Exposure to per- and polyfluoroalkyl substances (PFAS) has been associated with adverse cardiometabolic health across the lifespan. Due to their widespread use in consumer and industrial products, the developing fetus, infant, and child may be exposed via transplacental transfer, breast milk, dust ingestion, diet, and drinking water. The long biological half-lives of some PFAS, which can range from 2-7 years in humans, intensifies concerns about the risk of continued exposure and associated health effects. While elevated exposure to PFAS in utero and during childhood may predispose exposed children to increased adiposity, systolic blood pressure, and cholesterol levels, the biological mechanisms underlying the PFAS-cardiometabolic risk associations are not well-understood. Growing evidence suggests that one mechanism by which PFAS may contribute to cardiometabolic risk is through changes in DNA methylation (DNAm). As such, DNAm-derived epigenetic clocks have emerged as a promising biomarker of aging and disease. Recent studies suggest gestational and childhood exposure to environmental pollutants including phthalates, indoor air pollutants, and smoking influence the rate of epigenetic aging. However, the link between PFAS, epigenetic aging, and cardiometabolic health in children remains unknown. We will leverage data from the HOME Study, a prospective cohort of pregnant women and their children from Cincinnati, OH, to calculate novel epigenetic biomarkers of aging and disease. The HOME Study has repeated measures of serum PFAS concentrations across childhood, comprehensive assessments of cardiometabolic markers in early adolescence, and DNA methylation at birth and 12 years of age. This will allow us to: 1) determine if gestational and childhood PFAS are associated with epigenetic age acceleration (EGAA) at birth and epigenetic age acceleration (EAA) in early adolescence; 2) determine if EGAA and EAA are associated with increased cardiometabolic risk in early adolescence using multiple markers of cardiometabolic health; and 3) explore the mediating role of EGAA in the association between gestational PFAS exposure and cardiometabolic risk in early adolescence. By using these novel epigenetic clocks and quantifying the persistence of these effects into adolescence, we will gain valuable insights into the impact of PFAS toxicity on biological processes that may affect early life development and subsequent PFAS-associated cardiometabolic risk. This diversity supplement will train a promising graduate student to enhance her training in environmental epidemiology and biostatistical methods, and learn how to estimate and interpret biological aging measures derived from high dimensional DNA methylation data.