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Prenatal bisphenol a exposure and dysregulation of infant hypothalamic-pituitary-adrenal axis function: findings from the APrON cohort study.
Environ Health. 2017 05 19; 16(1):47.EH

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.

Authors+Show Affiliations

Department of Paediatrics, University of Calgary, 2500 University Drive, Calgary, AB, T2N 1N4, Canada. ggiesbre@ucalgary.ca. Department of Community Health Sciences, University of Calgary, Calgary, AB, Canada. ggiesbre@ucalgary.ca.Department of Community Health Sciences, University of Calgary, Calgary, AB, Canada.Department of Laboratory Medicine and Pathology, University of Alberta, Edmonton, AB, Canada.Department of Psychology, University of Calgary, Calgary, AB, Canada.Department of Paediatrics, University of Calgary, 2500 University Drive, Calgary, AB, T2N 1N4, Canada. Faculty of Nursing, University of Calgary, Calgary, AB, Canada.Department of Psychology, University of Calgary, Calgary, AB, Canada.Department of Laboratory Medicine and Pathology, University of Alberta, Edmonton, AB, Canada.Department of Paediatrics, University of Calgary, 2500 University Drive, Calgary, AB, T2N 1N4, Canada. Department of Community Health Sciences, University of Calgary, Calgary, AB, Canada.No affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

28526030

Citation

Giesbrecht, Gerald F., et al. "Prenatal Bisphenol a Exposure and Dysregulation of Infant Hypothalamic-pituitary-adrenal Axis Function: Findings From the APrON Cohort Study." Environmental Health : a Global Access Science Source, vol. 16, no. 1, 2017, p. 47.
Giesbrecht GF, Ejaredar M, Liu J, et al. Prenatal bisphenol a exposure and dysregulation of infant hypothalamic-pituitary-adrenal axis function: findings from the APrON cohort study. Environ Health. 2017;16(1):47.
Giesbrecht, G. F., Ejaredar, M., Liu, J., Thomas, J., Letourneau, N., Campbell, T., Martin, J. W., & Dewey, D. (2017). Prenatal bisphenol a exposure and dysregulation of infant hypothalamic-pituitary-adrenal axis function: findings from the APrON cohort study. Environmental Health : a Global Access Science Source, 16(1), 47. https://doi.org/10.1186/s12940-017-0259-8
Giesbrecht GF, et al. Prenatal Bisphenol a Exposure and Dysregulation of Infant Hypothalamic-pituitary-adrenal Axis Function: Findings From the APrON Cohort Study. Environ Health. 2017 05 19;16(1):47. PubMed PMID: 28526030.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Prenatal bisphenol a exposure and dysregulation of infant hypothalamic-pituitary-adrenal axis function: findings from the APrON cohort study. AU - Giesbrecht,Gerald F, AU - Ejaredar,Maede, AU - Liu,Jiaying, AU - Thomas,Jenna, AU - Letourneau,Nicole, AU - Campbell,Tavis, AU - Martin,Jonathan W, AU - Dewey,Deborah, AU - ,, Y1 - 2017/05/19/ PY - 2016/12/14/received PY - 2017/05/11/accepted PY - 2017/5/21/entrez PY - 2017/5/21/pubmed PY - 2017/10/4/medline KW - Bisphenol-A KW - Cortisol KW - Fetal exposure KW - Hypothalamic-pituitary-adrenal axis KW - Infant stress reactivity SP - 47 EP - 47 JF - Environmental health : a global access science source JO - Environ Health VL - 16 IS - 1 N2 - 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. SN - 1476-069X UR - https://www.unboundmedicine.com/medline/citation/28526030/Prenatal_bisphenol_a_exposure_and_dysregulation_of_infant_hypothalamic_pituitary_adrenal_axis_function:_findings_from_the_APrON_cohort_study_ L2 - https://ehjournal.biomedcentral.com/articles/10.1186/s12940-017-0259-8 DB - PRIME DP - Unbound Medicine ER -