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Environ Int. 2017 Oct;107:258-265. doi: 10.1016/j.envint.2017.07.021. Epub 2017 Jul 29.

Early life bisphenol A exposure and neurobehavior at 8years of age: Identifying windows of heightened vulnerability.

Author information

1
Department of Epidemiology, Brown University, Providence, RI 02912, United States.
2
Department of Biostatistics, Brown University, Providence, RI 02912, United States.
3
Division of Laboratory Sciences, National Center for Environmental Health, Centers for Disease Control and Prevention, Atlanta, GA 30341, United States.
4
Division of Epidemiology, Department of Environmental Health, University of Cincinnati College of Medicine, Cincinnati, OH 45267, United States.
5
Department of Pediatrics, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, United States.
6
Child and Family Research Institute, BC Children's Hospital and the Faculty of Health Sciences, Simon Fraser University, Vancouver, British Columbia V5A 1S6, Canada.
7
Department of Epidemiology, Brown University, Providence, RI 02912, United States. Electronic address: joseph_braun_1@brown.edu.

Abstract

BACKGROUND:

Early life BPA exposure could affect neurobehavior, but few studies have investigated whether there are developmental periods when the fetus or child is more vulnerable to these potential effects.

OBJECTIVES:

We explored windows of vulnerability to BPA exposure in a multiethnic cohort of 228 mothers and their children from Cincinnati, Ohio.

METHODS:

We measured urinary BPA concentrations at up to two prenatal and six postnatal time points from the 2nd trimester of pregnancy until the child was age 8years. At age 8years, we administered the Behavioral Assessment System for Children-2 (BASC-2), Behavior Rating Inventory of Executive Function, and Wechsler Intelligence Scale for Children-IV. We estimated covariate-adjusted differences in composite scores from each instrument using a multiple informant model designed to identify heightened windows of vulnerability.

RESULTS:

Among all children, there was not strong evidence that the associations between BPA and neurobehavior varied by the timing of exposure (Visit x BPA p-values≥0.16). However, child sex modified the associations of repeated BPA measures with BASC-2 scores (Visit x Sex x BPA p-values=0.02-0.23). For example, each 10-fold increase in prenatal BPA was associated with more externalizing behaviors in girls (β=6.2, 95% CI: 0.8, 11.6), but not boys (β=-0.8, 95% CI: -5.0, 3.4). In contrast, a 10-fold increase in 8-year BPA was associated with more externalizing behaviors in boys (β=3.9, 95% CI: 0.6, 7.2), but not girls (β=0.3, 95% CI: -3.5, 4.1).

CONCLUSIONS:

We found that sex-dependent associations between BPA and child neurobehavior may depend on the timing of BPA exposure.

KEYWORDS:

Bisphenol A; Children; Epidemiology; Neurodevelopment

PMID:
28764921
PMCID:
PMC5567845
DOI:
10.1016/j.envint.2017.07.021
[Indexed for MEDLINE]
Free PMC Article

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