Emerging evidence from a research study in rabbits suggests that environmental toxicants may influence inflammation-promoted chronic disease susceptibility during early life. BPA exposure just before or after birth leads to reduced gut bacterial diversity, bacterial metabolites such as short-chain fatty acids (SCFA) and elevated gut permeability – three common early markers of inflammation-promoted chronic diseases.

The 16S rRNA amplicon sequencing analysis revealed differences in beta diversity with a significant reduction in the relative abundances of short-chain fatty acid (SCFA) producers such as Oscillospira and Ruminococcaceae due to BPA exposure. Furthermore, BPA exposure reduced fecal SCFA levels and increased systemic lipopolysaccharide (LPS) levels. BPA exposure-increased intestinal permeability was ameliorated by the addition of SCFA in vitro. Metabolic fingerprints revealed alterations in global metabolism and amino acid metabolism.

The results, published in the journal mSystems show that perinatal BPA exposure may cause gut bacterial dysbiosis and altered metabolite profiles that lead to chronic colon and liver inflammation. The study suggests that correcting bacterial dysbiosis induced by environmental toxins early in life may reduce the risk for chronic diseases later in life.