We assessed the association between perfluorooctanoic acid (PFOA) and pregnancy outcome in an area with elevated exposure to PFOA from drinking water contaminated by chemical plant releases.
Serum PFOA was measured, and reproductive and residential histories were obtained during 2005–2006. We estimated serum PFOA levels at the time of pregnancy for 11,737 pregnancies occurring between 1990 and 2006, based on historical information on PFOA releases, environmental distribution, pharmacokinetic modeling, and residential histories. We assessed the association between PFOA and the odds of miscarriage, stillbirth, preeclampsia, preterm birth, term low birthweight, and birth defects, controlling for calendar time, age, parity, education, and smoking. PFOA exposure was evaluated as a continuous measure (with and without log transformation) and in quintiles, combining the lowest 2 quintiles (<6.8 ng/mL) as the referent.
Measures of association between PFOA and miscarriage, preterm birth, term low birthweight, and birth defects were close to the null. Odds of stillbirth were elevated in the fourth quintile only. For preeclampsia, the odds ratio was 1.13 (95% confidence interval = 1.00–1.28) for an interquartile shift in log-transformed PFOA, and the odds ratios were 1.1–1.2 across the upper 3 quintiles of exposure.
In this large, population-based study in a region with markedly elevated PFOA exposure, we found no associations between estimated serum PFOA levels and adverse pregnancy outcomes other than possibly preeclampsia. Conclusions are tempered by inherent limitations in exposure reconstruction and self-reported pregnancy outcome information.
From the aDepartment of Epidemiology, Brown University, Providence, Rhode Island; bDepartment of Obstetrics and Gynecology, Brown University, Providence, Rhode Island; cDepartment of Preventive Medicine, Mount Sinai School of Medicine, New York, NY; and dProgram in Public Health, University of California, Irvine, Irvine, CA.
Submitted 22 July 2011; accepted 15 November 2011; posted online 27 February 2012.
This research was funded by the C8 class action settlement agreement (Jack W. Leach, et al. v. E.I. du Pont de Nemours & Company [no. 01-C-608 W.Va., Wood County Circuit Court, West Virginia, USA]) between DuPont and plaintiffs. Funds were administered by the Garden City Group (Melville, New York) that reports to the court. Our work and conclusions are independent of either party to the lawsuit. Cheryl Stein was supported by grant K01 ES019156 from the National Institute of Environmental Health Sciences (NIEHS). Gregory Wellenius was supported by grant R00-ES015774 from NIEHS. The authors reported no other financial interests related to this research. The contents of this report are solely the responsibility of the authors and do not necessarily represent the official views of NIEHS or NIH.
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Correspondence: David A. Savitz, Department of Epidemiology, Brown University, Box G-S121–2, Providence, RI 02912. E-mail: firstname.lastname@example.org.