BPA was first developed in the 1890s as a synthetic estrogen which in the 1930s has been shown to possess estrogenic activity comparable to estrone in stimulating the female reproductive system in rats [
9]. Surprisingly, data on the estrogenic properties of this compound have been forgotten and nowadays BPA is the most abundant chemical used in many consumer products [
10]. It is mostly used in the production of polycarbonate plastics and epoxy resins, food packaging, dental sealants, and thermal receipts. Therefore, BPA can migrate into dust from laminate flooring, adhesives containing epoxy resins, paints, toys and household electronic equipment [
11]. BPA is also widely used as the inside coating of cans used for food preservation and storage. Heating cans during sterilization or food preparation causes BPA to leak into the can content and therefore, BPA is also found in many food products [
12]. Consequently, we are now exposed to this chemical not only via inhalation of household dust but mostly by eating foods stored in plastic containers or cans [
10]. Due to the phenolic structure, BPA has been shown to interact with estrogen receptors (ERs) and estrogen signaling pathways [
13]. The binding affinity of BPA with both ERs has been estimated to be 0.1–0.01 % of the affinity of 17β-estradiol (E2) [
14] but data from the
in vitro experiments on ER positive human MCF-7 breast cancer cells show that although it competes more effectively for binding with the ERα it induces the ERα- and ERβ-mediated gene expression with comparable efficacy [
15]. BPA has also been shown to activate the expression of the target genes by signaling via so-called membrane estrogen receptors [G-protein coupled ERs (GPER)] with the potency comparable to the E2 or through related signal-transduction cascades [
16]. Although BPA is generally considered to be an ER agonist in some tissues it has been shown to have antagonistic effects (i.e., brain and uterus) [
17]. In addition to binding to ERs, BPA has also been shown to have an influence on their expression. Data from
in vitro as well as
in vivo experiments showed that exposure to this phenolic compound leads to the upregulation of ERα gene expression in different cell types and tissues [
18‐
21]. Apart from the apparent affinity of this chemical to the ERs, BPA has also been shown to bind androgen receptors (AR) [
22,
23], thyroid hormone receptors (TR) [
24] and peroxisome proliferator activated receptors gamma (PPARγ) [
25]. Therefore, BPA may not only cause adverse effects in the reproductive tissues but may also greatly influence metabolic aspects of human health (reviewed in ref. [
26,
27]).