Airborne fine dust pollution poses a significant threat to both respiratory and skin health, yet the skin’s physiological response to such exposure has been underexplored. This study investigates the impact of fine dust on skin cells, focusing on their metabolic activity, inflammatory responses, and aging-related changes. We found that exposure to fine dust model compounds led to dose-dependent cytotoxicity, with PM2.5-Ions exhibiting higher toxicity compared to PM10-PAHs. Human epithelial keratinocytes (HEKn) showed heightened sensitivity to fine dust, marked by increased inflammation, particularly with elevated IL-8 expression in response to PM2.5-Ions. Additionally, fine dust exposure resulted in reduced cell density, slower proliferation, and decreased migration, notably at higher concentrations of PM2.5-Ions. These changes are indicative of accelerated aging processes, including compromised cell function and structural integrity. Live cell imaging and correlation analyses highlighted significant links between metabolic activity, cell morphology, and IL-8 secretion. These findings provide critical insights into the differential impacts of fine dust components on skin cells, emphasizing the potential acceleration of aging processes and underscoring the need for further research on cellular responses to environmental stress and the development of protective measures against urban fine dust exposure. Overall, this study, which contributes to addressing the skin health risks posed by air pollutants, could be actively used in environmental science, dermatology, and public health.
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