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.
Wang et al. (Tue,) studied this question.