Neither direct nor developmental exposure to bisphenol A alters the severity of experimental inflammatory colitis in mice. (28th December 2012)

• Record Type: Journal Article
• Authors: Roy, Anirban; Gaylo, Alison; Cao, Wenqing; Saubermann, Lawrence J.; Lawrence, B. Paige
• Is Part Of: Journal of immunotoxicology. Volume 10:Number 4(2013)
• Page Start: 334
• Page End: 340
• Publication Date: 2012-12-28
• Subjects: Bisphenol A -- developmental immunotoxicity -- endocrine disruptor -- inflammatory bowel disease; Immunotoxicology -- Periodicals; Poisons -- Immunology -- Periodicals; Environmental health -- Periodicals; 616.97
• DOI: 10.3109/1547691X.2012.747231
• Languages: English
• ISSNs: 1547-691X

Abstract

Abstract: Bisphenol A (BPA) is a high production volume endocrine disrupting chemical that is widely used in many consumer products and prevalent in human biological fluids. Recent studies suggest that BPA is active even at low levels, raising concern about its potential harm to human health. Given that the main route of exposure to BPA is oral, via the consumption of BPA-tainted foods and beverages, intestinal tissues could be particularly vulnerable to BPA-induced changes. A novel examination is reported here of whether oral exposure to BPA affects inflammatory bowel disease (IBD), an immune-mediated disease of the colon, using a mouse model of inflammatory colitis. In addition to direct exposure, the possible contribution of maternal BPA exposure to disease later in life is explored. It was found that daily oral exposure to BPA at the US Environmental Protection Agency described oral reference dose (50 µg/kg/day), either via direct oral route or through maternal sources (i.e. developmental exposure), did not significantly alter disease outcomes of body weight, survival, or colonic pathology. These observations suggest that oral BPA exposure, at this dose and for this exposure duration, has minimal influence on aspects of the inflammatory response that regulate immune mediated diseases of the gastrointestinal tract.