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Long-term Behavioral and Reproductive Consequences of Embryonic Exposure to Low-dose Toxicants

Long-term Behavioral and Reproductive Consequences of Embryonic Exposure to Low-dose Toxicants

Published on: March 6, 2018

Prenatal bisphenol a exposure and dysregulation of infant hypothalamic-pituitary-adrenal axis function: findings from

Gerald F Giesbrecht^1,2, Maede Ejaredar³, Jiaying Liu⁴

¹Department of Paediatrics, University of Calgary, 2500 University Drive, Calgary, AB, T2N 1N4, Canada. ggiesbre@ucalgary.ca.

Environmental Health : a Global Access Science Source

|May 21, 2017

Insights

Prenatal exposure to bisphenol A (BPA) affects infant hypothalamic-pituitary-adrenal (HPA) axis function differently in males and females. This study reveals sex-specific impacts of BPA on cortisol levels and reactivity in 3-month-old infants.

Area of Science:

Endocrinology
Neuroscience
Environmental Health

Background:

Animal studies indicate prenatal bisphenol A (BPA) exposure causes sex-specific neuroendocrine disruption, particularly in the hypothalamic-pituitary-adrenal (HPA) axis.
Human data linking prenatal BPA exposure to sex-specific behavioral issues and potential HPA axis dysregulation are emerging.

Purpose of the Study:

To investigate sex differences in the association between maternal urinary BPA concentrations during pregnancy and infant HPA axis function at three months of age.

Main Methods:

Longitudinal study of 132 mother-infant pairs from the Alberta Pregnancy Outcomes and Nutrition cohort.
Maternal urine samples (2nd trimester) analyzed for BPA; infant saliva samples analyzed for cortisol before and after blood draw.
Linear growth curve models used to assess infant cortisol changes in relation to prenatal BPA exposure.

Main Results:

Higher maternal BPA was linked to increased baseline cortisol in female infants but decreased baseline cortisol in male infants.
Prenatal BPA exposure was associated with increased cortisol reactivity in males and decreased reactivity in females.

Conclusions:

Prenatal BPA exposure is associated with sex-specific alterations in infant HPA axis function.
Findings align with rodent model evidence and support the hypothesis that BPA-induced behavioral changes in children are mediated by sex-specific HPA axis modifications.

Read full analysis

Abstract

Background:

Animal models show that prenatal bisphenol A (BPA) exposure leads to sexually dimorphic disruption of the neuroendocrine system in offspring, including the hypothalamic-pituitary-adrenal (HPA) neuroendocrine system, but human data are lacking. In humans, prenatal BPA exposure is associated with sex-specific behavioural problems in children, and HPA axis dysregulation may be a biological mechanism. The objective of the current study was to examine sex differences in associations between prenatal maternal urinary BPA concentration and HPA axis function in 3 month old infants.

Methods:

Mother-infant pairs (n = 132) were part of the Alberta Pregnancy Outcomes and Nutrition study, a longitudinal birth cohort recruited (2010-2012) during pregnancy. Maternal spot urine samples collected during the 2nd trimester were analyzed for total BPA and creatinine. Infant saliva samples collected prior to and after a blood draw were analyzed for cortisol. Linear growth curve models were used to characterize changes in infant cortisol as a function of prenatal BPA exposure.

Results:

Higher maternal BPA was associated with increases in baseline cortisol among females (β = 0.13 log μg/dL; 95% CI: 0.01, 0.26), but decreases among males (β = -0.22 log μg/dL; 95% CI: -0.39, -0.05). In contrast, higher BPA was associated with increased reactivity in males (β = .30 log μg/dL; 95% CI: 0.04, 0.56) but decreased reactivity in females (β = -0.15 log μg/dL; 95% CI: -0.35, 0.05). Models adjusting for creatinine yielded similar results.

Conclusions:

Prenatal BPA exposure is associated with sex-specific changes in infant HPA axis function. The biological plausibility of these findings is supported by their consistency with evidence in rodent models. Furthermore, these data support the hypotheses that sexually dimorphic changes in children's behaviour following prenatal BPA exposure are mediated by sexually dimorphic changes in HPA axis function.

Keywords:

Bisphenol-A Cortisol Fetal exposure Hypothalamic-pituitary-adrenal axis Infant stress reactivity

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