Peretz Jackye, Vrooman Lisa, Ricke William A, Hunt Patricia A, Ehrlich Shelley, Hauser Russ, Padmanabhan Vasantha, Taylor Hugh S, Swan Shanna H, VandeVoort Catherine A, Flaws Jodi A
Comparative Biosciences, University of Illinois at Urbana-Champaign, Urbana, Illinois, USA.
Environ Health Perspect. 2014 Aug;122(8):775-86. doi: 10.1289/ehp.1307728. Epub 2014 Jun 4.
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.
In this review, we summarize data obtained since 2007, focusing on a) findings from human and animal studies, b) the effects of BPA on a variety of reproductive end points, and c) mechanisms of BPA action.
We reviewed the literature published from 2007 to 2013 using a PubMed search based on keywords related to BPA and male and female reproduction.
Because BPA has been reported to affect the onset of meiosis in both animal and in vitro models, interfere with germ cell nest breakdown in animal models, accelerate follicle transition in several animal species, alter steroidogenesis in multiple animal models and women, and reduce oocyte quality in animal models and women undergoing in vitro fertilization (IVF), we consider it an ovarian toxicant. In addition, strong evidence suggests that BPA is a uterine toxicant because it impaired uterine endometrial proliferation, decreased uterine receptivity, and increased 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 these associations. Studies also suggest that BPA may be a testicular toxicant in animal models, but the data in humans are equivocal. Finally, insufficient evidence exists regarding effects of BPA on the oviduct, the placenta, and pubertal development.
Based on reports that BPA impacts female reproduction and has the potential to affect male reproductive systems in humans and animals, we conclude that BPA is a reproductive toxicant.
2007年，一个专家小组审查了双酚A（BPA）暴露与生殖健康结果之间的关联。自那时以来，已经开展了关于BPA对生殖影响的新研究。
在本综述中，我们总结2007年以来获得的数据，重点关注：a）人类和动物研究的结果；b）BPA对各种生殖终点的影响；c）BPA的作用机制。
我们使用基于与BPA以及男性和女性生殖相关关键词的PubMed搜索，回顾了2007年至2013年发表的文献。
因为据报道BPA在动物模型和体外模型中都会影响减数分裂的开始，在动物模型中干扰生殖细胞巢的解体，在多个动物物种中加速卵泡过渡，在多个动物模型和女性中改变类固醇生成，并降低动物模型和接受体外受精（IVF）的女性的卵母细胞质量，所以我们认为它是一种卵巢毒物。此外，有力证据表明BPA是一种子宫毒物，因为它在动物模型中损害子宫内膜增殖、降低子宫接受性并增加着床失败率。BPA暴露可能与人类不良出生结局、高雄激素血症、性功能障碍和着床受损有关，但需要更多研究来证实这些关联。研究还表明BPA在动物模型中可能是一种睾丸毒物，但人类方面的数据并不明确。最后，关于BPA对输卵管、胎盘和青春期发育的影响，现有证据不足。
基于BPA影响人类和动物的女性生殖并有可能影响男性生殖系统的报道，我们得出结论，BPA是一种生殖毒物。
