An Extensive New Literature Concerning Low-Dose Effects of Bisphenol A Shows the Need for a New Risk Assessment

Abstract

Bisphenol A (BPA) is the monomer used to manufacture polycarbonate plastic, the resin lining of cans, and other products, with global capacity in excess of 6.4 billion lb/year. Because the ester bonds in these BPA-based polymers are subject to hydrolysis, leaching of BPA has led to widespread human exposure. A recent report prepared by the Harvard Center for Risk Analysis and funded by the American Plastics Council concluded that evidence for low-dose effects of BPA is weak on the basis of a review of only 19 studies; the report was issued after a delay of 2.5 years. A current comprehensive review of the literature reveals that the opposite is true. As of December 2004, there were 115 published in vivo studies concerning low-dose effects of BPA, and 94 of these report significant effects. In 31 publications with vertebrate and invertebrate animals, significant effects occurred below the predicted “safe” or reference dose of 50 μg/kg/day BPA. An estrogenic mode of action of BPA is confirmed by in vitro experiments, which describe disruption of cell function at 10−12 M or 0.23 ppt. Nonetheless, chemical manufacturers continue to discount these published findings because no industry-funded studies have reported significant effects of low doses of BPA, although > 90% of government-funded studies have reported significant effects. Some industry-funded studies have ignored the results of positive controls, and many studies reporting no significant effects used a strain of rat that is inappropriate for the study of estrogenic responses. We propose that a new risk assessment for BPA is needed based on a) the extensive new literature reporting adverse effects in animals at doses below the current reference dose; b) the high rate of leaching of BPA from food and beverage containers, leading to widespread human exposure; c) reports that the median BPA level in human blood and tissues, including in human fetal blood, is higher than the level that causes adverse effects in mice; and d) recent epidemiologic evidence that BPA is related to disease in women.

Cited by papers we hold 18

• Potential Mechanisms of Bisphenol A (BPA) Contributing to Human Disease · 2020
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• Guideline levels for PFOA and PFOS in drinking water: the role of scientific uncertainty, risk assessment decisions, and social factors · 2019
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• Bisphenol A Exposure Disrupts Genomic Imprinting in the Mouse · 2013
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• Peroxisome Proliferator-Activated Receptor γ Is a Target for Halogenated Analogs of Bisphenol A · 2011
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• Similarity of Bisphenol A Pharmacokinetics in Rhesus Monkeys and Mice: Relevance for Human Exposure · 2010
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• Association between Serum Perfluorooctanoic Acid (PFOA) and Thyroid Disease in the U.S. National Health and Nutrition Examination Survey · 2010
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• A Perspective on the Scientific, Philosophical, and Policy Dimensions of Hormesis · 2009
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• Low Doses of Bisphenol A Promote Human Seminoma Cell Proliferation by Activating PKA and PKG via a Membrane G-Protein–Coupled Estrogen Receptor · 2009
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• Biodegradation of Bisphenol A, Bisphenol F and Bisphenol S in Seawater · 2009
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• Polycarbonate Bottle Use and Urinary Bisphenol A Concentrations · 2009
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• Perinatal Exposure to Bisphenol A Alters Early Adipogenesis in the Rat · 2009
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• Molecular Toxicology of Substances Released from Resin–Based Dental Restorative Materials · 2009
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• Exposure to Bisphenol A and Other Phenols in Neonatal Intensive Care Unit Premature Infants · 2008
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• Pancreatic Insulin Content Regulation by the Estrogen Receptor ERα · 2008
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• Why Public Health Agencies Cannot Depend on Good Laboratory Practices as a Criterion for Selecting Data: The Case of Bisphenol A · 2008
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• Exposure of the U.S. Population to Bisphenol A and 4- tertiary -Octylphenol: 2003–2004 · 2007
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• Pilot Study of Urinary Biomarkers of Phytoestrogens, Phthalates, and Phenols in Girls · 2006
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• The Estrogenic Effect of Bisphenol A Disrupts Pancreatic β-Cell Function In Vivo and Induces Insulin Resistance · 2005
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