Academic journal article Environmental Health Perspectives

Vehicular Traffic-Related Polycyclic Aromatic Hydrocarbon Exposure and Breast Cancer Incidence: The Long Island Breast Cancer Study Project (LIBCSP)

Academic journal article Environmental Health Perspectives

Vehicular Traffic-Related Polycyclic Aromatic Hydrocarbon Exposure and Breast Cancer Incidence: The Long Island Breast Cancer Study Project (LIBCSP)

Article excerpt


Breast cancer is the most common malignancy among women in the United States [American Cancer Society (ACS) 2011]. Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous pollutants formed from incomplete combustion (Bostrom et al. 2002). PAHs are genotoxic prooxidants, confirmed human lung carcinogens, and potent mammary carcinogens in laboratory animals [International Agency for Research on Cancer (IARC) 2010]. However, the association between PAHs and breast cancer in women is unclear (Gammon and Santella 2008). Previous population studies have reported associations between PAH-related exposures and breast cancer. For example, PAHs bind to DNA, including in breast tissue, and the resulting DNA adducts have been associated with breast cancer in epidemiological studies, although the research is scant (Gammon et al. 2002b; Rundle et al. 2000). PAH-DNA adducts reflect short-term exposures (Gammon et al. 2002b), whereas breast cancer is thought to develop over many years. Thus, it is of interest to evaluate longer-term PAH exposures in relation to breast cancer risk.

Vehicular traffic is a major ambient source of PAH exposure, especially near urban areas (Fromme et al. 2004). To our knowledge, all previous studies on traffic or air pollution exposure and breast cancer have reported some positive associations between breast cancer and at least one air pollution exposure surrogate (Bonner et al. 2005; Crouse et al. 2010; Lewis-Michl et al. 1996; Nie et al. 2007; Raaschou-Nielsen et al. 2011). In some cases, the effect estimates were close to the null [for example, 1.16 (0.89, 1.51); Raaschou-Nielsen et al. 2011]. The exposure assessment methods in these previous reports varied. Some investigations relied on simple traffic density data or sparse monitors, evaluated relatively brief periods of exposure, or focused on nitrogen oxides rather than carcinogenic particulate pollution. Further progress requires sophisticated modeling to reconstruct long-term cumulative exposures to ambient PAHs.

Breast cancer risk factor profiles differ by menopausal status and tumor subtype (ACS 2011; Chen and Colditz 2007), and fruits and vegetables may modify the carcinogenic effects of PAHs via antioxidant and other chemopreventive properties (Hecht 2000; Jin et al. 2006). However, whether the association between ambient PAHs and breast cancer varies by fruit/vegetable intake, tumor characteristics, or menopausal status is not well understood.

Our population-based study aimed to estimate the association between breast cancer incidence and vehicular traffic, overall and within subgroups of women classified according to fruit/vegetable intake, menopausal status, and tumor subtype. For the study reported here, we used long-term, individualized residential traffic benzo[a] pyrene (B[a]P) exposure estimates (as a proxy for exposure to particulate traffic PAHs), which were reconstructed using a historical, geographic exposure model that was consistent with a varied set of environmental measurements (Beyea et al. 2006). It is important to help clarify the association between traffic PAHs and breast cancer given the high incidence of breast cancer and broad exposure to traffic pollution worldwide.

Materials and Methods

We used resources from the case-control component of the Long Island Breast Cancer Study Project (LIBCSP), a population-based investigation conducted among women residing in Nassau and Suffolk counties in Long Island, New York (Gammon et al. 2002a). All participating institutions provided institutional review board approval for this study, and all participants gave their written informed consent prior to study enrollment.

Study population. Eligible case participants were diagnosed with a first primary invasive or in situ breast cancer between August 1996 and July 1997 and were identified via rapid case ascertainment through contact with local pathology departments (Gammon et al. …

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