Articles

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

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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

Polycyclic Aromatic Hydrocarbons and Respiratory Toxicity: A Review

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Polycyclic aromatic hydrocarbons (PAHs) are environmental pollutants primarily associated with chronic respiratory illness. Increased epidemiological findings necessitate a concentrated effort to raise awareness regarding the influence of air quality on the prevalence of highlighted PAHs in airborne particles. PAHs have been associated with respiratory problems including asthma, asthma exacerbation, chronic bronchitis, and emphysema The review gives an insight into the recent PAHs exposure and its toxicity effects on the respiratory system. A literature search across four scientific databases yielded 120 relevant studies, including articles analyzing urinary concentrations of various persistent PAHs and their biomarkers. The study also highlighted the risk posed by PM2.5-PAHs conjugates in causing mutagenesis, carcinogenesis, teratogenesis, disrupting signalling pathways resulting in oxidative stress, acute and/or chronic respiratory morbidity, cognitive impairment, cardiovascular morbidity, and mortality. The study further emphasizes PAHs’ and their metabolites’ significant toxicity to the respiratory system, inducing AhR/nonAhR interlinked signalling mechanisms that lead to oxidative stress, immune system damage, asthma/COPD, and cancer. In conclusion, the study predominantly indicates positive correlations between PAHs and respiratory toxicity.