Pharmacokinetics
There is no agreement between scientists of a physiologically based pharmacokinetic (PBPK) BPA model for humans. The effects of BPA on an organism depend on how much free BPA is available and for how long cells are exposed to it. Glucuronidation in the liver, by conjugation with glucuronic acid to form the metabolite BPA-glucuronide (BPAG), reduces the amount of free BPA, however BPAG can be deconjugated by beta-glucuronidase, an enzyme present in high concentration in placenta and other tissues. Free BPA can also be inactivated by sulfation, a process that can also be reverted by arylsulfatase C.
A 2009 research study found that some drugs, like naproxen, salicylic acid, carbamazepine and mefenamic acid can, in vitro, significantly inhibit BPA glucuronidation. A 2010 study on rats embryos has found that genistein may enhance developmental toxicity of BPA, and another 2010 vitro study has shown that placenta P-glycoprotein may efflux BPA from placenta.
A 2010 review of 80+ biomonitoring studies concluded that the general population is internally exposed to significant amounts of unconjugated BPA (in the ng/ml blood range). Using GC/MS on 20 samples, BPA was detected in 100% of urine samples with a median of 1.25 ng/ml, and 10% of blood samples (LOD 0.5 ng/ml). In a 2011 study, researchers found that after a 5-day consumption of 1 serving of canned vegetarian soup, subjects exhibited a 1200% increase in urinary BPA concentrations compared to controls, suggesting that such a diet induces a peak of BPA elevation of unknown duration and of unknown biological safety.
The best test methods for studying BPA effects are currently under discussion with scientists sharing different opinions.
Read more about this topic: Bisphenol A