An article published on April 14, 2016 in the peer-reviewed journal Food and Chemical Toxicology compares the pharmacokinetics of bisphenol A (BPA, CAS 80-05-7) in sheep after gavage or diet exposure routes. Davy Guignard and colleagues from the TOXALIM Research Centre in Food Toxicology, University of Toulouse, France, exposed ewes to BPA via two different routes: First, through nasogastric gavage, and 13 days later, via food pellets. The plasma concentrations of BPA and its main metabolite, glucuronidated BPA (BPA-G), were followed for 24 hours after each exposure treatment. This approach allowed modeling and comparing BPA pharmacokinetics after different exposure scenarios in the same animals.
Compared to gavage, the dietary route was found to result in threefold higher bioavailability of BPA. Moreover, the metabolism of BPA after diet exposure was delayed, with BPA-G appearing much later than after the gavage treatment. This indicated that, when BPA is ingested with food, it is absorbed and consequently metabolized via two different mechanisms. A significant amount of BPA is absorbed directly in the mouth cavity (buccal absorption), thus surpassing the inactivation by the so-called first-pass metabolism, which takes place in the liver following intestinal absorption.
This report underscores the significance of previous findings in dogs, where high absorption of BPA was demonstrated following sublingual administration (FPF reported). This 2013 study raised a debate (FPF reported) and was later claimed to be irrelevant for the situation in humans, since no particularly high absorption of BPA could be observed after consumption of BPA-contaminated tomato soup by human volunteers (FPA reported). However, Guignard and colleagues point out that the low internal BPA concentrations in this case could be at least partially explained by the short time of contact with the buccal mucosa, typical for liquid foods. Indeed, it has been observed that internal concentrations of BPA in humans were higher after eating BPA-contaminated cookies than after consuming a BPA-contaminated soup. Therefore, buccal absorption of BPA may be particularly relevant for solid foods that require chewing and are thus subject to longer contact with the mouth’s epithelium.
Guignard, D. et al. (2016). “Characterization of the contribution of buccal absorption to internal exposure to bisphenol A through the diet.” Food and Chemical Toxicology (published online April 14, 2016).
Thayer, K. et al. (2015). “Pharmacokinetics of bisphenol A in humans following a single oral administration.” Environment International 83:107-115.
Teeguarden, J. et al. (2015). “24-hour human urine and serum profiles of bisphenol A: Evidence against sublingual absorption following ingestion in soup.” Toxicology and Applied Pharmacology 288:131-142.
Gayrard, V. et al. (2013). “High bioavailability of bisphenol A from sublingual exposure.” Environmental Health Perspectives 121:951-956.