Institute of Clinical Physiology, National Research Council, 56124 Pisa, Italy.
Int J Environ Res Public Health. 2020 Apr 13;17(8):2654. doi: 10.3390/ijerph17082654.
Bisphenols (BPs), and especially bisphenol A (BPA), are known endocrine disruptors (EDCs), capable of interfering with estrogen and androgen activities, as well as being suspected of other health outcomes. Given the crucial role of thyroid hormones and the increasing incidence of thyroid carcinoma in the last few decades, this review analyzes the effects of BPS on the thyroid, considering original research in vitro, in vivo, and in humans published from January 2000 to October 2019. Both in vitro and in vivo studies reported the ability of BPs to disrupt thyroid function through multiple mechanisms. The antagonism with thyroid receptors (TRs), which affects TR-mediated transcriptional activity, the direct action of BPs on gene expression at the thyroid and the pituitary level, the competitive binding with thyroid transport proteins, and the induction of toxicity in several cell lines are likely the main mechanisms leading to thyroid dysfunction. In humans, results are more contradictory, though some evidence suggests the potential of BPs in increasing the risk of thyroid nodules. A standardized methodology in toxicological studies and prospective epidemiological studies with individual exposure assessments are warranted to evaluate the pathophysiology resulting in the damage and to establish the temporal relationship between markers of exposure and long-term effects.
双酚类物质（BPs），尤其是双酚 A（BPA），是众所周知的内分泌干扰物（EDCs），能够干扰雌激素和雄激素的活性，并且还被怀疑会对其他健康结果产生影响。鉴于甲状腺激素的重要作用以及过去几十年间甲状腺癌发病率的不断上升，本综述分析了 BPS 对甲状腺的影响，考虑了从 2000 年 1 月到 2019 年 10 月发表的体外、体内和人类的原始研究。体外和体内研究均报道了 BPs 通过多种机制干扰甲状腺功能的能力。BPs 与甲状腺受体（TRs）的拮抗作用，影响 TR 介导的转录活性，BPs 对甲状腺和垂体水平基因表达的直接作用，与甲状腺转运蛋白的竞争性结合，以及在几种细胞系中诱导毒性，可能是导致甲状腺功能障碍的主要机制。在人类中，结果更为矛盾，尽管有一些证据表明 BPs 有增加甲状腺结节风险的潜力。需要标准化的毒理学研究方法和具有个体暴露评估的前瞻性流行病学研究，以评估导致损伤的病理生理学，并确定暴露标志物与长期影响之间的时间关系。
