However, the study has a number of limitations which suggest that it is not applicable to humans:
- Importantly, previous and on-going human studies have not found any evidence of unconjugated BPA in serum [Volkel, Csanady, Filser, Dekant. 2002. Metabolism and kinetics of bisphenol A in humans at low doses following oral administration. Chem Res Toxicol 15: 1281-7.]
- A number of human studies have not found evidence of bioaccumulation, regardless of the method of dosing. Perhaps most persuasive are intervention-biomonitoring studies. These suggest BPA does not bioaccumulate since levels in the urine rapidly decreases when intake is reduced [Rudel RA, Gray JM, Engel CL, Rawsthorne TW, Dodson RE, Ackerman JM, Rizzo J, Nudelman JL, Brody JG. 2011. Food Packaging and Bisphenol A and Bis(2-Ethylhexyl) Phthalate Exposure: Findings from a Dietary Intervention. Environ. Health Perspec. doi:10.1289/ehp.1003170.].
- Rodents are not necessarily good models for human toxicokinetics. Rodents have enterohepatic recirculation that is likely to lead to the persistence of BPA in the bloodstream [Kurebayashi, Betsui, Ohno. 2003. Disposition of a low dose of C14-bisphenol A in male rats and its main biliary excretion as BPA glucuronide. Toxicol Sci 73:17-25.]. Humans have a more direct route for excretion of BPA and therefore are likely to have a smaller internal dose from the same external dose.
- The doses tested were 100,000 times higher than the expected human dose and thus there likely are issues with accurate extrapolation to realistic dose levels.