Abstract 4699: Environmental tobacco smoke in relation to bladder cancer risk: The Shanghai Bladder Cancer Study

Abstract

Abstract Tobacco use is an established risk factor for bladder cancer. However, data on exposure to environmental tobacco smoke (ETS) are sparse. Given the important roles of hepatic cytochrome P450 (CYP1A2) in activation and N-acetyltransferase (NAT2) in detoxification of tobacco carcinogens, we examined ETS and bladder cancer risk association among lifelong nonsmokers and for subgroups stratified by CYP1A2/NAT2 phenotype status. As part of the Shanghai Bladder Cancer Study, a population based case-control study in Shanghai, China, we enrolled 202 case patients (101 women) who were lifelong nonsmokers aged 25-74 at diagnosis in 1995-1998 and 268 lifelong nonsmoking control subjects (130 women) who were comparable to cases in gender-age distributions. An in-person interview was administered. In addition to lifestyle factors, subjects were asked about smoking history (number of cigarettes/day and number of years of living together) of their mother, father, spouse, other relatives in the household and smoking habits of coworkers at workplace. CYP1A2 and NAT2 phenotype status were determined by ratios of specific caffeine metabolites in overnight urine samples collected from each subject after ingestion of 70mg of caffeine. Odds ratios (ORs) and 95% confidence intervals (CIs) for bladder cancer were calculated using unconditional logistic regression methods. Exposure to ETS was related to a statistically non-significant 20-30% increased bladder cancer risk in all lifelong nonsmokers. The positive ETS-bladder cancer association varied according to the source of ETS, and primarily was confined to women. Living with a smoking mother during childhood was associated with an OR of 1.59 (95% CI=0.79-3.21, P=0.19) in all lifelong nonsmokers and an OR of 2.02 (95% CI=0.71-5.78, P=0.19) in women only. Among all lifelong nonsmokers, bladder cancer risk increased with increasing number of cigarettes/day (OR=2.92, 95% CI=0.95-8.96, P=0.06, for more than 10 cigarettes/day), number of years of smoking (OR=2.47, 95% CI=0.94-6.46, P=0.07, for more than 10 years), and pack-years of smoking (OR=3.51, 95% CI=1.08-11.35, P<0.01 for more than 10 pack-years) by mothers who smoked. When all lifelong nonsmokers were stratified by CYP1A2 (below or above median in all controls) and NAT2 (slow or rapid) phenotype status, ORs (95% CI) of bladder cancer for ETS vs. non-ETS exposure were 0.98 (0.56-1.73, P=0.95) for subjects possessing both a low CYP1A2 and a rapid NAT2 phenotypes, 1.36 (0.78-2.32, P=0.26) for subjects with either a low CYP1A2 or a rapid NAT2 phenotypes, and 2.07 (0.98-4.38, P=0.06) among those possessing both a high CYP1A2 and a slow NAT2 acetylation phenotypes (P for trend=0.04). Exposure to ETS, especially during childhood, was associated with an increased risk of bladder cancer among lifelong nonsmokers. CYP1A2 and NAT2 acetylation phenotypes exert a moderate modifying effect on the ETS-bladder cancer association. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 4699.