| Polycyclic aromatic hydrocarbons (PAHs) are an important component of air pollution and potential human carcinogens. While they have been shown to cause mammary cancer in animal studies, the association between PAH exposure and breast cancer risk is not well understood. Growing biological evidence has suggested that there may be critical time periods of exposure and of gene-environment interactions in breast cancer initiation and development. Using data collected from the Western New York Exposures and Breast Cancer (WEB) study, a population based case control study in western New York, I examined the association between breast cancer risk and exposure to PAHs from traffic emission estimated for each woman at menarche, at the time when she had her first pregnancy and birth, and at 20 and 10 years prior to interviews, estimating historical exposure from a validated geographic traffic model. In addition, I examined variants in two genes, CYP1A1 and GSTM1, both involved in metabolism of PAHs to determine if there are gene-environment interactions with risk. All participants were women, aged 35--79, residents of Erie and Niagara Counties. Cases had incident, primary, histologically-confirmed breast cancer. Controls were randomly selected and frequency matched to cases on age, race and county. In-person interviews were used to collect the data on potential breast cancer risk factors including self-reported lifetime residential histories. We found evidence that higher exposure to traffic PAH emissions at menarche was associated with increased risk of premenopausal breast cancer (OR 2.07, 95% CI 0.91--4.72, p for trend 0.03), and emissions at the time of a woman's first birth was associated with postmenopausal breast cancer (OR 2.58, 95% CI 1.15--5.83, p for trend 0.19). This association was limited to lifetime non-smokers, and to women with GSTM1 null genotypes. There was no evidence of a main effect of either GSTM1 null or the CYP1A1 variant genotype in association with risk. These findings provide evidence both of the importance of early exposures and of the potential importance of an environmental agent and genetic polymorphism in risk of breast cancer. |
