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Perfluoroalkyl substances and preterm birth

Journal of Perinatology volume 45, pages 539–541 (2025)Cite this article

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Per- and polyfluoroalkyl substances (PFAS) are synthetic chemicals applied to products such as clothing, cookware, and carpets to repel water, oil, and stains. Exposure occurs commonly through drinking water and food and PFAS remain in human tissues for years [1]. PFAS can pass through the placenta and may contribute to adverse birth outcomes, including preterm birth (PTB) [1]. While a large study of PFAS and PTB was null [2], few studies have analyzed associations of PFAS with specific PTB phenotypes such as spontaneous PTB (sPTB) and medically indicated PTB (mPTB). However, a prior study of the Boston-based birth cohort LIFECODES found that some PFAS were associated with higher odds of mPTB [1] and another study of the Boston-based cohort Project Viva found associations of PFAS with gestational hypertension [3], which is a driver of mPTB. Analyzing associations of PFAS with specific PTB phenotypes may reveal potential mechanisms and associations that could be missed when PTB is analyzed as a single heterogeneous outcome. We sought to quantify associations of the two most common PFAS, perfluorooctanoate (PFOA) and perfluorooctane sulfonate (PFOS), with sPTB and mPTB and determine if associations differed between PTB phenotypes.

We performed a nested, case-control study of 40 participants with PTB (<37 weeks’ gestation, 17 sPTB, 23 mPTB) and 43 full-term controls ( > 39 weeks’ gestation) from the Spontaneous Prematurity and Epigenetics of the Cervix (SPEC) cohort in Boston (2013–2019). Details of enrollment are published elsewhere [4]. Cases of sPTB and mPTB were matched 1:2 with controls on age and race/ethnicity. Cases were classified as sPTB if there were preterm labor or spontaneous rupture of membranes and mPTB if birth was initiated by a medical provider due to a maternal or fetal condition such as preeclampsia or intrauterine growth restriction. We used blood samples from glucose tolerance testing at 24–28 weeks gestation to measure plasma PFOA and PFOS concentrations by liquid-chromatography tandem mass-spectrometry and analyzed them independently and then as the sum of PFOA and PFOS [5]. The limit of quantification (LOQ) was defined as the lowest concentration for which values were within 20% of the specified control amounts. For PFOA and PFOS, the LOQ was 0.16 ng/mL and all samples were above the LOQ. We measured 14 additional PFAS but excluded them from our analysis because fewer than 25% of samples exceeded the LOQ. We log2 transformed PFAS concentrations and performed multinomial logistic regression adjusted for parity, body mass index, and insurance. We used linear hypothesis testing to compare sPTB and mPTB effect estimates to one another.

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References

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Funding

This work was supported with funds from the following sources: NIH (R01ES3030101, PI Fleisch); Charles H Hood Foundation (PI Burris); Harvard TH Chan NIEHS Center for Environmental Health Pilot Grant, pilot study PI Hacker (NIH P30ES000002, PI Weisskopf); Center of Excellence in Environmental Toxicology (CEET) Translational Biomarkers Core, core PI Mesaros (P30 ES013508, PI Penning).

Author information

Authors and Affiliations

  1. Tufts University School of Medicine, Boston, MA, USA

    Anne M. Mullin

  2. Center for Interdisciplinary Population & Health Research, Maine Health Institute for Research, Westbrook, ME, USA

    Abby F. Fleisch

  3. Pediatric Endocrinology and Diabetes, Maine Medical Center, Portland, ME, USA

    Abby F. Fleisch

  4. Department of Systems Pharmacology and Translational Therapeutics, University of Pennsylvania, Philadelphia, PA, USA

    Clementina Mesaros

  5. Center of Excellence in Environmental Toxicology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA

    Clementina Mesaros & Heather H. Burris

  6. Division of Neonatology, Children’s Hospital of Philadelphia, University of Pennsylvania, Philadelphia, PA, USA

    Rachel Ledyard & Heather H. Burris

  7. Department of Obstetrics and Gynecology, Beth Israel Deaconess Medical Center, Boston, MA, USA

    Michele R. Hacker

  8. Department of Obstetrics, Gynecology, and Reproductive Biology, Harvard Medical School, Boston, MA, USA

    Michele R. Hacker

  9. Department of Pediatrics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA

    Heather H. Burris

  10. Department of Obstetrics and Gynecology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA

    Heather H. Burris

Authors
  1. Anne M. Mullin
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  2. Abby F. Fleisch
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  3. Clementina Mesaros
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  4. Rachel Ledyard
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  5. Michele R. Hacker
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  6. Heather H. Burris
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Contributions

AM contributed to the analysis and interpretation of the data and drafting and review of the manuscript. AF contributed to the interpretation of the data and review of the manuscript. CM contributed to the analyses of the data and review of the manuscript. RL contributed to the acquisition and analyses of the data and review of the manuscript. MH contributed to the conception and design of the study, acquisition and interpretation of the data, and review of the manuscript. HB contributed to the conception and design of the study, acquisition, analysis, and interpretation of the data, drafting and review of the manuscript.

Corresponding author

Correspondence to Heather H. Burris.

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The authors declare no competing interests.

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Mullin, A.M., Fleisch, A.F., Mesaros, C. et al. Perfluoroalkyl substances and preterm birth. J Perinatol 45, 539–541 (2025). https://doi.org/10.1038/s41372-025-02231-2

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