Bisphenol A (BPA) is a monomer that is widely used in the manufacturing of polycarbonate
plastics (including storage plastics and baby bottles) and is considered to be one of the most
widely used synthetic compounds in the manufacturing industry. Exposure to BPA mainly occurs
after oral ingestion and results from leaks into food and water from plastic containers. According to
epidemiological data, exposure is widespread and estimated to occur in 90% of individuals. BPA
exhibits pleiotropic and estrogen-like effects; thus, it is considered an endocrine-disrupting chemical.
A growing body of evidence highlights the role of BPA in modulating immune responses and
signaling pathways, which results in a proinflammatory response by enhancing the differential polarization
of immune cells and cytokine production profile to one that is consistent with proinflammation.
Indeed, epidemiological studies have uncovered associations between several autoimmune
diseases and BPA exposure. Data from animal models provided consistent evidence, which highlighted
the role of BPA in the pathogenesis, exacerbation, and perpetuation of various autoimmune
phenomena including neuroinflammation in the context of multiple sclerosis, colitis in inflammatory
bowel disease, nephritis in systemic lupus erythematosus, and insulitis in type 1 diabetes mellitus.
Owing to the widespread use of BPA and its effects on immune system dysregulation, a call
for careful assessment of patients’ risks and public health measures are needed to limit exposure
and subsequent deleterious effects. The purpose of this study is to explore the autoimmune triggering
mechanisms and present the current literature supporting the role of BPA in the pathogenesis of