A study published today in Environmental Health Perspectives outlines a new method for assessing how synthetic chemicals and pollutants may contribute to breast cancer risk. In addition to developing the chemical testing approach, the authors identify two critical needs: the need for new chemical safety testing methods, and the need to screen more chemicals.
Inherited genes only explain about a quarter of a woman’s risk of developing breast cancer. Exposure to synthetic chemicals and pollutants in air, water, food, workplaces, and consumer products may account for a significant portion of breast cancer risk.
Over 34 million tons of synthetic chemicals are produced or imported into the United States every year, and hundreds of these chemicals are commonly found in women’s blood, urine, and breast tissue. Most have not been tested for their carcinogenic potential. Among those that have, hundreds have been shown to increase mammary tumors in laboratory animals. Animal tests are both time- and resource-intensive and they rarely evaluate the effects of chemical exposure during early life or prenatal development.
To address these issues, a panel of 18 experts—representing fields including toxicology, biology, epidemiology, endocrine disruption, and risk assessment—developed a new method of distinguishing safer chemicals from more hazardous chemicals.
“The basic question is, what would you need to know about a chemical to be able to say with confidence that it doesn't raise the risk of breast cancer?” says Megan Schwarzman, a physician and environmental health researcher at UC Berkeley and the lead author of the study.
The panel of scientists first identified biological processes that, when disturbed, could increase breast cancer risk. They then determined what tests exist to assess whether chemicals interfere with those vulnerable biological processes.
“These are pretty complex chains of causation,” Schwarzman says, “so we tried to build a hazard assessment approach to recognize that complexity.”
The scientists reached three important conclusions: First, both genotoxicity (a chemical’s ability to damage genetic information in a cell) and endocrine disruption (interfering with normal hormonal activity) are significant contributors to breast cancer potential, so any comprehensive chemical assessment must evaluate both categories of biological mechanisms. Second, while useful test methods exist for evaluating chemicals’ genotoxicity and estrogen-like activity, there are insufficient methods for testing chemical effects on other biological processes relevant to breast cancer, including progesterone activity. Finally, they found large gaps in available test data even for chemicals generally thought of as well-tested.
“Developing rapid, inexpensive chemical tests to fill the gaps identified in this study will make it easier for manufacturers to choose safer chemicals for consumer products,” said Ruthann Rudel, a toxicologist at Silent Spring Institute and a coauthor of the study.
“There are so many places we can use this information today—regulators can consider requiring these recommended tests now; manufacturers can choose to use chemicals that pass these tests; and consumers can request that their suppliers use products that have undergone these tests. Meanwhile, we are funding research to fill the gaps that were identified,” says Mhel Kavanaugh-Lynch, director of the California Breast Cancer Research Program, which funded this study.
The authors also hope that the methods they developed can be applied to other diseases that may be affected by chemical exposure, such as other cancers or neurological disorders.
“We're actively trying to use the results to change how chemicals are tested and the decisions that are made in public policy,” Schwarzman says.” We see the potential for chemical testing to contribute to breast cancer prevention and other disease prevention efforts.”
Other UC Berkeley coauthors include Dale Johnson, Department of Nutritional Sciences and Toxicology and Kathleen M. Navarro, Department of Environmental Health.