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Environ Health. 2017 May 19;16(1):47. doi: 10.1186/s12940-017-0259-8.

Prenatal bisphenol a exposure and dysregulation of infant hypothalamic-pituitary-adrenal axis function: findings from the APrON cohort study.

Author information

1
Department of Paediatrics, University of Calgary, 2500 University Drive, Calgary, AB, T2N 1N4, Canada. ggiesbre@ucalgary.ca.
2
Department of Community Health Sciences, University of Calgary, Calgary, AB, Canada. ggiesbre@ucalgary.ca.
3
Department of Community Health Sciences, University of Calgary, Calgary, AB, Canada.
4
Department of Laboratory Medicine and Pathology, University of Alberta, Edmonton, AB, Canada.
5
Department of Psychology, University of Calgary, Calgary, AB, Canada.
6
Department of Paediatrics, University of Calgary, 2500 University Drive, Calgary, AB, T2N 1N4, Canada.
7
Faculty of Nursing, University of Calgary, Calgary, AB, Canada.

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

PMID:
28526030
PMCID:
PMC5437646
DOI:
10.1186/s12940-017-0259-8
[Indexed for MEDLINE]
Free PMC Article

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