Free radical-induced DNA damage in environmental pollutant exposure

Abstract

Environmental pollution accounts for an estimated 9 million premature deaths annually worldwide, with oxidative stress serving as a primary mechanism linking pollutant exposure to cellular damage. This prospective cohort research investigated the relationship between occupational environmental pollutant exposure and free radical-induced DNA damage among industrial workers in the Osaka-Kobe industrial corridor of Japan. A total of 847 workers from petrochemical, steel manufacturing, and electronics assembly facilities were enrolled between January 2020 and June 2022, with biological sampling conducted at baseline, 12 months, and 24 months following initial assessment. Personal air monitoring quantified exposure to particulate matter (PM2.5, PM10), heavy metals (lead, cadmium, arsenic), polycyclic aromatic hydrocarbons, volatile organic compounds, and nitrogen oxides during work shifts. DNA damage biomarkers included urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG) measured by ELISA, serum malondialdehyde (MDA) assessed through thiobarbituric acid reactive substances assay, comet assay tail moment in peripheral lymphocytes, gamma-H2AX foci quantification by immunofluorescence microscopy, and cytokinesis-block micronucleus frequency in cultured lymphocytes. Participants demonstrated mean PM2.5 exposure of 47.3±18.6 μg/m³, substantially exceeding ambient air quality guidelines. Heavy metal concentrations varied by facility type, with steel workers showing highest lead (blood lead 8.7±3.2 μg/dL) and cadmium (urinary cadmium 2.1±0.9 μg/g creatinine) levels. Significant positive correlations emerged between pollutant exposure indices and all DNA damage markers. The strongest associations were observed for 8-OHdG with PM2.5 (r=0.72, p