarette smoking and lung cancer was conducted during 1981-1985 in Toronto, St. Catharine's, and Niagara Falls, Ontario, Canada. In total, 442 female and 403 male histologically verified cancer cases were individually matched by age and area of residence to each other and to 410 female and 362 male randomly selected population controls. Subjects were interviewed concerning their exposures to various life-style factors, and in particular, they received detailed questioning regarding their lifelong histories of usage of tobacco products. It was found that, for both sexes, a greatly elevated risk of developing lung cancer was associated with cigarette consumption, increasing with pack-years of cigarettes smoked and declining with duration of time since quitting smoking. Furthermore, the association was significantly (p = 0.010) and appreciably stronger for females than for males. At a history of 40 pack-years relative to lifelong nonsmoking, the odds ratio for women was 27.9 (95% confidence interval (CI) 14.9-52.0) and that for men was 9.60 (95% CI 5.64-16.3). Higher odds ratios for females were also seen within each of the major histologic groupings. Thus, the higher elevated risk of lung cancer currently observed in other studies for female ever smokers compared with male ever smokers, while possibly attributable in part to greater smoking cessation among males, may be due to higher susceptibility among females.

The association between tobacco use and risk of bladder cancer was investigated in a population-based case-control study conducted in Alberta and south-central Ontario, Canada, between 1979 and 1982. In all, 826 histologically-confirmed cancer cases and 792 randomly selected controls, individually matched to cases for age, sex, and area of residence, were recruited into the study. Compared to those who had never smoked cigarettes, males and females who had ever smoked cigarettes had a statistically highly significant 2-fold increase in risk of bladder cancer; for ex-smokers, the risk was intermediate between that for current smokers and never-smokers. There was a dose-dependent increase in risk of bladder cancer with total lifetime cigarette consumption, of similar magnitude for males and females. In males, risk increased with self-reported degree of inhalation in ex-smokers and in current smokers (statistically significant trend), while in females there was no association in current smokers, and a statistically significant inverse association in ex-smokers. Overall, risks of bladder cancer associated with lifetime consumption of plain and filter cigarettes were similar, and there was little evidence to suggest that switching from plain to filter cigarettes was beneficial. Neither passive smoking nor other forms of tobacco consumption (pipes, cigars, chewing tobacco, or snuff) were associated with altered risk of bladder cancer. The population attributable risk for cigarette smoking was about 47% in males and about 33% in females.

A case-control study of diet and bladder cancer was conducted during 1979-1982 in Edmonton, Calgary, Toronto, and Kingston, Canada. A total of 826 histologically verified cancer cases were individually matched by age, sex, and area of residence to 792 randomly selected population controls. Subjects were interviewed concerning their histories of exposure to a number of dietary factors, including table-top artificial sweeteners, low calorie foods and drinks, beverages containing caffeine or ethanol, and certain other food items. Also, subjects provided information on their past medical, occupational, and residential histories, in addition to their exposures to tobacco and other life-style factors. For the analysis, conditional logistic regression methods were used. Under adjustment for cumulative lifetime amount of cigarette smoking, the dietary factors, with little exception, were not associated with significant alteration of risk for bladder cancer. In particular, ever regular use of artificial sweeteners did not appear to be associated with increased risk, either among men (odds ratio = 0.95, p = 0.70) or among women (odds ratio = 1.15, p = 0.53). However, daily intake of cholesterol, calculated from reported frequencies of consumption of nine relevant food items, suggested a mild increase in risk; the odds ratio estimate of trend was 1.07/100 mg average daily intake (i.e., 1.07(5.5) = 1.45 for 550 mg cholesterol per day, as might be consumed in one egg; p = 0.009). A history of diabetes mellitus of onset after age 20 years also seemed to be associated with increased risk of bladder cancer (odds ratio = 1.65, p = 0.019), but this increase did not appear to be the result of use of insulin or other medications, or use of artificial sweeteners or low calorie foods. Thus, this study tends to confirm reports of a lack of association between use of artificial sweeteners and subsequent risk of bladder cancer.

The interpretation and interpretability of epidemiologic studies of environmental tobacco smoke (ETS) depend largely on the validity of self-reported exposure. To investigate to what extent questionnaires can indicate exposure levels to ETS, an international study was conducted in 13 centers located in 10 countries, and 1,369 nonsmoking women were interviewed. The present paper describes the results of the analysis of self-reported recent exposure to ETS from any source in relation to urinary concentrations of cotinine. Of the total, 19.7 percent of the subjects had nondetectable cotinine levels, the median value was 6 ng/mg, and the cut-point of the highest decile was 24 ng/mg. The proportion of subjects misreporting their active smoking habit was estimated at between 1.9 and 3.4 percent, depending on whether cut-points of 50 or 100 ng/mg creatinine were used. Large and statistically significant differences were observed between centers, with the lowest values in Honolulu, Shanghai, and Chandigarh, and the highest in Trieste, Los Angeles, and Athens. Mean cotinine/creatinine levels showed a clear linear increase from the group of women not exposed either at home or at work, to the group of those exposed both at home and at work. Values were significantly higher for women exposed to ETS from the husband but not at work, than for those exposed at work but not from the husband. The results of linear regression analysis indicated that duration of exposure and number of cigarettes to which the subject reported being exposed were strongly related to urinary cotinine. ETS exposure from the husband was best measured by the number of cigarettes, while exposure at work was more strongly related to duration of exposure. After adjustment of number of cigarettes for volume of indoor places, a similar increase in cotinine (5 ng/mg) was predicted by the exposure to 7.2 cigarettes/8 h/40 m3 from the husband and 17.9 cigarettes/8 h/40 m3 at work. The results indicate that, when appropriately questioned, nonsmoking women can provide a reasonably accurate description of ETS exposure. Assessment of individual exposure to ETS should focus on daily duration and volume of indoor places where exposure occurred.

There are very few large scale studies that have examined the association of prostate cancer with alcohol and other beverages. This relationship was examined in a case‐control study conducted in 3 geographical areas of Canada [Metropolitan Toronto (Ontario), Montreal (Quebec), and Vancouver (British Columbia)] with 617 incident cases and 637 population controls. Complete history of beverage intake was assessed by a personal interview with reference to a 1‐year period prior to diagnosis or interview. In age‐ and energy‐adjusted models for all centers combined, the odds ratio (OR) for the highest quintile of total alcohol intake was 0.89. For alcoholic beverages separately, it was 0.68 for the highest tertile of beer, 1.12 for wine and 0.86 for liquor. The decreasing trend was significant for beer intake. The results were only significant for British Columbia out of all the 3 centers studied. Whereas coffee and cola intake was not associated with prostate cancer, a decrease in risk was observed with tea intake of more than 500 g per day (OR 0.70). Our results do not support a positive association between total alcohol, coffee and prostate cancer. Int. J. Cancer 78:707–711, 1998. © 1998 Wiley‐Liss, Inc.