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.

Zinc oxide nanoparticles (ZnO NPs) rank among the highest-volume engineered nanomaterials, and their partial dissolution generates a composite particle and ion exposure that converges on three measurable molecular layers. This review consolidates quantitative endpoints reported across in vitro, rodent, avian, piscine and controlled human exposures and organises them into mitochondrial, redox and epigenetic signature classes. Reported responses include mitochondrial membrane potential loss to 55 percent of control, mitochondrial DNA copy number shifts spanning 290 percent to 80 percent of control, PGC-1 alpha suppression to 48.6 percent, global 5-methylcytosine reduction to 42 percent, histone G9a induction near 50-fold, and transcriptomic responses reaching 2703 differentially expressed genes. Cross-layer convergence is anchored by zinc homeostasis regulators, heme oxygenase 1, one carbon metabolite accumulation and ferroptotic lipid remodelling across species. A candidate integrated biomarker panel is proposed here together with the analytical and dosimetric constraints that presently limit its regulatory adoption.