Prenatal and Childhood Per‐ and Polyfluoroalkyl Substance (PFAS) Exposures and Blood Pressure Trajectories From Birth to Late Adolescence in a Prospective US Prebirth Cohort

Author:

Zhang Mingyu1ORCID,Aris Izzuddin M.1ORCID,Lin Pi‐I Debby1ORCID,Rifas‐Shiman Sheryl L.1ORCID,Brady Tammy M.2ORCID,James‐Todd Tamarra3ORCID,Oken Emily14ORCID,Hivert Marie‐France15ORCID

Affiliation:

1. Department of Population Medicine Harvard Medical School and Harvard Pilgrim Health Care Institute Boston MA USA

2. Department of Pediatrics Johns Hopkins University School of Medicine Baltimore MD USA

3. Departments of Environmental Health and Epidemiology Harvard T.H. Chan School of Public Health Boston MA USA

4. Department of Nutrition Harvard T.H. Chan School of Public Health Boston MA USA

5. Diabetes Unit Massachusetts General Hospital Boston MA USA

Abstract

Background Evidence is limited regarding the associations of prenatal and childhood per‐ and polyfluoroalkyl substance (PFAS) exposures with blood pressure (BP) trajectories in children. Methods and Results Participants are from Project Viva, a prospective prebirth cohort in eastern Massachusetts. We measured PFAS in early‐pregnancy maternal (median, 9.6 weeks) and midchildhood (median, 7.7 years) plasma samples. We conducted standardized BP measurements at 6 research visits: birth, infancy (median, 6.3 months), early childhood (median, 3.2 years), midchildhood (median, 7.7 years), early adolescence (median, 12.9 years), and late adolescence (median, 17.5 years). We used linear regression to examine associations of individual PFASs with BP at each visit, linear spline mixed‐effects regression to model BP trajectories, and a mixture approach to estimate PFAS exposure burden. We included 9036 BP measures from 1506 participants. We observed associations between particular individual prenatal PFASs and child BP at specific time points, for example, prenatal 2‐(N‐ethyl‐perfluorooctane sulfonamido) acetate (EtFOSAA) and 2‐(N‐methyl‐perfluorooctane sulfonamido) acetate (MeFOSAA) with higher systolic BP at birth; prenatal perfluorooctane sulfonate (PFOS) and EtFOSAA with lower diastolic BP in infancy; and prenatal PFOS, perfluorooctanoate (PFOA), and EtFOSAA with higher systolic BP at midchildhood. No prenatal or childhood PFAS was consistently associated with BP across all visits. Diastolic BP trajectories from 0 to 20 years differed slightly by prenatal PFOA, perfluorohexane sulfonate (PFHxS), and perfluorononanoate (PFNA) ( P values 0.01–0.09). Diastolic BP trajectories from 6 to 20 years differed slightly by midchildhood PFHxS and MeFOSAA ( P ‐values 0.03–0.08). Prenatal or childhood PFAS mixture burden scores were not associated with BP. Conclusions We found associations of prenatal and childhood PFAS exposures with BP at specific time points between birth and late adolescence but no consistent associations across all time points or PFAS types.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Cardiology and Cardiovascular Medicine

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