Format

Send to

Choose Destination
Crit Rev Toxicol. 2019 May;49(5):371-386. doi: 10.1080/10408444.2019.1621263. Epub 2019 Jul 1.

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

Author information

1
Department of Oncologic Sciences, University of South Alabama Mitchell Cancer Institute, Mobile, AL, USA.
2
Department of Physiology and Cell Biology, University of South Alabama College of Medicine, Mobile, AL, USA.

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.

KEYWORDS:

Bisphenol A; adverse effects; animal models; cell lines; co-exposure; environmental stressors

PMID:
31256736
PMCID:
PMC6823117
[Available on 2020-07-01]
DOI:
10.1080/10408444.2019.1621263

Supplemental Content

Full text links

Icon for Taylor & Francis
Loading ...
Support Center