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

Abstract

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 (PM 2.5) 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 PM 2.5 significantly enhanced malondialdehyde activity (P<0.05), decreased superoxide dismutase activity (P<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<0.05). Western blot analysis indicated that PM 2.5 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<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 PM 2.5 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.

Expectorant Effects of Immature Asian Pear Extract on PM2.5-Induced Subacute Pulmonary Injury in Mice

“…COX-2 is an important enzyme involved in the synthesis of prostaglandin, a chemical mediator of infammation, and is known to be involved in angiogenesis and the progression of infammation [93,94]. Signifcant increases in COX-2 occur during PM 2.5 -induced lung injury [25,95,96]. At present, the suppression of COX-2 immunoreactivity is used as an important index for evaluating anti-infammatory efects [97,98].…”

Air-pollutant particulate matter 2.5 (PM2.5)-induced inflammation and oxidative stress in diseases: Possible therapeutic approaches

“…Interestingly, exposures of mice to printing room generated PM2.5 (5µg, 10µg or 15µg/g BW on day 1 and 3) significantly increased malondialdehyde (MDA) activity, increased expression of inflammatory cytokines like IL-1β, TNF-, and IL-6 and decreased expression of antioxidant SOD on day 4 of exposure. In addition, primary profibrogenic signaling mediator TGF--induced pERK1-MAPK activity is also increased by PM2.5 indicating exposure for a significant amount of time to print room-generated PM2.5 is a major risk factor for increased lung oxidative stress, inflammation, pyroptosis and pulmonary fibrosis [36].…”

Health risk analysis from volatile organic compounds and fine particulate matter in the printing industry

“…There were many reports on the health impact of indoor air pollution in the printing press. For example, the exposure to PM 2.5 from the printing room significantly increased inflammation, fibrosis, apoptosis, and the abundance of pathogenic bacteria, indicating that exposure is a potential threat to individuals who spend a significant amount of time in printing rooms (Zou et al 2020 ). A study in the printing industry in Serbia found that the presence of volatile organic compounds in the printing process had an adverse health effect on the workers (Kiurski et al 2013 ).…”