Personalized oxidative toxicity exposure assessment: Unveiling feasibility of linking respiratory PM10 oxidative potential to human oxidative damage

Atmospheric particulate matter-driven oxidative stress is a crucial benchmark in evaluating health risk, yet the direct evidence linking environmental oxidability to human internal oxidative damage remains elusive. Here, we systematically quantified oxidative potential (OP) in respirable size-segregated PM 10 collected longitudinally from waste recycling plants in Southern China, and monitored oxidative damage to DNA, lipids and proteins in workers using biomarker techniques. By self-developed high-throughput microplate dithiothreitol (DTT) assay, we found that maximum OP values (both mass and volume normalized) were primarily derived from fine particles (0.43–0.65 μm), with 62 %–82 % of oxidability in pulmonary alveoli attributed to <2.1 μm fractions. Each unit increase (1 × 10 16 spins/g) of environmentally persistent free radicals (EPFRs) was associated with 1.316 pmol/μg/min rise in OP DTT_m . Critically, we introduced “respirable particle-bound oxidability (RPO)” metric, integrating OP with individualized respiratory rates to capture bioavailable exposure. Mixed-effect modeling revealed a robust association between that RPO and lipid peroxidation, with each 1 % increase correlating with a 2.92 % (95 % CI: 1.66 %, 4.17 %) increase in urinary malondialdehyde (MDA), particularly in pulmonary alveoli. While no significant effect is observed for DNA or protein oxidation. These findings successfully established the quantitative linkage between ambient PM oxidizing capacity and internal oxidative injury, highlighting RPO as an advanced metric for environmental risk assessment and offering new insight into the mechanistic evaluation of air pollution toxicity. • Maximum oxidative potential is primarily derived from 0.43 to 0.65 μm fractions. • 62 %–82 % of PM oxidability in pulmonary alveoli is attributed to <2.1 μm particle. • EPFRs partially contribute to the generation of oxidative potential in PM 10 . • Respirable particle-bound oxidability exposure is linked to urinary MDA increase. • PM oxidation exposure in deep respiratory tract induce severe lipid peroxidation.