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Children's Health Advance Publication

Environ Health Perspect; DOI:10.1289/ehp.1408258

Early-Life Bisphenol A Exposure and Child Body Mass Index: A Prospective Cohort Study

Joseph M. Braun,1 Bruce P. Lanphear,2,3 Antonia M. Calafat,4 Sirad Deria,3 Jane Khoury,5 Chanelle J. Howe,1 and Scott A. Venners
Author Affiliations close
1Department of Epidemiology, Brown University School of Public Health, Brown University, Providence, Rhode Island, USA; 2Child and Family Research Institute, BC Children’s and Women’s Hospital, Vancouver, Canada; 3Faculty of Health Sciences, Simon Fraser University, Burnaby, Canada; 4Centers for Disease Control and Prevention, Atlanta, Georgia, USA; 5Division of Biostatistics and Epidemiology, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio, USA
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This EHP Advance Publication article has been peer-reviewed, revised, and accepted for publication. EHP Advance Publication articles are completely citable using the DOI number assigned to the article. This document will be replaced with the copyedited and formatted version as soon as it is available. Through the DOI number used in the citation, you will be able to access this document at each stage of the publication process.

Citation: Braun JM, Lanphear BP, Calafat AM, Deria S, Khoury J, Howe CJ, Venners SA. Early-Life Bisphenol A Exposure and Child Body Mass Index: A Prospective Cohort Study. Environ Health Perspect;

Received: 10 February 2014
Accepted: 25 July 2014
Advance Publication: 29 July 2014

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Background: Early life bisphenol A (BPA) exposure may increase childhood obesity risk, but few prospective epidemiological studies have investigated this relationship.

Objective: To determine if early life BPA exposure was associated with increased body mass index (BMI) at 2-5 years of age in 297 mother-child pairs from Cincinnati, OH (HOME Study).

Methods: Urinary BPA concentrations were measured in samples collected from pregnant women during the 2nd and 3rd trimesters and their children at 1 and 2 years of age. BMI z-scores were calculated from weight/height measures conducted annually from 2-5 years of age. We used linear mixed models to estimate BMI differences or trajectories with increasing creatinine-normalized BPA concentrations.

Results: After confounder adjustment, each 10-fold increase in prenatal (β = -0.1, 95% confidence limit [CL]: -0.5, 0.3) or early childhood (β = -0.2, CL: -0.6, 0.1) BPA concentrations was associated with a modest and non-significant reduction in child BMI. These inverse associations were suggestively stronger in girls compared to boys (prenatal effect measure modification [EMM] p-value = 0.30, early childhood EMM p-value = 0.05), but sex-specific associations were imprecise. Children in the highest early childhood BPA tercile had lower BMI at 2 years (difference = -0.3; CL: -0.6, 0) and larger increases in their BMI slope from 2-5 years (BMI increase per year = 0.12; CL: 0.07, 0.18) than children in the lowest tercile (BMI increase per year = 0.07; CL: 0.01, 0.13). All associations were attenuated without creatinine-normalization.

Conclusions: Prenatal and early childhood BPA exposures were not associated with increased BMI at 2-5 years, but higher early childhood BPA exposures were associated with accelerated growth during this period.

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