Environmental exposures offer one of the greatest opportunities to reduce breast cancer risk, according to a recent article published in Breast Diseases: A Year Book Quarterly, an interdisciplinary publication for medical professionals. While both scientific literature and mainstream media tend to focus breast cancer research and coverage on primary genetic mutations, these account for just five-to-seven percent of breast cancer risk.
In fact, women who carry the BRCA 1 or BRCA 2 mutations are still susceptible to environmental exposures, which may interact with genes to increase breast cancer risk. For example, women carrying BRCA mutations who were born after 1940 were shown to have breast cancer rates that were 2.8 times higher than those born before 1940. While factors like diet, exercise, childbearing practices, etc. impact breast cancer risk, there has also been an exponential increase in exposure to toxic environmental chemicals, many of which are known to disrupt our endocrine systems.
“Unlike drugs aimed at modulating the endocrine system under strict medical supervision, an unknown number of environmental chemicals with hormone-disrupting properties are present in consumer products, and most Americans are routinely exposed to them.” That includes chemicals in food, cosmetics, toys and furniture.
Many authoritative reports endorse the importance of research into the role of environmental exposure in breast cancer incidence, including the President’s Cancer Panel Report: Reducing Environmental Cancer Risk, which concluded that “the true burden of environmentally induced cancer has been grossly underestimated,” and the Interagency Breast Cancer and Environmental Research Coordinating Committee, which concluded that “prevention is key to reducing the burden of breast cancer.”
Critical Periods of Susceptibility
Endocrine-disrupting chemicals exert effects on later health outcomes during “critical periods of susceptibility” such as gestation, childhood and pregnancy, and the authors include three examples of human epidemiological/clinical literature supporting the notion that early exposures lead to disruptions in breast development and subsequent risk for developing breast cancer:
Between 1938 and 1971 doctors prescribed a drug called DES for millions of pregnant women to prevent miscarriages, culminating in a medical tragedy that has affected at least 5 million people. Daughters who were exposed prenatally to DES had a nearly 2-fold increase in breast cancer risk for women over 40 years old. These results indicate direct effects of fetal exposure to DES on later development of breast cancer.
Rachel Carson made DDT famous in 1961 with the publication of Silent Spring, a groundbreaking book that spurred the environmental movement—and the passage of important legislation to regulate environmental toxicants. Exposure to DDT during childhood and early adolescence was associated with a 5-fold increase in the risk of developing breast cancer before age 50. In a follow up study, higher maternal DDT levels were associated with an almost 4-fold increase in breast cancer occurrence in their daughters over the next five decades, passing the toxic load on to subsequent generations.
- Camp Lejeune
Over the past several years, former marines and family members of marines stationed at Camp Lejeune in North Carolina have come forward, documenting development of male breast cancer decades after exposures to trichloroethylene (TCE) and other toxic industrial solvents that were found in the water supplies on the base. By the middle of 2014, some 84 cases of breast cancer had been documented among men who were exposed to the solvents at Camp Lejeune in utero or in childhood. This extraordinarily high rate of male breast cancer is further evidence of the link between exposures to environmental toxicants and increased risk of breast cancer at critical windows of development.
At the end of the day, we cannot change our genetic makeup, but we can limit exposures to toxic chemicals. The authors recommend additional research in the following areas:
- Regular testing of exposures at neonatal, prenatal, and pubertal periods;
- Examining mammary glands as standard endpoints in basic EDC and toxicology research;
- Studying the development of breast cancer in males and females in both rodent models and humans;
- Improving the design of epidemiologic studies to unravel the complex roles of exposure to environmental chemicals in the development of breast cancer;
- Improving risk assessment methods to include cumulative adverse effects of chemicals and mixtures of chemicals.
About the authors:
Janet Gray, Ph.D.
Vassar professor and director of the college’s Science, Technology, and Society Program, Janet Gray has a background in behavioral neuroscience,and her laboratory research has focused on the effects of estrogens and mixed antiestrogens, especially tamoxifen, on brain activity and behavior. She chairs the Breast Cancer Fund’s Science Advisory Panel and serves on the Board of Directors. In recent years, her research and writing focus has turned toward engaging the public in the complex issues surrounding breast cancer and environmental risks. Gray is the editor of the fifth (2008) and sixth (2010) editions of the Breast Cancer Fund’s groundbreaking report, State of the Evidence: The Connection Between Breast Cancer and the Environment.
Maricel V. Maffini, Ph.D.
Maricel Maffini is a private contractor on issues related to chemical safety, food additive regulation, science and public health. She also serves on the Breast Cancer Fund’s Science Advisory Panel. Prior to her current role she was a senior scientist in the health and environment program at the Natural Resources Defense Council (NRDC) in Washington, DC. She joined NRDC in 2013 after completing a three-year research project evaluating the U.S. food additive regulatory system at The Pew Charitable Trusts. Before joining Pew, she was an investigator at Tufts University in Boston, MA. Her research areas included breast cancer, endocrine disruption and tissue engineering.