Environmental pollutants and breast cancer

Laboratory research has shown that numerous environmental pollutants cause mammary gland tumors in animals; are hormonally active, specifically mimicking estrogen, which is a breast cancer risk factor; or affect susceptibility of the mammary gland to carcinogenesis. An assessment of epidemiologic research on these pollutants identified in toxicologic studies can guide future research and exposure reduction aimed at prevention.

The PubMed database was searched for relevant literature and systematic critical reviews were entered in a database available at URL: silentspring.org/sciencereview and URL: komen.org/environment (accessed April 10, 2007). Based on a relatively small number of studies, the evidence to date generally supports an association between breast cancer and polycyclic aromatic hydrocarbons (PAHs) and polychlorinated biphenyls (PCBs) in conjunction with certain genetic polymorphisms involved in carcinogen activation and steroid hormone metabolism.

Evidence regarding dioxins and organic solvents is sparse and methodologically limited but suggestive of an association. Methodologic problems include inadequate exposure assessment, a lack of access to highly exposed and unexposed populations, and a lack of preclinical markers to identify associations that may be obscured by disease latency. Among chemicals identified in toxicologic research as relevant to breast cancer, many have not been investigated in humans. The development of better exposure assessment methods is needed to fill this gap. In the interim, weaknesses in the epidemiologic literature argue for greater reliance on toxicologic studies to develop national policies to reduce chemical exposures that may be associated with breast cancer. Substantial research progress in the last 5 years suggests that the investigation of environmental pollutants will lead to strategies to reduce breast cancer risk.

RATIONALE

Laboratory research provides evidence that environmental pollutants may contribute to breast cancer risk by damaging DNA, promoting tumor growth, or increasing susceptibility by altering mammary gland development. Although to our knowledge most chemicals have never been tested for these effects, 216 potential mammary carcinogens have been identified in animals. In vitro assays have identified approximately 250 chemicals that mimic or interfere with estrogen, which stimulates proliferation of estrogen-sensitive breast cancer cells in laboratory studies and presumably underlies many of the established breast cancer risk factors. In an emerging area of research into developmental toxicity, animal studies show that maternal exposure during pregnancy to atrazine or bisphenol A affects differentiation of the mammary glands in the offspring, which remain in a less differentiated state that is more susceptible to carcinogen exposure.

If these mechanisms similarly affect humans, reducing or eliminating chemical exposures could have substantial public health benefits, because breast cancer is the mostly commonly diagnosed invasive cancer in women and the leading cause of cancer death in women ages 25 to 60 years. Furthermore, exposure to the chemicals identified as animal mammary carcinogens and estrogen mimics is substantial; these compounds are widely detected in human tissues and in environments, such as homes, where women spend time. Compounds of interest include, for example, benzene from gasoline, polycyclic aromatic hydrocarbons (PAHs) from vehicle exhaust and air pollution, disinfection products from chlorinated drinking water, polychlorinated biphenyls (PCBs), dioxin, chlorinated solvents, and some pesticides.