Abstract 37: Associations of Prenatal Per- and Polyfluoroalkyl Substances (PFAS) Exposures and Childhood Blood Pressure in the Environmental influences on Child Health Outcomes (ECHO) Cohort
Abstract
Background: PFAS are widespread, persistent chemicals that cross the placenta and may affect fetal development. Animal studies suggest prenatal PFAS exposure increases offspring blood pressure (BP); however, epidemiologic evidence is limited and inconsistent. Hypothesis: We hypothesized that prenatal PFAS exposure is associated with higher childhood BP. Methods: We included children aged 3-13 years in the U.S. ECHO Cohort with data on gestational plasma or serum concentrations of PFOA, PFOS, PFHxS, PFNA, PFDA, and MeFOSAA. Children’s BP was obtained from study visits or medical records. We derived age-, sex-, and height-specific BP percentiles according to the 2017 American Academy of Pediatrics Guidelines and defined elevated BP as systolic BP (SBP) or diastolic BP (DBP) ≥90 th percentile. We used multivariable linear and modified Poisson models with generalized estimating equations and repeated BP measures clustered by participant (adjustment variables shown in Figure 1 footnotes ) and addressed missing data using multiple imputation by chained equations. We conducted subgroup analyses by child sex, ethnicity, and race, and we examined trimester-specific associations. Results: Among 2,435 children (50% female, 21% Hispanic, 25% Black), 22% had elevated BP at their last visit at a median age of 7.3 years ( Table 1 ). In adjusted analyses ( Figure 1 ), each doubling of PFOA was associated with a 1.23 (95% CI: 0.02, 2.45) higher SBP percentile, a 0.95 (0.10, 1.79) higher DBP percentile, and 1.07 (1.00, 1.15) times the risk of elevated BP. Each doubling of PFOS and PFNA was associated with a 1.14 (0.01, 2.27) and 0.85 (0.09, 1.61) higher DBP percentile, respectively. The PFOA-SBP association was stronger in males, and associations of PFOA, PFOS, and PFNA with DBP were stronger in females and non-Hispanic children. In trimester-specific analyses ( Figure 2 ), first-trimester PFOA, PFOS, and PFDA were associated with elevated BP; second-trimester PFOA and PFNA were associated with higher SBP percentiles; and third-trimester PFOS and MeFOSAA were associated with higher DBP percentiles. Conclusions: Prenatal exposure to PFOA, PFOS, and PFNA was associated with higher childhood BP. The trimester-specific associations should be interpreted with caution as they may also reflect cohort differences in PFAS profiles. PFAS may contribute to early-life programming of elevated lifelong cardiovascular risk, reinforcing the importance of population-level prevention.
Article Details
Authors (30)
Frances Wang
Beth Israel Deaconess Med Center, Diamond Bar, California, United States
Pi-i Lin
Harvard Medical School and Harvard Pilgrim Health Care Institute, Boston, Massachusetts, United States
Izzuddin Aris
Harvard Medical School and Harvard Pilgrim Health Care Institute, Boston, Massachusetts, United States
Theresa Bastain
University of Southern California, Los Angeles, California, United States
Courtney Carignan
Michigan State University, East Lansing, Michigan, United States
Andrea Cassidy-Bushrow
Henry Ford Health, Detroit, Michigan, United States
Whitney Cowell
NYU Grossman School of Medicine, New York, New York, United States
Lisa Croen
Kaiser Permanente Northern California, Pleasanton, California, United States
Dana Dabelea
Anne Dunlop
Assiamira Ferrara
Kaiser Permanente Northern California, Pleasanton, California, United States
Shohreh Farzan
University of Southern California, Los Angeles, California, United States
Sarah Geiger
University of Illinois, Urbana, Illinois, United States
Rachel Kelly
Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, United States
Margaret Karagas
Dartmouth College, Lebanon, New Hampshire, United States
MICHELE LEVINE
University Of Pittsburgh, Pittsburgh, Pennsylvania, United States
Zeyu Li
Beijing National Laboratory for Molecular Sciences
Donghai Liang
Zhongzheng Niu
Thomas OConnor
University of Rochester Medical Center, Rochester, New York, United States
Jiwon Oh
St. Michael’s Hospital, University of Toronto, Toronto
Alicia Peterson
Kaiser Permanente Northern California, Pleasanton, California, United States
Christina Porucznik
University of Utah, Salt Lake City, Utah, United States
Megan Romano
Dartmouth College, Lebanon, New Hampshire, United States
Anne Starling
University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States
Julia Varshavsky
Northeastern University, Boston, Massachusetts, United States
Qi Zhao
Marie-France Hivert
Emily Oken
Mingyu Zhang
Hubei Key Laboratory of Electrochemical Power Sources, College of Chemistry and Molecular Sciences