Experimental Study on the Systemic Toxic Effects of PM2.5 Exposure on Oxidative Stress and Systemic Toxicity

Abstract

Particulate matter 2.5 (PM2.5) refers to fine particulate matter with a diameter of 2.5 micrometers or less. It poses a serious threat to health, causing respiratory and cardiovascular diseases and potentially triggering other health problems. Its main sources include industrial emissions, vehicle exhaust, agricultural activities, and waste incineration. (PM2.5) has emerged as a significant global health concern, contributing to substantial morbidity and mortality worldwide. This comprehensive review examines the mechanistic pathways through which PM2.5 exposure induces systemic oxidative stress and inflammation, leading to multi-organ toxicity. We synthesize evidence from recent toxicological, epidemiological, and experimental studies highlighting how PM2.5 components trigger cellular oxidative damage through direct generation of reactive oxygen species (ROS) and disruption of endogenous antioxidant systems. The complex relationship between PM2.5 physicochemical characteristics and their biological reactivity is explored, with particular emphasis on size-dependent deposition, chemical composition-dependent toxicity, and temporal patterns of exposure. Furthermore, we discuss emerging therapeutic approaches to mitigate PM2.5-induced damage, including natural compounds and pharmaceutical agents targeting oxidative stress pathways. Current research gaps and future directions are identified, emphasizing the need for more precise exposure assessment, multi-organ system investigations, and translational studies to bridge experimental findings and clinical applications. This review underscores the urgent need for comprehensive strategies addressing air pollution-related health burdens through integrated environmental, public health, and biomedical approaches.