A Review on Pollutant-Induced Inflammation: Molecular Mechanisms and Implications for Disease Pathogenesis

Environmental pollutants, including persistent organic pollutants (POPs), heavy metals, and airborne particulate matter (PM), disrupt immune homeostasis by triggering oxidative stress, cytokine release, and activation of key inflammatory pathways such as AhR, HIF-1α, Nrf2, NF-ĸB, MAPK, JAK/STAT, and EGFR. These molecular mechanisms amplify or sustain inflammation, contributing to diseases spanning the respiratory, cardiovascular, neurological, and oncogenic spectrum. This review synthesizes the current mechanistic insights into pollutant-induced inflammation, emphasizing the regulatory crosstalk among these pathways and the health implications. Understanding how pollutants modulate inflammation provides a foundation for developing targeted preventive and therapeutic strategies. Future research should focus on integrating both human and animal data, in vitro and in vivo studies, to clarify dose-response concentrations, identify biomarkers of exposure, and enhance translational relevance for public health.