Bisphenol A co-exposure effects: a key factor in understanding BPA’s complex mechanism and health outcomes

Abstract

Bisphenol A (BPA) is an environmental endocrine disrupting chemical widely used in the production of consumer products, such as polycarbonate plastics, epoxies and thermal receipt paper. Human exposure to BPA is ubiquitous due to its high-volume production and use. BPA exposure has been associated with obesity, diabetes, reproductive disorders and cancer. Yet, the molecular mechanisms or modes of action underlying these disease outcomes are poorly understood due to the pleiotropic effects induced by BPA. A further confounding factor in understanding BPA's impact on human health is that co-exposure of BPA with endogenous and exogenous agents occurs during the course of daily life. Studies investigating BPA exposure effects and their relationship to adverse health outcomes often ignore interactions between BPA and other chemicals present in the environment. This review examines BPA co-exposure studies to highlight potentially unexplored mechanisms of action and their possible associations with the adverse health effects attributed to BPA. Importantly, both adverse and beneficial co-exposure effects are observed between BPA and natural chemicals or environmental stressors in in vitro and in vivo models. These interactions clearly influence cellular responses and impact endpoint measures and need to be considered when evaluating BPA exposures and their health effects.

Bisphenol a Induces Autophagy Defects and AIF-Dependent Apoptosis via HO-1 and AMPK to Degenerate N2a Neurons

“…Thus, concern regarding whether BPA exposure causes brain health problems in humans has grown. Reliable evidence supports the supposition that BPA impairs brain development (e.g., neural stem cell proliferation and differentiation) and induces neurodegeneration [2,5,6,37]. Herein, we demonstrated that BPA is directly toxic to differentiating N2a neurons, leading to insults including AIF-dependent apoptosis and impaired autophagy flux.…”

“…Bisphenol A (BPA) is a common endocrine-disrupting chemical widely used in the manufacture of polycarbonate plastics and epoxy resins, and people inevitably come into contact with it in daily life [1][2][3][4]. Growing evidence suggests close correlations between BPA exposure, pathogenetic brain degeneration (e.g., Alzheimer's disease (AD)), and altered neurobehaviors (e.g., cognitive decline) [5,6], which implies that BPA is an emerging risk factor for cognitive dysfunction.…”

Adult Male Rats Show Resilience to Adolescent Bisphenol A Effects on Hormonal and Behavioral Responses While Co-Exposure With Hop Extracts Supports Synergistic Actions

“…Notably, however, adolescent exposure to BPA inhibited hops-induced open arm entries in co-exposed rats. This co-exposure effect in regulating behavioral response substantiates a number of studies that have reported the ability of various dietary/naturally occurring compounds to regulate different BPA genomic and biochemical effects upon co-exposure at physiological and pharmacological dose regimens (Sonavane and Gassman, 2019). Interestingly, the behavioral trends observed in the EPM are concordant with BPA-induced anxiety reported at other developmental stages (Matsuda et al, 2012;Patisaul et al, 2012;Diaz Weinstein et al, 2013;Xu et al, 2015).…”

Plastics in Cyanobacterial Blooms—Genotoxic Effects of Binary Mixtures of Cylindrospermopsin and Bisphenols in HepG2 Cells

“…However, combined exposure to these pollutants has not been studied thus far. Recently, a review highlighted the importance of BPA co-exposure studies with other chemicals and environmental stressors for the assessment of outcomes that common co-exposures can exert on human health [52]. Considering their simultaneous presence in the environment, exposure to mixtures of different pollutants is the only realistic exposure scenario.…”