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Comparative Toxicogenomics Database (CTD)

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Environmental Health Perspectives Volume 117, Number 5, May 2009 Open Access
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Bisphenol A Data in NHANES Suggest Longer than Expected Half-Life, Substantial Nonfood Exposure, or Both

Richard W. Stahlhut,1 Wade V. Welshons,2 and Shanna H. Swan3

1Environmental Health Sciences Center, University of Rochester Medical Center, Rochester, New York, USA; 2Department of Biomedical Sciences, University of Missouri-Columbia, Columbia, Missouri, USA; 3Department of Obstetrics and Gynecology, University of Rochester Medical Center, Rochester, New York, USA

Abstract
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” (pop˝) for a fasting time of 0–24 hr, < 4.5 hr, 4.5–8.5 hr, and > 8.5 hr.

Results: The overall pop˝ 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 pop˝ 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.

Key words: , , , . Environ Health Perspect 117:784–789 (2009) . doi:10.1289/ehp.0800376 available via http://dx.doi.org/ [Online 28 January 2009]


Address correspondence to R.W. Stahlhut, University of Rochester Medical Center, 601 Elmwood Ave., Box 668, Rochester, New York 14642 USA. Telephone: (585) 275-9204. Fax: (585) 276-2171. E-mail: richard_stahlhut@urmc.rochester.edu

We thank M. Elumalai for SAS programming and H. Lockhart and M. Yuki for Japanese translation.

This work was supported by National Institute of Environmental Health Sciences Training Grant ES07026 and University of Rochester Environmental Health Sciences Center Grant ES01247.

The authors declare they have no competing financial interests.

Received 7 November 2008 ; accepted 16 January 2009.


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