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    Bisphenol A: developmental toxicity from early prenatal exposure.

    Source

    Office of Environmental Health Hazard Assessment, Reproductive and Cancer Hazard Assessment Branch, Sacramento, California, USA. mgolub@oehha.ca.gov

    Erratum in

    • Birth Defects Res B Dev Reprod Toxicol. 2011 Feb;92(1):95.

    Abstract

    Bisphenol A (BPA) exposure has been documented in pregnant women, but consequences for development are not yet widely studied in human populations. This review presents research on the consequences for offspring of BPA exposure during pregnancy. Extensive work in laboratory rodents has evaluated survival and growth of the conceptus, interference with embryonic programs of development, morphological sex differentiation, sex differentiation of the brain and behavior, immune responsiveness, and mechanism of action. Sensitive measures include RAR, aryl hydrocarbon receptor, and Hox A10 gene expression, anogenital distance, sex differentiation of affective and exploratory behavior, and immune hyperresponsiveness. Many BPA effects are reported at low doses (10-50 µg/kg d range) by the oral route of administration. At high doses (>500,000 µg/kg d) fetal viability is compromised. Much of the work has centered around the implications of the estrogenic actions of this agent. Some work related to thyroid mechanism of action has also been explored. BPA research has actively integrated current knowledge of developmental biology, concepts of endocrine disruption, and toxicological research to provide a basis for human health risk assessment.

    © 2010 Wiley-Liss, Inc.

    PMID:
    21136531
    [PubMed - indexed for MEDLINE]

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