Chapel Hill bisphenol A expert panel consensus statement: integration of mechanisms, effects in animals and potential to impact human health at current levels of exposure.

By F. S. V. Saal, B. Akingbemi, Scott M. Belcher, Linda S. Birnbaum, D. Crain, M. Eriksen, F. Farabollini, L. Guillette, Russ Hauser, J. Heindel and 28 more. Reproductive Toxicology, 2007

734 citations recorded by the source corpus.

This document is a summary statement of the outcome from he meeting: “Bisphenol A: An Examination of the Relevance of cological, In vitro and Laboratory Animal Studies for Assessng Risks to Human Health” sponsored by both the NIEHS and IDCR at NIH/DHHS, as well as the US-EPA and Commonweal n the estrogenic environmental chemical bisphenol A (BPA, ,2-bis(4-hydroxyphenyl)propane; CAS# 80-05-7). The meetng was held in Chapel Hill, NC, 28–30 November 2006 due o concerns about the potential for a relationship between BPA nd negative trends in human health that have occurred in recent ecades. Examples include increases in abnormal penile/urethra evelopment in males, early sexual maturation in females, an ncrease in neurobehavioral problems such as attention deficit yperactivity disorder (ADHD) and autism, an increase in childood and adult obesity and type 2 diabetes, a regional decrease n sperm count, and an increase in hormonally mediated cancers, uch as prostate and breast cancers. Concern has been elevated y published studies reporting a relationship between treatment ith “low doses” of BPA and many of theses negative health outomes in experimental studies in laboratory animals as well as n vitro studies identifying plausible molecular mechanisms that ould mediate such effects. Importantly, much evidence suggests hat these adverse effects are occurring in animals within the ange of exposure to BPA of the typical human living in a develped country, where virtually everyone has measurable blood, issue and urine levels of BPA that exceed the levels produced y doses used in the “low dose” animal experiments. Issues relating to BPA were extensively discussed by five anels of experts prior to and during the meeting, and are sumarized in five reports included in this issue: (1) human exposure o bisphenol A (BPA) [1]; (2) in vitro molecular mechanisms of isphenol A action [2]; (3) in vivo effects of bisphenol A in aboratory animals [3]; (4) an ecological assessment of bispheol A: evidence from comparative biology [4]; (5) an evaluation

Subfields: Health, Toxicology and Mutagenesis, Small Animals

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In Small Animals

Citations in the corpus

Prenatal environmental exposures, epigenetics, and disease (2011, positive): “Recent studies, however, have suggested that non-dietary sources may be important as well [101,102].”
Endocrine disruptors: from endocrine to metabolic disruption. (2011, background): “These U-shaped curves suggest the existence of two independent mechanisms for low doses and high doses (151, 152).”
Urinary, Circulating, and Tissue Biomonitoring Studies Indicate Widespread Exposure to Bisphenol A (2010, background): “Whatever the mechanism, BPA can cause effects in animal models at doses in the range of human exposures, indicating that it can act at lower doses than predicted from some in vitro and in vivo assays (Richter et al. 2007; Vandenberg et al. 2007; vom Saal et al. 2007; Wetherill et al. 2007).”
Hormones and endocrine-disrupting chemicals: low-dose effects and nonmonotonic dose responses. (2012, positive): “BPA binds to the nuclear and membrane ER, and thus most of the effects of this chemical have been attributed to its estrogenic activity (27).”
Bisphenol A and human health: a review of the literature. (2013, background): “detrimental to human health [13], there is less research examining BPA effects in humans.”