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There have been few studies investigating the potential effects of indoor sources of particulate matter on human health. In this study, the effect of different concentrations of fine particulate matter (PM2.5) collected from a printing room on lung health was examined using cultured cells and a mouse model. Further, the mechanism of lung injury was examined. The results indicated that PM2.5 significantly enhanced malondialdehyde activity (P&lt;0.05), decreased superoxide dismutase activity (P&lt;0.05), upregulated the expression of pro‑inflammatory factors including interleukin (IL)‑1β, tumor necrosis factor‑, IL‑6 and downregulated the expression of the inflammatory factor IL‑2 (P&lt;0.05). Western blot analysis indicated that PM2.5 significantly enhanced expression of phosphorylated (p)‑ERK relative to total ERK, cyclooxygenase‑2, p‑anti‑nuclear‑factor‑κB (p‑NF‑κB) relative to NF‑κB, transforming growth factor‑β1 and Bax relative to Bcl‑2 in inflammation (P&lt;0.05), fibrosis and apoptosis signaling pathways. Furthermore, the results revealed that exposure was associated with an increased abundance of pathogens including Burkholderiales, Coriobacteriia, and Betaproteobacteria in in the lungs. In conclusion, exposure to PM2.5 from a printing room significantly increased inflammation, fibrosis, apoptosis and the abundance of pathogenic bacteria, indicating that exposure is potential threat to individuals who spend a significant amount of time in printing rooms.

Potential hazardous effects of printing room PM2.5 exposure include promotion of lung inflammation and subsequent injury