This Article Full Text Full Text (PDF) Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Welshons, W. V. Articles by vom Saal, F. S. Search for Related Content PubMed PubMed Citation Articles by Welshons, W. V. Articles by vom Saal, F. S.

Large Effects from Small Exposures. III. Endocrine Mechanisms Mediating Effects of Bisphenol A at Levels of Human Exposure

Department of Biomedical Sciences (W.V.W.), Department of Obstetrics, Gynecology, and Women’s Health (S.C.N.), and Division of Biological Sciences (F.S.v.S.), University of Missouri-Columbia, Columbia, Missouri 65211

Address all correspondence and requests for reprints to: Dr. Wade V. Welshons, Department of Biomedical Sciences, E102 Veterinary Medicine, University of Missouri-Columbia, Columbia, Missouri 65211-5120. E-mail: WelshonsW{at}missouri.edu.

Abstract

Over 6 billion pounds per year of the estrogenic monomer bisphenol A (BPA) are used to manufacture polycarbonate plastic products, in resins lining metal cans, in dental sealants, and in blends with other types of plastic products. The ester bond linking BPA molecules in polycarbonate and resins undergoes hydrolysis, resulting in the release of free BPA into food, beverages, and the environment, and numerous monitoring studies now show almost ubiquitous human exposure to biologically active levels of this chemical. BPA exerts estrogenic effects through the classical nuclear estrogen receptors, and BPA acts as a selective estrogen receptor modulator. However, BPA also initiates rapid responses via estrogen receptors presumably associated with the plasma membrane. Similar to estradiol, BPA causes changes in some cell functions at concentrations between 1 pM and 1 nM, and the mean and median range of unconjugated BPA measured by multiple techniques in human pregnant maternal, fetal, and adult blood and other tissues exceeds these levels. In contrast to these published findings, BPA manufacturers persist in describing BPA as a weak estrogen and insist there is little concern with human exposure levels. Our concern with human exposure to BPA derives from 1) identification of molecular mechanisms mediating effects in human and animal tissues at very low doses, 2) in vivo effects in experimental animals caused by low doses within the range of human exposure, and 3) widespread human exposure to levels of BPA that cause adverse effects in animals.

This article has been cited by other articles:

				I. A. Lang, T. S. Galloway, A. Scarlett, W. E. Henley, M. Depledge, R. B. Wallace, and D. Melzer Association of Urinary Bisphenol A Concentration With Medical Disorders and Laboratory Abnormalities in Adults JAMA, September 17, 2008; 300(11): 1303 - 1310. [Abstract] [Full Text] [PDF]

				F. S. vom Saal and J. P. Myers Bisphenol A and Risk of Metabolic Disorders JAMA, September 17, 2008; 300(11): 1353 - 1355. [Full Text] [PDF]