Molecular Mechanisms Linking Air Pollution-Induced Oxidative Stress to Inflammation and Human Disease

Air pollution is a major public health problem worldwide, causing millions of premature deaths every year due to its association with diseases of the respiratory, cardiovascular, neurological, metabolic and carcinogenic systems. A major mechanism of pollutant-induced toxicity has been well identified as oxidative stress. The overproduction of reactive oxygen/nitrogen species causes direct damage to cellular redox homeostasis and activation of inflammatory signaling pathways. This review provides a broad overview of the molecular mechanisms linking ambient air pollutants, such as particulate matter, nitrogen oxides, ozone, sulphur dioxide and volatile organic compounds, with health effects mediated by oxidative stress. Mitochondrial dysfunction, endoplasmic reticulum stress, and epigenetic reprogramming were critically discussed with key signalling pathways such as nuclear factor erythroid 2-related factor 2, nuclear factor kappa B (NF-κB), mitogen-activated protein kinase, and NOD-like receptor protein 3 inflammasome. Tissue-specific effects on respiratory, cardiovascular and nervous systems are also discussed. Susceptible populations and critical exposure windows are identified. Emerging advances in biomarker discovery, and mechanistic in vitro and in vivo approaches, are also summarized as promising tools to improve exposure assessment and disease prediction. Finally, current therapeutic approaches targeting oxidative stress and inflammation, as well as preventive measures to reduce pollutant exposure, are discussed to support precision environmental health and evidence-based air quality management.