- Full (HTML) - Full (PDF) - Related EHP Articles - PubMed:Related Articles - PubMed:Citation - Cited in PMC - Purchase This Issue

Gilbert Schönfelder,¹ Werner Wittfoht,¹ Hartmut Hopp,² Chris E. Talsness,¹ Martin Paul,¹ and Ibrahim Chahoud¹

¹Institute of Clinical Pharmacology and Toxicology, Department of Toxicology, and ²Department of Gynaecology and Obstetrics, Benjamin Franklin Medical Center, Freie Universität, Berlin, Berlin, Germany

Abstract

Bisphenol A (BPA) , an endocrine disruptor, is employed in the manufacture of a wide range of consumer products. The suggestion that BPA, at amounts to which we are exposed, alters the reproductive organs of developing rodents has caused concern. At present, no information exists concerning the exposure of human pregnant women and their fetuses to BPA. We therefore investigated blood samples from mothers (n = 37) between weeks 32 and 41 of gestation. Afer the births, we also analyzed placental tissue and umbilical cord blood from the same subjects. We developed a novel chemical derivatization-gas chromatography/mass spectrometry method to analyze parent BPA at concentrations < 1 µg/mL in plasma and tissues. Concentrations of BPA ranged from 0.3 to 18.9 ng/mL (median = 3.1 ng/mL) in maternal plasma, from 0.2 to 9.2 ng/mL (median = 2.3 ng/mL) in fetal plasma, and from 1.0 to 104.9 ng/g (median = 12.7 ng/g) in placental tissue. BPA blood concentrations were higher in male than in female fetuses. Here we demonstrate parent BPA in pregnant women and their fetuses. Exposure levels of parent BPA were found within a range typical of those used in recent animal studies and were shown to be toxic to reproductive organs of male and female offspring. We suggest that the range of BPA concentrations we measured may be related to sex differences in metabolization of parent BPA or variable maternal use of consumer products leaching BPA. Key words: bisphenol A, endocrine disruptor, fetus, human, maternal blood, placenta, sex differences. Environ Health Perspect 110:A703-A707 (2002) . [Online 10 October 2002]

http://ehpnet1.niehs.nih.gov/docs/2002/110pA703-A707schonfelder/ abstract.html

Address correspondence to G. Schönfelder, Institute of Clinical Pharmacology and Toxicology, Department of Toxicology, Universitätsklinikum Benjamin Franklin der Freie Universität Berlin, Garystr. 5, 14195 Berlin Germany. Telephone: +49 30 8445 1702. Fax: +49 30 8445 1761. E-mail: schoenfe@zedat.fu-berlin.de

G. Schönfelder and W. Wittfoht contributed equally to this work.

This work was supported by the Benjamin Franklin Medical Center.

Received 15 April 2002 ; accepted 15 July 2002.