Bisphenol A BPA is a Reproductive Toxicant and has the Potential to affect Male Reproductive System

BPA is a reproductive toxicant because it impacts female reproduction, and has the potential to affect male reproductive systems in humans and animals

Abstract

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EHP Report: BPA is a female reproductive toxicant.

Background:
In 2007, an expert panel reviewed associations between bisphenol A (BPA) exposure and reproductive health outcomes. Since then, new studies have been conducted on the impact of BPA on reproduction.

Objective:
This review summarizes the data obtained since 2007, focusing on:

  1. findings from human and animal studies,
  2. the effects of BPA on a variety of reproductive endpoints,
  3. and mechanisms of BPA action.

Methods:
We reviewed the literature using a PubMed search from 2007-2013 based on keywords related to BPA and male and female reproduction.

Discussion:
BPA is an ovarian toxicant because it affects the onset of meiosis in both animal and in vitro models, interferes with germ cell nest breakdown in animal models, accelerates follicle transition in several animal species, alters steroidogenesis in multiple animal models and women, and reduces oocyte quality in animal models and women undergoing IVF. BPA is a uterine toxicant because it impairs uterine endometrial proliferation, decreases uterine receptivity, and increases implantation failure in animal models. BPA exposure may be associated with adverse birth outcomes, hyperandrogenism, sexual dysfunction, and impaired implantation in humans, but additional studies are required to confirm whether this is the case. BPA is a testicular toxicant in animal models, but the data in humans are equivocal. Finally, insufficient evidence exists regarding effects of BPA on the oviduct, placenta, and pubertal development.

Conclusion:
BPA is a reproductive toxicant because it impacts female reproduction, and has the potential to affect male reproductive systems in humans and animals.

Sources
  • Bisphenol A and Reproductive Health: Update of Experimental and Human Evidence, 2007–2013, Environ Health Perspect ; DOI:10.1289/ehp.1307728, 4 June 2014
  • Full text PDF
  • Supplemental Material PDF

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