Early-Life Exposure to Perfluoroalkyl Substances and Childhood Metabolic Function

• Abby F. Fleisch ^[1] ; Sheryl L. Rifas-Shiman ^[4] ; Ana M. Mora ^[2] ; Antonia M. Calafat ^[3] ; Xiaoyun Ye ^[3] ; Heike Luttmann-Gibson ^[5] ; Matthew W. Gillman ^[6] ; Emily Oken ^[6] ; Sharon K. Sagiv ^[7]
  1. [1] Boston Children's Hospital

     Boston Children's Hospital

     City of Boston, Estados Unidos

     
  2. [2] Boston University

     Boston University

     City of Boston, Estados Unidos

     
  3. [3] Centers for Disease Control and Prevention

     Centers for Disease Control and Prevention

     Estados Unidos

     
  4. [4] 2 Obesity Prevention Program, Department of Population Medicine, Harvard Medical School and Harvard Pilgrim Health Care Institute, Boston, Massachusetts, USA
  5. [5] 6 Department of Environmental Health, and
  6. [6] 2 Obesity Prevention Program, Department of Population Medicine, Harvard Medical School and Harvard Pilgrim Health Care Institute, Boston, Massachusetts, USA; 7 Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts, USA
  7. [7] 8 Center for Environmental Research and Children’s Health (CERCH), School of Public Health, University of California, Berkeley, Berkeley, California, USA

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• Localización: Environmental health perspectives, ISSN 0091-6765, Vol. 125, Nº. 3, 2017, págs. 481-487
• Idioma: inglés
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• Resumen

  • Perfluoroalkyl substances (PFASs) are synthetic chemicals that may persist in the environment and in humans. There is a possible association between early-life PFAS exposure and metabolic dysfunction in later life, but data are limited.

    We studied 665 mother–child pairs in Project Viva, a Boston, Massachusetts-area cohort recruited 1999–2002. We quantified concentrations of PFASs [perfluorooctanoate (PFOA), perfluorooctane sulfonate (PFOS), perfluorononanoate (PFNA), perfluorohexane sulfonate (PFHxS), and perfluorodecanoate (PFDeA)] in maternal plasma collected at the first prenatal visit (median, 9.6 weeks gestation) and in child plasma from the mid-childhood research visit (median, 7.7 years). We assessed leptin, adiponectin, and homeostatic model assessment of insulin resistance (HOMA-IR) in mid-childhood. We fit covariate-adjusted linear regression models and conducted stratified analyses by child sex.

    Children with higher PFAS concentrations had lower HOMA-IR [e.g., –10.1% (95% CI: –17.3, –2.3) per interquartile range increment in PFOA]. This inverse association between child PFAS and HOMA-IR was more pronounced in females [e.g., PFOA: –15.6% (95% CI: –25.4, –4.6) vs. –6.1% (95% CI: –16.2, 5.2) for males]. Child PFAS plasma concentrations were not associated with leptin or adiponectin. Prenatal PFAS plasma concentrations were not associated with leptin, adiponectin, or HOMA-IR in offspring.

    We found no evidence for an adverse effect of early-life PFAS exposure on metabolic function in mid-childhood. In fact, children with higher PFAS concentrations had lower insulin resistance.

    Fleisch AF, Rifas-Shiman SL, Mora AM, Calafat AM, Ye X, Luttmann-Gibson H, Gillman MW, Oken E, Sagiv SK. 2017. Early-life exposure to perfluoroalkyl substances and childhood metabolic function. Environ Health Perspect 125:481–487; http://dx.doi.org/10.1289/EHP303