Night work might influence cancer risk, possibly via suppression of melatonin release. In a population-based case-control study conducted in Montreal, Quebec, Canada, between 1979 and 1985, job histories, including work hours, were elicited from 3,137 males with incident cancer at one of 11 anatomic sites and from 512 controls. Compared with men who never worked at night, the adjusted odds ratios among men who ever worked at night were 1.76 (95% confidence interval (CI): 1.25, 2.47) for lung cancer, 2.03 (95% CI: 1.43, 2.89) for colon cancer, 1.74 (95% CI: 1.22, 2.49) for bladder cancer, 2.77 (95% CI: 1.96, 3.92) for prostate cancer, 2.09 (95% CI: 1.40, 3.14) for rectal cancer, 2.27 (95% CI: 1.24, 4.15) for pancreatic cancer, and 2.31 (95% CI: 1.48, 3.61) for non-Hodgkin's lymphoma. Equivocal evidence or no evidence was observed for cancers of the stomach (odds ratio (OR) = 1.34, 95% CI: 0.85, 2.10), kidney (OR = 1.42, 95% CI: 0.86, 2.35), and esophagus (OR = 1.51, 95% CI: 0.80, 2.84) and for melanoma (OR = 1.04, 95% CI: 0.49, 2.22). There was no evidence of increasing risk with increasing duration of night work, with risks generally being increased across all duration categories. Results suggest that night work may increase cancer risk at several sites among men.

Wood dust is one of the oldest and one of the most common occupational exposures in the world. The present analyses examine the effect of lifetime exposure to wood dust in diverse occupational settings on lung cancer risk. We conducted two population-based case–control studies in Montreal: Study I (1979–1986) included 857 cases and two sets of controls (533 population and 1349 cancer controls), and Study II (1996–2001) comprised 736 cases and 894 population controls. Detailed job histories were obtained by interview and each job was evaluated by expert chemist–hygienists to estimate the likelihood and level of exposure to many substances, one of which was wood dust. Odds ratios (ORs) were computed in relation to different indices of exposure to wood dust, adjusting for several covariates including smoking. Three datasets were analysed: Study I with population controls, Study I with cancer controls, and Study II. The most frequently exposed occupations in our study population were in construction, timber and furniture making industries. We found increased risks of lung cancer for substantial cumulative exposure to wood dust in Study I with cancer controls, (OR = 1.4: 95% confidence interval 1.0;-2.0) and in Study II (OR = 1.7: 95% confidence interval 1.1-2.7). There were no excess risks of lung cancer in any of the three datasets among workers whose cumulative exposure was not substantial. These tendencies held equally within strata of low smokers and heavy smokers. There was evidence of increased risk of lung cancer among workers with substantial cumulative exposure to wood dust.

Objectives There is a paucity of information on environmental risk factors for prostate cancer. We conducted a case–control study in Montreal to estimate associations with exposure to ground-level nitrogen dioxide (NO₂), a marker for traffic-related air pollution. Methods Cases were 803 men with incident prostate cancer, ≤75 years of age, and diagnosed across all French hospitals in Montreal. Concurrently, 969 controls were drawn from electoral lists of French-speaking individuals residing in the same electoral districts as the cases and frequency-matched by age. Concentrations of NO₂ were measured across Montreal in 2005–2006. We developed a land use regression model to predict concentrations of NO₂ across Montreal for 2006. These estimates were back-extrapolated to 1996. Estimates were linked to residential addresses at the time of diagnosis or interview. Unconditional logistic regression was used, adjusting for potential confounding variables. Results For each increase of 5 parts per billion of NO₂, as estimated from the original land use regression model in 2006, the OR_5ppb adjusted for personal factors was 1.44 (95% CI 1.21 to 1.73). Adding in contextual factors attenuated the OR_5ppb to 1.27 (95% CI 1.03 to 1.58). One method for back-extrapolating concentrations of NO₂ to 1996 (about 10 years before the index date) gave the following OR_5ppb: 1.41 (95% CI 1.24 to 1.62) when personal factors were included, and 1.30 (95% CI 1.11 to 1.52) when contextual factors were added. Conclusions Exposure to ambient concentrations of NO₂ at the current address was associated with an increased risk of prostate cancer. This novel finding requires replication.

Pollution from motor vehicles constitutes a major environmental health problem. The present paper describes associations between diesel and gasoline engine emissions and lung cancer, as evidenced in a 1979–1985 population-based case-control study in Montreal, Canada. Cases were 857 male lung cancer patients. Controls were 533 population controls and 1,349 patients with other cancer types. Subjects were interviewed to obtain a detailed lifetime job history and relevant data on potential confounders. Industrial hygienists translated each job description into indices of exposure to several agents, including engine emissions. There was no evidence of excess risks of lung cancer with exposure to gasoline exhaust. For diesel engine emissions, results differed by control group. When cancer controls were considered, there was no excess risk. When population controls were studied, the odds ratios, after adjustments for potential confounders, were 1.2 (95% confidence interval: 0.8, 1.8) for any exposure and 1.6 (95% confidence interval: 0.9, 2.8) for substantial exposure. Confidence intervals between risk estimates derived from the two control groups overlapped considerably. These results provide some limited support for the hypothesis of an excess lung cancer risk due to diesel exhaust but no support for an increase in risk due to gasoline exhaust.