Perinatal Exposure to Low Doses of Bisphenol A Affects Body Weight, Patterns of Estrous Cyclicity, and Plasma LH Levels

Environmental Health Perspectives v.109, n.7, Jul01

Beverly S. Rubin, Mary K. Murray, David A. Damassa, Joan C. King, and Ana M. Soto

Department of Anatomy and Cellular Biology, Tufts Medical School, Boston, Massachusetts, USA

Abstract
The nonsteroidal estrogenic compound bisphenol A (BPA) is a monomer used in the manufacture of polycarbonate plastics and resins. BPA may be ingested by humans as it reportedly leaches from the lining of tin cans into foods, from dental sealants into saliva, and from polycarbonate bottles into their contents. Because BPA is weakly estrogenic--approximately 10,000-fold less potent than 17ß-estradiol--current environmental exposure levels have been considered orders of magnitude below the dose required for adverse effects on health. Herein we demonstrate measurable effects on the offspring of Sprague-Dawley female rats that were exposed, via their drinking water, to approximately 0.1 mg BPA/kg body weight (bw)/day (low dose) or 1.2 mg BPA/kg bw/day (high dose) from day 6 of pregnancy through the period of lactation. Offspring exposed to BPA exhibited an increase in body weight that was apparent soon after birth and continued into adulthood. In addition, female offspring exposed perinatally to the high dose of BPA exhibited altered patterns of estrous cyclicity and decreased levels of plasma luteinizing hormone (LH) in adulthood. Administration of neither the doses of BPA that caused effects during perinatal exposure nor a 10-fold higher dose was able to evoke a uterotropic response in ovariectomized postpubertal females. These data indicate an increased sensitivity to BPA during the perinatal period and suggest the need for careful evaluation of the current levels of exposure to this compound. Key words: Bisphenol A, body weight, BPA, development, endocrine disruptors, environmental estrogens, estrous cycles, reproductive function, xenoestrogen. Environ Health Perspect 109:675-680 (2001). [Online 22 June 2001]

http://ehpnet1.niehs.nih.gov/docs/2001/109p675-680rubin/abstract.html

Address correspondence to A. Soto, Department of Anatomy and Cellular Biology, Tufts Medical School, 136 Harison Avenue, Boston, MA 02111 USA. Telephone: (617) 636-6954. Fax: (617) 636-6536. E-mail: Ana.Soto@tufts.edu

We acknowledge the technical assistance of C. Lee, C. Michaelson, R. O'Donnell, P. Ronsheim, and G. Shin.

Support for these studies was provided by the Tufts Institute of the Environment and NIH-ES 08314.

Received 23 August 2000; accepted 26 January 2001.