Background: Preterm birth (PTB), a leading cause of infant mortality and morbidity, has a complex etiology with a multitude of interacting causes and risk factors. The role of environmental contaminants, particularly bisphenol A (BPA), is understudied with regard to PTB.

Objectives: In the present study we examined the relationship between longitudinally measured BPA exposure during gestation and PTB.

Methods: A nested case–control study was performed from women enrolled in a prospective birth cohort study at Brigham and Women’s Hospital in Boston, Massachusetts, during 2006–2008. Urine samples were analyzed for BPA concentrations at a minimum of three time points during pregnancy on 130 cases of PTB and 352 randomly assigned controls. Clinical classifications of PTB were defined as “spontaneous,” which was preceded by spontaneous preterm labor or preterm premature rupture of membranes, or “placental,” which was preceded by preeclampsia or intrauterine growth restriction.

Results: Geometric mean concentrations of BPA did not differ significantly between cases and controls. In adjusted models, urinary BPA averaged across pregnancy was not significantly associated with PTB. When examining clinical classifications of PTB, urinary BPA late in pregnancy was significantly associated with increased odds of delivering a spontaneous PTB. After stratification on infant’s sex, averaged BPA exposure during pregnancy was associated with significantly increased odds of being delivered preterm among females, but not males.

Conclusions: These results provide little evidence of a relationship between BPA and prematurity, though further research may be warranted given the generalizability of participant recruitment from a tertiary teaching hospital, limited sample size, and significant associations among females and within the clinical subcategories of PTB.

Citation: Cantonwine DE, Ferguson KK, Mukherjee B, McElrath TF, Meeker JD. 2015. Urinary bisphenol A levels during pregnancy and risk of preterm birth. Environ Health Perspect 123:895–901;  http://dx.doi.org/10.1289/ehp.1408126

Address correspondence to D.E. Cantonwine, Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA 02115 USA. Telephone: (734) 239-4040. E-mail: dcantonwine@partners.org

We thank the participants and field staff at Brigham and Women’s Hospital (A. Thomas and J. Bloom), National Science Foundation International in Ann Arbor, Michigan (K. Kneen, S. Clipper, G. Pace, D. Weller, and J. Bell) for urine BPA analysis, and R. Hauser of Harvard School of Public Health for guidance on study design.

Funding was provided by the National Institute of Environmental Health Sciences, National Institutes of Health (R01ES018872, P42ES017198, R21 ES02811, and P30ES017885).

The authors declare they have no actual or potential competing financial interests.

Received: 14 January 2014 Accepted: 24 March 2015 Advance Publication: 27 March 2015 Final Publication: 1 September 2015

Note to readers with disabilities: EHP strives to ensure that all journal content is accessible to all readers. However, some figures and Supplemental Material published in EHP articles may not conform to 508 standards due to the complexity of the information being presented. If you need assistance accessing journal content, please contact ehp508@niehs.nih.gov . Our staff will work with you to assess and meet your accessibility needs within 3 working days.

Note to readers with disabilities: EHP has provided a 508-conformant table of contents summarizing the Supplemental Material for this article (see below) so readers with disabilities may determine whether they wish to access the full, nonconformant Supplemental Material. If you need assistance accessing this or any other content on this site, please contact ehp508@niehs.nih.gov . Our staff will work with you to assess and meet your accessibility needs within 3 working days.

Supplemental Table of Contents PDF (105 KB)