BPA and the Struggle to define the Safety of Chemicals
Traces of BPA are widely detected in our bodies and environment. Is this chemical, and its presence in the human body, safe? What is meant by safety? Who defines it, and according to what information?
Is it Safe?
We are all just a little bit plastic. Traces of Bisphenol-A (BPA), a chemical used in plastics production, are widely detected in our bodies and environment. Is this chemical, and its presence in the human body, safe? What is meant by safety? Who defines it, and according to what information?
Is It Safe? narrates how the meaning of the safety of industrial chemicals has been historically produced by breakthroughs in environmental health research, which in turn trigger contests among trade associations, lawyers, politicians, and citizen activists to set new regulatory standards. Drawing on archival research and extensive interviews, author Sarah Vogel explores the roots of the contemporary debate over the safety of BPA, and the concerns presented by its estrogen-like effects even at low doses. Ultimately, she contends that science alone cannot resolve the political and economic conflicts at play in the definition of safety. To strike a sustainable balance between the interests of commerce and public health requires recognition that powerful interests will always try to shape the criteria for defining safety, and that the agenda for environmental health research should be protected from capture by any single interest group.
Dose-Dependent Incidence of Hepatic Tumors in Adult Mice following Perinatal Exposure to Bisphenol A
Background: Bisphenol-A (BPA) is a high production – volume chemical with hormone – like properties that has been implicated as a potential carcinogen. Early life exposure has been linked to increased risk for precancerous lesions in mammary and prostate glands and the uterus, but no prior study has shown a significant association between BPA exposure and cancer development.
Objective: We explored the effects of exposure to BPA during gestation and lactation on adult incidence of hepatic tumors in mice.
Methods: Isogenic mice were perinatally exposed to BPA through maternal diets containing one of four environmentally relevant doses (0, 50 ng, 50 µg, or 50 mg of BPA per kg diet) and approximately one male and one female per litter were followed until 10 months of age. Animals were tested for known risk factors for hepatocellular carcinoma, including bacterial and viral infections.
We report dose-dependent incidence of hepatic tumors in exposed 10-month mice. 23% of offspring presented with hepatic tumors or preneoplastic lesions. A statistically significant dose-response relationship was observed, with an odds ratio for neoplastic and preneoplastic lesions of 7.23 (95% CI: 3.23, 16.17) for mice exposed to 50 mg BPA per kg diet compared with unexposed controls. Observed early disease onset, absence of bacterial or viral infection, and lack of characteristic sexual dimorphism in tumor incidence support a non-classical etiology.
To our knowledge, this is the first report of a statistically significant association between BPA exposure and frank tumors in any organ. Our results link early life exposure to BPA with the development of hepatic tumors in rodents, with potential implications for human health and disease.