Smoking (active and passive), N-acetyltransferase 2, and risk of breast cancer

• Main Author: Conlon, Michael S. C
• Format: Dissertation
• Language: English
• Published: ProQuest Dissertations & Theses 01.01.2007
• Subjects: Epidemiology
• ISBN: 9780494307960; 049430796X

The relationship between passive and active smoking and breast cancer risk has been controversial. Many early studies concluded a null association; more recent studies often suggested a positive association. To explore the risks between exposure to passive or active smoking and breast cancer, and smoking effect modification by N-acetyltransferase2 ( NAT2) genotype, we collected and analyzed data through a population-based case-control study conducted in Northeastern Ontario, Canada from 347 women recently diagnosed (2002-2004) with breast cancer and 775 population-based controls. The mailed study package contained a questionnaire requesting information about known breast cancer risk factors and a lifetime residential and occupational history of exposure to passive smoking, and a buccal swab to be returned for genetic analyses. Among women who were never-active smokers, a long duration of passive smoking was associated with an increased risk of breast cancer, highest quartile age-adjusted OR of 1.86, 95% confidence interval (CI) 1.01-3.44, when compared to women who received the lowest quartile of passive smoke exposure. Results appeared stronger in slow acetylators rather than fast acetylators. However, a test for interaction was nonsignificant. In post hoc analyses results were strongest in a homogenous subset of extremely slow acetylators. Active smoking of long duration was associated with increased breast cancer risk, highest quartile of active smoking risk-factor-adjusted OR of 1.58, 95% CI 1.00-2.50 (p for trend 0.50) using a refined referent group that excluded never-active smokers, and never-active smokers with high passive smoke exposure. Higher risk also occurred in women who quit smoking most recently. Active smoking metrics generally appeared stronger in fast rather than slow acetylators, although a test for interaction was non-significant. These results suggest that exposure to long periods of passive smoking may be associated with risk of breast cancer in never-active smoking women, and effects may be stronger in women who are slow NAT2 acetylators. Long periods of active smoking may also be associated with risk of breast cancer, and these effects may be stronger in women who are fast acetylators. Further research into the potential genetic modification of a breast cancer smoking relationship may help to reconcile earlier discrepant findings. Keywords: active smoking, passive smoking, NAT2, breast cancer, case-control study, Northeastern Ontario.