Abstract P169: Prenatal Per- and Polyfluoroalkyl Substance (PFAS) Exposures and Offspring Blood Pressure From Birth to Late Adolescence: A Prospective Study in Project Viva

Abstract

Introduction: Mice studies showed that prenatal PFAS exposures increase offspring blood pressure (BP), but findings in human studies are inconsistent. Prior studies did not have repeated BP measurements from birth to late adolescence or use a mixture approach to investigate the interactions or overall effects of prenatal PFAS exposures. Methods: Participants are from the prospective pre-birth cohort Project Viva. We measured PFAS in maternal plasma samples collected in the 1 st -trimester (median: 9.6w) and child systolic (SBP) and diastolic BP (DBP) at six follow-up visits: 1) birth; 2) infancy (median: 6m); 3) early childhood (median: 3.2y); 4) mid-childhood (median: 7.7y); 5) early adolescent (median: 13.0y), 6) mid-adolescent (median: 17.5y). At each study visit, BP was measured 4-5 times, and the average value was taken. We used linear regression to examine associations of each individual PFAS, and Bayesian kernel machine regression (BKMR) to examine PFAS mixtures, with BP at each visit, adjusting for maternal age, race/ethnicity, education, pre-pregnancy body mass index, parity, smoking status, and chronic hypertension before pregnancy. Results: Sample sizes at each visit ranged from 549-919 ( Legend ). Prenatal PFAS was not consistently associated with offspring SBP or DBP across all visits. PFOS was associated with higher SBP in mid-childhood ( Panel A1 ), EtFOSAA was associated with higher SBP in infancy and in mid-childhood ( Panel A5 ), and MeFOSAA was associated with higher SBP in infancy ( Panel A6 ). PFOS, PFNA, EtFOSAA, and MeFOSAA were associated with lower DBP only in early childhood but not at other visits ( Panels B1, B4, B5, B6 ). BKMR did not suggest prenatal PFAS interactions or the overall effects of exposure to multiple PFAS on offspring SBP or DBP. Conclusions: There are no consistent associations between prenatal PFAS exposures and BP from birth to late adolescence. Future studies should examine whether there are other critical windows (e.g., mid- or late pregnancy) of susceptibility for PFAS on offspring BP.