Bisphenols as Environmental Triggers of Thyroid Dysfunction: Clues and Evidence

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 ofother health outcomes. Given the crucial role of thyroid hormones and the increasing incidence ofthyroid 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 toOctober 2019. Both in vitro and in vivo studies reported the ability of BPs to disrupt thyroid functionthrough multiple mechanisms. The antagonism with thyroid receptors (TRs), which affects TRmediatedtranscriptional activity, the direct action of BPs on gene expression at the thyroid and thepituitary level, the competitive binding with thyroid transport proteins, and the induction of toxicityin 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 increasingthe risk of thyroid nodules. A standardized methodology in toxicological studies and prospectiveepidemiological studies with individual exposure assessments are warranted to evaluate thepathophysiology resulting in the damage and to establish the temporal relationship betweenmarkers of exposure and long-term effects.