Prenatal Per- and Polyfluoroalkyl Substance Exposures and Longitudinal Blood Pressure Measurements in Children Aged 3 to 18 Years: Findings From a Racially and Ethnically Diverse US Birth Cohort.

Background: Prenatal per- and polyfluoroalkyl substance (PFAS) exposures may influence offspring blood pressure (BP), but long-term studies in diverse populations remain limited.

Methods: Participants were from the Boston Birth Cohort. We measured PFAS in maternal plasma collected 24 to 72 hours after delivery and extracted children's BP from medical records. We calculated age-, sex-, and height-specific BP percentiles and defined elevated BP as systolic/diastolic BP ≥90th percentile (ages 3 to <13 years) or ≥120/80 mm Hg (ages 13 to <18 years). We used adjusted mixed-effects linear and modified Poisson models to examine associations of PFAS with BP percentiles and elevated BP. We used linear spline mixed-effects models to predict BP trajectories at ages 3 to 18 years by PFAS levels.

Results: We included 13 404 BP measurements from 1094 children (median follow-up: 12 years [interquartile range, 9-15 years]; 61% Black and 22% Hispanic). Overall, higher perfluorodecanoic acid (PFDeA), perfluorononanoic acid (PFNA), and perfluoroundecanoic acid (PFUnA) were associated with higher systolic BP percentile. The associations differed by child life stage, sex, race and ethnicity. For example, associations of PFDeA with systolic BP percentile were stronger in older (β=0.40; β=1.06; β=2.55), male (β=1.51; β=0.52), and Black (β=1.75; β=0.45) children. In male children, each doubling of perfluoroheptanesulfonic acid (PFHpS) was associated with a 9% higher risk of elevated BP at ages 6 to 12 years and a 17% higher risk at 13 to 18 years, with no increased risk at 3 to 5 years. PFHpS was associated with a dose-dependent divergence in BP trajectories beginning at age 13 years.

Conclusions: Prenatal exposures to certain PFAS were associated with offspring BP, with stronger associations in adolescents, male children, and Black children. Prenatal PFAS exposures may have intergenerational, long-term, and latent hypertensive effects.