Ana M Mora1, Abby F Fleisch2, Sheryl L Rifas-Shiman3, Jennifer A Woo Baidal4, Larissa Pardo5, Thomas F Webster6, Antonia M Calafat7, Xiaoyun Ye7, Emily Oken8, Sharon K Sagiv9. 1. Center for Environmental Research and Children's Health (CERCH), School of Public Health, University of California, Berkeley, Berkeley, CA, USA; Central American Institute for Studies on Toxic Substances, Universidad Nacional, Heredia, Costa Rica. Electronic address: animora@berkeley.edu. 2. Pediatric Endocrinology and Diabetes, Maine Medical Center, Portland, ME, USA; Center for Outcomes Research and Evaluation, Maine Medical Center Research Institute, Portland, ME, USA. 3. Division of Chronic Disease Research Across the Lifecourse, Department of Population Medicine, Harvard Medical School and Harvard Pilgrim Health Care Institute, Boston, MA, USA. 4. Division of Pediatric Gastroenterology, Hepatology, and Nutrition, Columbia University Medical Center, New York, NY, USA. 5. Central American Institute for Studies on Toxic Substances, Universidad Nacional, Heredia, Costa Rica. 6. Department of Environmental Health, Boston University School of Public Health, Boston, MA, USA. 7. Division of Laboratory Sciences, National Center for Environmental Health, Centers for Disease Control and Prevention, Atlanta, GA, USA. 8. Division of Chronic Disease Research Across the Lifecourse, Department of Population Medicine, Harvard Medical School and Harvard Pilgrim Health Care Institute, Boston, MA, USA; Department of Nutrition, Harvard T. H. Chan School of Public Health, Boston, MA, USA. 9. Center for Environmental Research and Children's Health (CERCH), School of Public Health, University of California, Berkeley, Berkeley, CA, USA; Division of Epidemiology, School of Public Health, University of California, Berkeley, Berkeley, CA, USA.
Abstract
BACKGROUND: Growing evidence suggests that exposure to per- and polyfluoroalkyl substances (PFASs) may disrupt lipid homeostasis and liver function, but data in children are limited. OBJECTIVE: We examined the association of prenatal and mid-childhood PFAS exposure with lipids and alanine aminotransferase (ALT) levels in children. METHODS: We studied 682 mother-child pairs from a Boston-area pre-birth cohort. We quantified PFASs in maternal plasma collected in pregnancy (median 9.7weeks gestation, 1999-2002) and in child plasma collected in mid-childhood (median age 7.7years, 2007-2010). In mid-childhood we also measured fasting total (TC), high-density lipoprotein cholesterol (HDL-C), triglycerides (TG), and ALT. We then derived low-density lipoprotein cholesterol (LDL-C) from TC, HDL-C, and TG using the Friedewald formula. RESULTS: Median (interquartile range, IQR) perfluorooctane sulfonate (PFOS), perfluorooctanoate (PFOA), and perfluorodecanoate (PFDeA) concentrations in child plasma were 6.2 (5.5), 4.3 (3.0), and 0.3 (0.3) ng/mL, respectively. Among girls, higher child PFOS, PFOA, and PFDeA concentrations were associated with detrimental changes in the lipid profile, including higher TC and/or LDL-C [e.g., β per IQR increment in PFOS=4.0mg/dL (95% CI: 0.3, 7.8) for TC and 2.6mg/dL (-0.5, 5.8) for LDL-C]. However, among both boys and girls, higher plasma concentrations of these child PFASs were also associated with higher HDL-C, which predicts better cardiovascular health, and slightly lower ALT, which may indicate better liver function. Prenatal PFAS concentrations were also modestly associated with improved childhood lipid and ALT levels. CONCLUSIONS: Our data suggest that prenatal and mid-childhood PFAS exposure may be associated with modest, but somewhat conflicting changes in the lipid profile and ALT levels in children.
BACKGROUND: Growing evidence suggests that exposure to n class="Chemical">per- and polyfluoroalkyl substances (PFASs) may disrupt lipid homeostasis and liver function, but data in children are limited. OBJECTIVE: We examined the association of prenatal and mid-childhood PFAS exposure with lipids and alanine aminotransferase (ALT) levels in children. METHODS: We studied 682 mother-child pairs from a Boston-area pre-birth cohort. We quantified PFASs in maternal plasma collected in pregnancy (median 9.7weeks gestation, 1999-2002) and in child plasma collected in mid-childhood (median age 7.7years, 2007-2010). In mid-childhood we also measured fasting total (TC), high-density lipoprotein cholesterol (HDL-C), triglycerides (TG), and ALT. We then derived low-density lipoprotein cholesterol (LDL-C) from TC, HDL-C, and TG using the Friedewald formula. RESULTS: Median (interquartile range, IQR) perfluorooctane sulfonate (PFOS), perfluorooctanoate (PFOA), and perfluorodecanoate (PFDeA) concentrations in child plasma were 6.2 (5.5), 4.3 (3.0), and 0.3 (0.3) ng/mL, respectively. Among girls, higher childPFOS, PFOA, and PFDeA concentrations were associated with detrimental changes in the lipid profile, including higher TC and/or LDL-C [e.g., β per IQR increment in PFOS=4.0mg/dL (95% CI: 0.3, 7.8) for TC and 2.6mg/dL (-0.5, 5.8) for LDL-C]. However, among both boys and girls, higher plasma concentrations of these childPFASs were also associated with higher HDL-C, which predicts better cardiovascular health, and slightly lower ALT, which may indicate better liver function. Prenatal PFAS concentrations were also modestly associated with improved childhood lipid and ALT levels. CONCLUSIONS: Our data suggest that prenatal and mid-childhood PFAS exposure may be associated with modest, but somewhat conflicting changes in the lipid profile and ALT levels in children.
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