Environmental exposures in early life are increasingly recognised as key determinants of pediatric cardiovascular health. Beyond genetic susceptibility, insults during fetal development and childhood can shape risk for congenital and acquired cardiac conditions. This review synthesizes epidemiological data and plausible biological mechanisms linking four exposure domains to pediatric cardiovascular outcomes: (1) climate-related maternal heat exposure and other prenatal stressors associated with increased risk of congenital heart defects; (2) air pollution, especially traffic-related pollutants and sulfur dioxide, as a trigger for Kawasaki disease via immune activation and systemic inflammation; (3) early-life heavy metals, notably prenatal lead exposure, associated with modest but clinically meaningful increases in childhood blood pressure; and (4) endocrine-disrupting chemicals that promote early alterations in adiposity and metabolic regulation, elevating cardiometabolic risk. Collectively, the evidence highlights critical developmental windows when environmental insults exert lasting cardiovascular effects and supports incorporating environmental risk reduction into early-life prevention strategies.
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