Particulate matter (PM) is a significant environmental pollutant and a growing public health concern. Chronic exposure to PM has been identified as a risk factor for various skin conditions—yet the cellular mechanisms underlying these effects remain poorly understood. In this study, we investigated the effects of PM on HaCaT cells to present how fine dust triggers intracellular damage. HaCaT cells were exposed to PM in vitro and assessed for changes in viability and cell signaling pathways. We observed a marked reduction in cell viability upon PM treatment. These findings suggest that fine dust can directly compromise skin cell survival. Notably, PM exposure triggered an increase in intracellular calcium levels in HaCaT cells. Excessive Ca 2+ can involve mitochondrial function, leading to loss of mitochondrial function. These downstream events are hallmarks of the intrinsic cell death pathway, implicating Ca 2+ -dependent mitochondrial damage as a key mechanism of PM-induced cytotoxicity. In addition, we observed evidence of mitochondrial dysfunction in PM-treated cells. In our experiments, PM-exposed HaCaT cells showed signs of mitochondrial stress, suggesting that fine dust triggers structural and functional changes in this organelle. Mitochondrial impairment likely exacerbates cellular injury by amplifying oxidative stress and promoting apoptosis, as reported in prior studies. Collectively, our findings reveal that PM induces skin cell damage through a combination of disrupted calcium signaling and mitochondrial dysfunction. By elucidating these mechanistic insights, this work contributes to a better understanding of how air pollutants harm skin at the cellular level. This research was supported by Korea Basic Science Institute (National research Facilities and Equipment Center) grant funded by Ministry of Science and ICT (RS-2025-00555198) and by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education (RS-2025-00553251).
Seo et al. (Sun,) studied this question.