Abstract

Fine particulate matter with an aerodynamic diameter of ≤2.5 μm (PM₂.₅) remains a major environmental and public-health concern in South Korea despite improvements in national air quality. Rapid urbanization, industrial emissions, transportation, fossil-fuel combustion, secondary aerosol formation, seasonal atmospheric stagnation, and transboundary transport collectively shape the country’s complex exposure profile. PM₂.₅ is increasingly recognized as a systemic toxicant rather than solely a respiratory pollutant. Its adverse effects are determined not only by particle mass but also by chemical composition, surface reactivity, oxidative potential, exposure duration, and individual susceptibility.
This critical review synthesizes current mechanistic and population evidence linking PM₂.₅ exposure with oxidative stress and multiorgan cellular injury, with particular emphasis on South Korea. PM₂.₅-associated metals, organic compounds, and other redox-active constituents generate reactive oxygen and nitrogen species through particle-surface reactions, NADPH oxidase activation, mitochondrial dysfunction, and inflammatory-cell recruitment. Excessive oxidant production disrupts Nrf2–Keap1 antioxidant defenses and activates NF-κB, MAPK, NLRP3 inflammasome, endoplasmic-reticulum stress, and epigenetic pathways. The resulting inflammation, endothelial dysfunction, mitochondrial injury, DNA damage, autophagic impairment, and regulated cell death provide biologically plausible connections between pulmonary exposure and systemic disease.
Evidence from Korean and international populations associates PM₂.₅ exposure with respiratory disease, cardiovascular and cerebrovascular events, neurodegenerative disorders, renal dysfunction, metabolic abnormalities, adverse pregnancy outcomes, developmental impairment, malignancy, and premature mortality. Children, pregnant women, older adults, people with chronic cardiopulmonary or metabolic disease, outdoor workers, and socioeconomically disadvantaged populations may experience disproportionate risk. However, interpretation remains limited by exposure misclassification, residual confounding, heterogeneous particle composition, and insufficient integration of personal exposure measurements with molecular biomarkers. Effective prevention requires sustained source-directed emission reduction, stronger air-quality governance, regional cooperation, exposure-conscious community infrastructure, clinical protection of vulnerable populations, and evidence-based personal precautions. Future South Korean research should integrate particle composition and oxidative potential with longitudinal epidemiology, multi-omic biomarkers, and policy-based natural experiments.

Conclusion: PM₂.₅ remains an important systemic health threat in South Korea, with oxidative stress linking pulmonary exposure to multiorgan cellular injury. Effective protection requires sustained emission reduction, stronger regional air-quality cooperation, improved exposure assessment, and targeted clinical protection of vulnerable populations. Future research should integrate particle composition, oxidative potential, molecular biomarkers, and longitudinal population data to support more precise and equitable prevention.

Keywords: Air pollution; fine particulate matter; PM₂.₅; oxidative stress; reactive oxygen species; cellular injury.