Bisphenol A Data in NHANES Suggest Longer than Expected Half-Life, Substantial Nonfood Exposure, or Both

• Published in: Environmental health perspectives Vol. 117; no. 5; pp. 784 - 789
• Main Authors: Stahlhut, Richard W., Welshons, Wade V., Swan, Shanna H.
• Format: Journal Article
• Language: English
• Published: United States National Institute of Environmental Health Sciences. National Institutes of Health. Department of Health and Human Services 01.05.2009; National Institute of Environmental Health Sciences
• Subjects: Adipose tissues; Adjustment; Adult; Adults; Aged; Benzhydryl Compounds; Bisphenol A; Bisphenols; Business publications audits; Chemical hazards; Confidence intervals; Copyrights; Creatinine; Environmental Exposure; Environmental Monitoring; Fasting; Female; Foods; Half lives; Half-Life; Health; Health aspects; Health surveys; Human; Humans; Intervals; Kinetics; Male; Mathematical models; Median income; Middle Aged; Nutrition; Nutrition Surveys; Pharmacokinetics; Phenols - analysis; Phenols - pharmacokinetics; Phenols - urine; Physiological aspects; Reporting; Searching; Steels; Tissues (biology); Urine; Young Adult; United States; pharmacokinetics; NHANES; bisphenol A; exposure assessment
• ISSN: 0091-6765; 1552-9924
• DOI: 10.1289/ehp.0800376

Background: It is commonly stated in the literature on human exposure to bisphenol A (BPA) that food is the predominant BPA exposure source, and that BPA is rapidly and completely cleared from the body. If this is correct, BPA levels in fasting individuals should decrease with increased fasting time. Objectives: We set out to investigate the relationship between urine BPA concentration and fasting time in a population-based sample. Methods: We modeled log BPA urine concentration as a function of fasting time, adjusted for urine creatinine and other confounders, in 1,469 adult participants in the 2003-2004 National Health and Nutrition Examination Survey. We estimated the BPA "population-based half-life"$({\rm pop}^{{\textstyle\frac{1}{2}}})$for a fasting time of 0-24 hr, < 4.5 hr, 4.5-8.5 hr, and > 8.5 hr. Results: The overall${\rm pop}^{{\textstyle\frac{1}{2}}}$for the 0- to 24-hr interval was 43 hr [95% confidence interval (CI), 26-119 hr]. Among those reporting fasting times of 4.5-8.5 hr (n = 441), BPA declined significantly with fasting time, with a${\rm pop}^{{\textstyle\frac{1}{2}}}$of 4.1 hr (95% CI, 2.6-10.6 hr). However, within the fasting time intervals of 0-4.5 hr (n = 129) and 8.5-24 hr (n = 899), we saw no appreciable decline. Fasting time did not significantly predict highest (> 12 ng/mL) or lowest (below limit of detection) BPA levels. Conclusions: Overall, BPA levels did not decline rapidly with fasting time in this sample. This suggests substantial nonfood exposure, accumulation in body tissues such as fat, or both. Explaining these findings may require experimental pharmacokinetic studies of chronic BPA exposure, further examination of BPA levels and effects in fat, and a search for important nonfood sources.