Occupational Exposure to Factory‐Derived Particulate Matter 2.5 Induces Cutaneous Toxicity in Workers and HaCaT Keratinocytes Through Oxidative Stress and Inflammation

This study aimed to evaluate the toxicological effects of occupational exposure to factory-derived particulate matter (PM2.5) on human skin, emphasizing its role as a potential target organ of environmental toxicants. An epidemiological survey comparing factory and nonfactory workers was conducted by assessing their skin elasticity and color on the neck and forehead. Carbonylated proteins and inflammatory cytokines were quantified using tape stripping, and stratum corneum (SC) desquamation and cell area were analyzed using Brilliant Green staining. In addition, HaCaT keratinocytes were exposed to factory-derived PM2.5 (welding fumes), and oxidative stress, inflammation, and barrier function were assessed using gene expression analysis and reporter assays. Factory workers showed reduced dermal elasticity, increased skin redness, elevated levels of carbonylated proteins and inflammatory cytokines (IFN-γ and CXCL10), and enhanced SC desquamation with smaller cell areas. Consistently, in vitro exposure of HaCaT keratinocytes to PM2.5 induced oxidative stress (activation of the antioxidant response element pathway), inflammatory responses (nuclear factor kappa B activation), and suggested barrier impairment. These findings reveal that chronic occupational exposure to welding fumes impairs skin structure and function through oxidative stress, inflammation, and barrier disruption, highlighting the skin as a relevant target organ in occupational toxicology.