furthered by physiologic conditions such as obesity. It is likely that many such procarcinogenic events may never be entirely preventable because, although potentially modifiable, they are consequences of basic biologic processes, such as oxidative damage to DNA from endogenous metabolism, or stimulation of cell growth through normal hormonal processes.1 Although such biological “background” mutagenesis is unavoidable, highly efficient protective pathways, such as DNA repair and immune surveillance, are effective at reducing the impacts of procarcinongenic events (Loeb and Nishimura, 2010; Bissell and Hines, 2011).

Although more needs to be learned about both the mechanisms by which breast cancers arise and the array of factors that influence risk for them, much has been established. Among the factors generally accepted as increasing women’s risk are older age, having a first child at an older age or never having a child, exposure to ionizing radiation, and use of certain forms of postmenopausal hormone therapy (HT). Inherited mutations in the BRCA1 and BRCA2 genes also markedly increase risk for breast cancer (and other cancers as well), but these mutations are rare in the general population and account for only 5 to 10 percent of cases (ACS, 2011).

Even though aging, genetics, and patterns of childbearing account for some of the risk for breast cancer, they are not promising targets for preventive measures. More helpful would be identifying modifiable risk factors. For example, the publication of findings from the Women’s Health Initiative (Writing Group for the Women’s Health Initiative Investigators, 2002) confirming earlier indications that estrogen–progestin HT was contributing to an increase in the risk of postmenopausal breast cancer was followed by a rapid reduction in use of HT and in the incidence of invasive breast cancer. As reflected in NCI data, the incidence in 2002 was 136 cases per 100,000 women, compared with 127 in 2003 (NCI, 2011). A portion of the decline in breast cancer incidence since 1999 is attributed to this reduced use of HT (e.g., Ravdin et al., 2007; Farhat et al., 2010). But there are long-standing and still unresolved concerns that aspects of diet, ambient chemicals, or other potentially modifiable environmental exposures may be contributing to high rates of breast cancer.

At present, a large but incomplete body of evidence is available on the relationship between breast cancer and the wide variety of external factors that can be said to comprise the environment. Information on interactions between genetic susceptibility and environmental factors is particularly sparse. In contrast, knowledge of the complexity of breast cancer is growing, with the characterization of multiple tumor subtypes; the possibility

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1Loeb and Nishimura (2010, p. 4270) note that each normal cell in a person’s body may be exposed to as many as 50,000 DNA-damaging events each day, and that oxygen free radicals are a major source of DNA damage.



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