Epigenetics and Environmental Health: DNA Methylation Changes Induced by Air Pollution and Cardiovascular Disease

Cardiovascular disease (CVD) remains the leading global cause of mortality, driven by complex interactions between genetic predisposition and environmental factors, such as ambient air pollution.1 Fine particulate matter (), nitrogen oxides (), and sulfur oxides () are established nontraditional cardiovascular risk factors, triggering both acute events and chronic atherogenesis.3 This systematic review investigates the role of DNA methylation (DNAm)—a primary epigenetic modification—as the molecular transducer linking air pollution exposure to CVD pathology. A systematic search of biomedical databases (PubMed, EMBASE, Web of Science) was conducted to synthesize human observational studies focused on exposure, DNAm changes, and cardiovascular outcomes. The synthesized evidence demonstrates that air pollution induces rapid and systemic epigenetic alterations. Acute exposure to traffic particles (Black Carbon, ) is associated with global hypomethylation of repetitive elements (e.g., LINE-1) within days, suggesting a generalized collapse in cellular methylation capacity.4 Furthermore, gene-specific alterations, such as the hypomethylation of (Tissue Factor 3) and , drive prothrombotic states and increase the risk of myocardial infarction.5 Mechanistically, inhaled pollutants induce oxidative stress, which disrupts the S-adenosylmethionine () / Sadenosylhomocysteine () ratio, directly inhibiting DNA methyltransferases ().5 These alterations modulate key pathways of atherogenesis, including chronic systemic inflammation (NF- activation) and autonomic nervous system dysfunction (mtDNA D-loop hypomethylation).5 While methodological limitations—primarily heterogeneity in exposure assessment and reliance on peripheral blood cells—persist, the findings confirm that DNA methylation serves as a dynamic biomarker of individual susceptibility and provides compelling molecular targets for future intervention strategies aimed at mitigating the cardiovascular burden of environmental toxins.5