When BPA enters the body via the oral route, it is absorbed into the mesenteric blood vessels, transported to the liver, and rapidly metabolized in a process referred to as ‘first pass metabolism’ [31]. Such processes mean that the majority of BPA that circulates in the bloodstream following oral exposure is in the conjugated form (e.g., BPA-glucuronide, BPA-sulfate) although some unconjugated BPA does reach circulation [29, 32, 33]. In contrast, when BPA enters the body via alternative routes (e.g., dermal or inhalation), it circumvents first-pass metabolism, allowing significantly more unconjugated BPA to circulate in the bloodstream [29–31]. These toxicokinetic data suggest that the route of exposure can have a large influence on the concentration of BPA that circulates as unconjugated BPA [19, 34]. This is important because, for BPA, only the unconjugated form can bind to estrogen receptor, leading some groups to conclude that only the unconjugated form is biologically active and therefore hazardous [35, 36].