Bisphenol A is a widely used industrial chemical with many potential sources of 
human exposure. Bisphenol A is a weak estrogen and has been implicated as an 
"endocrine disruptor". This term is used for a variety of chemicals encountered 
in the environment which have estrogenic activity. It has been postulated that 
human exposure to these chemicals may elicit unwanted estrogenic effects in 
humans such as reduced fertility, altered development and cancer. Up to now the 
body burden of bisphenol A in humans is unknown. Therefore, we investigated the 
metabolism and toxicokinetics of bisphenol A in humans exposed to low doses 
since systemic bioavailability has a major influence on possible estrogenic 
effects in vivo. Human subjects (three males and three females, and four males 
for detailed description of blood kinetics) were administered d(16)-bisphenol A 
(5 mg). Blood and urine samples were taken in intervals (up to 96 h), 
metabolites formed were identified by GC/MS and LC-MS/MS and quantified by 
GC/MS-NCI and LC-MS/MS. d(16)-Bisphenol A glucuronide was the only metabolite of 
d(16)-bisphenol A detected in urine and blood samples, and concentrations of 
free d(16)-bisphenol A were below the limit of detection both in urine (6 nM) 
and blood samples (10 nM). d(16)-Bisphenol A glucuronide was cleared from human 
blood and excreted with urine with terminal half-lives of less than 6 h; the 
applied doses were completely recovered in urine as d(16)-bisphenol A 
glucuronide. Maximum blood levels of d(16)-bisphenol A glucuronide 
(approximately 800 nM) were measured 80 min after oral administration of 
d(16)-bisphenol A (5 mg). The obtained data indicate major species differences 
in the disposition of bisphenol A. Enterohepatic circulation of bisphenol A 
glucuronide in rats results in a slow rate of excretion, whereas bisphenol A is 
rapidly conjugated and excreted by humans due to the absence of enterohepatic 
circulation. The efficient glucuronidation of bisphenol A and the rapid 
excretion of the formed glucuronide result in a low body burden of the 
estrogenic bisphenol A in humans following oral absorption of low doses.