Reviews on Environmental Health
Editor-in-Chief: Carpenter, David O. / Sly, Peter
Editorial Board Member: Brugge, Doug / Diaz-Barriga, Fernando / Edwards, John W. / Field, R.William / Hales, Simon / Horowitz, Michal / Maibach, H.I. / Shaw, Susan / Stein, Renato / Tao, Shu / Tchounwou, Paul B.
SCImago Journal Rank (SJR) 2015: 0.776
Source Normalized Impact per Paper (SNIP) 2015: 0.676
Impact per Publication (IPP) 2015: 1.795
Human exposures to bisphenol A: mismatches between data and assumptions
1Center for Regenerative and Developmental Biology, Tufts University, Suite 4600, 200 Boston Avenue, Medford, MA 02155, USA
2School of Molecular Biosciences and Center for Reproductive Biology, Washington State University, Pullman, WA, USA
3Environmental Health Sciences, Charlottesville, VA, USA
4Division of Biological Sciences, University of Missouri-Columbia, Columbia, MO, USA
Citation Information: Reviews on Environmental Health. Volume 28, Issue 1, Pages 37–58, ISSN (Online) 2191-0308, ISSN (Print) 0048-7554, DOI: 10.1515/reveh-2012-0034, April 2013
- Published Online:
Human exposure to bisphenol A (BPA), a synthetic estrogen found in numerous consumer products, is widespread. However, scientific knowledge about the sources and routes of exposure remains incomplete. Although human biomonitoring studies report small amounts of bioactive BPA in the blood of most subjects, toxicokinetic models suggest that circulating levels should be undetectable. The conflict between reported data and toxicokinetic models has spurred considerable debate, with some suggesting that data from analyses of human blood should be dismissed in their entirety. This review addresses the assumptions used by previous risk assessment panels regarding the sources and routes of exposure to BPA (specifically, that BPA exposures occur solely via a few dietary sources) and how these assumptions have affected the interpretation of BPA studies. Given new experimental evidence that route of exposure influences BPA pharmacokinetics, we consider the implications of basing regulatory decisions on limited data that have provided incomplete information about the products that contain this chemical and how it enters the body. We also address evidence that challenges the assumption that humans metabolize BPA rapidly enough to result in undetectable levels in blood and therefore determine that there is a possibility of harm from current exposure levels. Our conclusions are consistent with the large number of hazards and adverse effects identified in laboratory animals exposed to low doses of BPA.
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