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Janet Gray, Ph.D.
Janet Gray, Ph.D.

As author of our 2008 and 2010 State of the Evidence reports, Dr. Gray drives the science behind all our work.

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Understanding breast cancer risk requires knowledge about the effects of mixtures of exposures, as well as the social and biological contexts in which those exposures occur. Characteristics such as age, genetics, diet, physical activity, alcohol use, smoking, and the cultural and environmental context of early life may interact with exposures to chemicals and radiation to alter risk.

At the biological level, genes may make some women more vulnerable to certain environmental exposures. This supports the conclusion that for many women, genetic and other commonly discussed factors may interact with environmental exposures in causing a large number of breast cancer cases. For instance, women who have BRCA1 and BRCA2 mutations (the primary "breast cancer genes") may be more sensitive to ionizing radiation exposure (Pijpe, 2012). These women are often screened for breast cancer more often and at earlier ages, raising genuine concerns about the use of radiation-based screening methods for breast cancer among this group. These kinds of gene-environment interactions are not unique to BRCA1 and BRCA2. Other genes can also make individuals more susceptible to different genetic, lifestyle, hormonal or environmental challenges (Bradbury, 2007; Conde, 2009; Silva, 2009). 

Race, ethnicity, socioeconomic status and other social factors also shape breast cancer risk. These interactions are complex, because access to health care, exposures to environmental chemicals (Evans, 2002; Forastiere, 2007; Quinn, 2007),  access to healthy foods and safe spaces for physical activity, occupation, and community stress and security are affected by the built environment, social networks, geographic location, poverty (Rauh, 2008) and race (Brulle, 2006). As a result, while health disparities associated with race, ethnicity and poverty are well documented, the actual causes of these disparities likely emerge from the complex social dimensions of class and race in the United States (Krieger, 2005). Socioeconomic status, race and ethnicity probably serve as markers for other activities or circumstances that influence the level of exposures to potentially toxic chemicals (Nelson, 2012).

Most data on disparities in exposure to chemicals of concern still use broad categories of race, ethnicity, nation of origin or socioeconomic status to compare groups. This may brush over complex social causes of these disparities. In addition, while the Centers for Disease Control collects data on chemical exposures in a national, representative sample, this is done using a relatively small sample that does not allow analysis of levels in Asian-Americans as a whole, or of distinct national/ethnic origin among individuals of Asian or Latino descent, with the exception of Mexican-Americans. Nevertheless, these data illustrate inequities in exposure. According to CDC scientists, blacks have higher body-burden levels than whites or Mexican-Americans of many chemicals, including PCBs, mercury, lead, PAHs, dioxins and phthalates (CDC, 2012). Mexican-Americans have higher levels of the pesticides DDT/DDE, lindane and 2,4,5-TCP (CDC, 2012). Yet many of these racial/ethnic differences may be explained, at least partially, by differences in economic resources (Borrell, 2004; Bellinger, 2008). Varying body burdens of some chemicals, including bisphenol A (BPA) and polyfluoroalkyl chemicals (PFCs), both commonly found in household products, are associated with both race/ethnicity and socioeconomic status (Calafat, 2008).

Better understanding of the social factors and inequities underlying individual and group differences in health outcomes may support the development of strategies for prevention.