Postmenopausal Breast Cancer Is Associated with Exposure to Traffic-Related Air Pollution in Montreal, Canada: A Case-Control Study

Article excerpt

BACKGROUND: Only about 30% of cases of breast cancer can be explained by accepted risk factors. Occupational studies have shown associations between the incidence of breast cancer and exposure to contaminants that are found in ambient air.

OBJECTIVES: We sought to determine whether the incidence of postmenopausal breast cancer is associated with exposure to urban air pollution.

METHODS: We used data from a case-control study conducted in Montreal, Quebec, in 1996-1997. Cases were 383 women with incident invasive breast cancer, and controls were 416 women with other incident, malignant cancers, excluding those potentially associated with selected occupational exposures. Concentrations of nitrogen dioxide ([NO.sub.2]) were measured across Montreal in 2005-2006. We developed a land-use regression model to predict concentrations of [NO.sub.2] across Montreal for 2006, and developed two methods to extrapolate the estimates to 1985 and 1996. We linked these estimates to addresses of residences of subjects at time of interview. We used unconditional logistic regression to adjust for accepted and suspected risk factors and occupational exposures.

RESULTS: For each increase of 5 ppb [NO.sub.2] estimated in 1996, the adjusted odds ratio was 1.31 (95% confidence interval, 1.00-1.71). Although the size of effect varied somewhat across periods, we found an increased risk of approximately 25% for every increase of 5 ppb in exposure.

CONCLUSIONS: We found evidence of an association between the incidence of postmenopausal breast cancer and exposure to ambient concentrations of [NO2.sub.2]. Further studies are needed to confirm whether [NO.sub.2] or other components of traffic-related pollution are indeed associated with increased risks.

KEY WORDS: air pollution, case-control study, Montreal, nitrogen dioxide, postmenopausal breast cancer. Environ Health Perspect 118:1578-1583 (2010). doi:10.1289/ehp.l002221 [Online 6 October 2010]


Breast cancer has the highest incidence rate of all cancers in women and is the second leading cause of death from cancer in both Canada (Canadian Cancer Society 2009) and the United States (American Cancer Society 2009). Accepted risk factors for breast cancer include genetic mutations, family history of breast cancer, aspects of reproductive history, and lifestyle factors, such as alcohol consumption. Only about one-third of new cases of breast cancer are attributable to known risk factors, and much of the etiology remains unexplained (Coyle 2004). There have been consistent findings of higher rates of breast cancer in urban areas compared with rural areas, in both Canada (Bako et al. 1984) and the United States (Hall et al. 2005; Reynolds et al. 2004).

Local vehicular traffic is the primary contributor to air pollution in urban areas. Vehicular emissions include gases, particles, volatile organic compounds, and polycyclic aromatic hydrocarbons (PAHs), many of which are accepted or potential carcinogens. Benzene, for example, is present in gasoline, is an accepted human carcinogen (International Agency for Research on Cancer 1987), and has been shown to cause mammary carcinomas in rodents (Huff et al. 1989; Maltoni et al. 1988, 1989). Exposure to other aromatic hydrocarbons associated with gasoline, including kerosene, toluene, and xylenes, has also produced increased rates of mammary cancers in female rats (Maltoni et al. 1997). Aromatic hydrocarbons are lipophilic and may therefore reach elevated concentrations in breast tissue and promote carcinogenesis in the cells of the breast (Morris and Seifter 1992). We postulated in the mid-1990s (Labreche and Goldberg 1997) that exposure to organic solvents and other lipophilic toxics may cause breast cancer. Santodonato (1997) concluded that, regarding the etiology of human breast cancer, current scientific literature provides "persuasive evidence for the hypothesis that certain carcinogenic PAHs produce a unique duality of pathologic effects encompassing both genotoxic and nongenotoxic components. …