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Environ Res. 2015 Apr;138:453-60. doi: 10.1016/j.envres.2015.03.003. Epub 2015 Mar 17.

Gestational urinary bisphenol A and maternal and newborn thyroid hormone concentrations: the HOME Study.

Author information

1
Department of Epidemiology, Brown University School of Public Health, Providence, RI, USA. Electronic address: megan_romano@brown.edu.
2
Child and Family Research Institute, BC Children's and Women's Hospital and Faculty of Health Sciences, Simon Fraser University, Vancouver, British Columbia, Canada.
3
Division of Epidemiology and Biostatistics, Department of Environmental Health, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
4
Department of Biology, University of Massachusetts, Amherst, MA, USA.
5
Department of Laboratory Medicine, University of Washington, Seattle, WA, USA.
6
Division of Laboratory Sciences, National Center for Environmental Health, Centers for Disease Control and Prevention, Atlanta, GA, USA.
7
Children's Environmental Health and Disease Prevention Research Center and Department of Community and Family Medicine, Geisel School of Medicine at Dartmouth, Hanover, NH, USA.
8
Division of General and Community Pediatrics, Department of Pediatrics, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
9
Department of Epidemiology, Brown University School of Public Health, Providence, RI, USA.

Abstract

Bisphenol A (BPA), an endocrine disruptor used in consumer products, may perturb thyroid function. Prenatal BPA exposure may have sex-specific effects on thyroid hormones (THs). Our objectives were to investigate whether maternal urinary BPA concentrations during pregnancy were associated with THs in maternal or cord serum, and whether these associations differed by newborn sex or maternal iodine status. We measured urinary BPA concentrations at 16 and 26 weeks gestation among pregnant women in the HOME Study (2003-2006, Cincinnati, Ohio). Thyroid stimulating hormone (TSH) and free and total thyroxine (T4) and triiodothyronine (T3) were measured in maternal serum at 16 weeks (n=181) and cord serum at delivery (n=249). Associations between BPA concentrations and maternal or cord serum TH levels were estimated by multivariable linear regression. Mean maternal urinary BPA was not associated with cord THs in all newborns, but a 10-fold increase in mean BPA was associated with lower cord TSH in girls (percent change=-36.0%; 95% confidence interval (CI): -58.4, -1.7%), but not boys (7.8%; 95% CI: -28.5, 62.7%; p-for-effect modification=0.09). We observed no significant associations between 16-week BPA and THs in maternal or cord serum, but 26-week maternal BPA was inversely associated with TSH in girls (-42.9%; 95% CI: -59.9, -18.5%), but not boys (7.6%; 95% CI: -17.3, 40.2%; p-for-effect modification=0.005) at birth. The inverse BPA-TSH relation among girls was stronger, but less precise, among iodine deficient versus sufficient mothers. Prenatal BPA exposure may reduce TSH among newborn girls, particularly when exposure occurs later in gestation.

KEYWORDS:

Bisphenol A; Endocrine disruptors; Epidemiology; Newborns; Pregnant women; Thyroid hormones; Thyroid stimulating hormone; Thyroxine; Triiodothyronine

PMID:
25794847
PMCID:
PMC4403004
DOI:
10.1016/j.envres.2015.03.003
[Indexed for MEDLINE]
Free PMC Article

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