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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 (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<0.05), decreased superoxide dismutase activity (P<0.05), upregulated the expression of pro?inflammatory factors including interleukin (IL)?1?, tumor necrosis factor?, IL?6 and downregulated the expression of the inflammatory factor IL?2 (P<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??B (p?NF??B) relative to NF??B, transforming growth factor??1 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 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.

SUBMITTER: Zou C

PROVIDER: S-EPMC7453667 | biostudies-literature | 2020 Oct

REPOSITORIES: biostudies-literature

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

Zou Changwei C Yang Hong H Cui Lanyue L Cao Xinyi X Huang Hong H Chen Tingtao T

Molecular medicine reports 20200731 4

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<0.05), decreased superoxide dismutase activity (P<0.05) ...[more]

PMID: 32945461

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Project description:Background Lung fibrosis is a severe lung disorder featured by chronic nonspecific inflammation of the interstitial lung and deposition of collagen, leading to lung dysfunction. It has been identified that ferroptosis is involved in the progression of lung injury. Particulate matter (PM2.5) is reported to be correlated with the incidence of pulmonary fibrosis. However, mechanisms underlying ferroptosis in PM2.5-related lung fibrosis is unclear. In this study, we aimed to explore the effect of PM2.5 on ferroptosis in lung fibrosis and the related molecular mechanisms. Methods PM2.5-treated mouse model and cell model were established. Fibrosis and tissue damage were measured by Masson's trichrome staining and HE staining. Fibrosis biomarkers, such as α-SMA, collagen I, and collagen III, were examined by histological analysis. The ferroptosis phenotypes, including the levels of iron, Fe2+, MDA, and GSH, were measured by commercial kits. ROS generation was checked by DCFH-DA. The oxidative stress indicators, 3-nitro-L-tyrosine (3′-NT), 4-HNE, and protein carbonyl, were checked by enzyme linked immunosorbent assay (ELISA). The thiobarbituric acid reactive substances (TBARS) and GSH/GSSG ratio were assessed by TBARS assay kit and GSH/GSSG assay kit, respectively. TGF-β signaling was detected by Western blotting. Results PM2.5 induced the lung injury and fibrosis in the mice model, along with elevated expression of fibrosis markers. PM2.5 enhanced oxidative stress in the lung of the mice. The SOD2 expression was reduced, and NRF2 expression was enhanced in the mice by the treatment with PM2.5. PM2.5 triggered ferroptosis, manifested as suppressed expression of GPX4 and SLC7A11, decreased levels of iron, Fe2+, and MDA, and increased GSH level in mouse model and cell model. The TGF-β and Smad3 signaling was inhibited by PM2.5. ROS inhibitor NAC reversed PM2.5-regulated ROS and ferroptosis in primary mouse lung epithelial cells. Conclusions Therefore, we concluded that PM2.5 exposure induced lung injury and fibrosis by inducing ferroptosis via TGF-β signaling.

Project description:Air pollution containing particulate matter (PM) less than 2.5 μm (PM2.5) plays an essential role in regulating hepatic disease. However, its molecular mechanism is not yet clear, lacking effective therapeutic strategies. In this study, we attempted to investigate the effects and mechanisms of PM2.5 exposure on hepatic injury by the in vitro and in vivo experiments. At first, we found that PM2.5 incubation led to a significant reduction of nuclear factor erythroid-derived 2-related factor 2 (Nrf2), along with markedly reduced expression of different anti-oxidants. Notably, suppressor of IKKε (SIKE), known as a negative regulator of the interferon pathway, was decreased in PM2.5-incubated cells, accompanied with increased activation of TANK-binding kinase 1 (TBK1) and nuclear factor-κB (NF-κB). The in vitro studies showed that Nrf2 positively regulated SIKE expression under the conditions with or without PM2.5. After PM2.5 treatment, Nrf2 knockdown further accelerated SIEK decrease and TBK1/NF-κB activation, and opposite results were observed in cells with Nrf2 over-expression. Subsequently, the gene loss- and gain-function analysis demonstrated that SIKE deficiency further aggravated inflammation and TBK1/NF-κB activation caused by PM2.5, which could be abrogated by SIKE over-expression. Importantly, SIKE-alleviated inflammation was mainly dependent on TBK1 activation. The in vivo studies confirmed that SIKE- and Nrf2-knockout mice showed significantly accelerated hepatic injury after long-term PM2.5 exposure through reducing inflammatory response and oxidative stress. Juglanin (Jug), mainly isolated from Polygonum aviculare, exhibits anti-inflammatory and anti-oxidant effects. We found that Jug could increase Nrf2 activation, and then up-regulated SIKE in cells and liver tissues, mitigating PM2.5-induced liver injury. Together, all these data demonstrated that Nrf2 might positively meditate SIKE to inhibit inflammatory and oxidative damage, ameliorating PM2.5-induced liver injury. Jug could be considered as an effective therapeutic strategy against this disease by improving Nrf2/SIKE signaling pathway.

Project description:BackgroundPrenatal exposure to ambient PM2.5, (i.e., fine particulate matter, aerodynamic diameter ? 2.5 ?m) has been associated with preterm birth and low birth weight. The association between prenatal PM2.5 exposure and intrauterine inflammation (IUI), an important risk factor for preterm birth and neurodevelopmental outcomes, has not been evaluated.ObjectivesWe aimed to investigate the association between maternal exposure to PM2.5 and IUI in the Boston Birth Cohort, a predominantly urban low-income minority population.MethodsThis analysis included 5,059 mother-infant pairs in the Boston Birth Cohort. IUI was assessed based on intrapartum fever and placenta pathology. PM2.5 exposure was assigned using data from the U.S. EPA's Air Quality System. Odds ratios (OR) and 95% confidence intervals (CI) quantified the association of maternal PM2.5 exposure during preconception and various periods of pregnancy with IUI.ResultsComparing the highest with the lowest PM2.5 exposure quartiles, the multi-adjusted association with IUI was significant for all exposure periods considered, including 3 months before conception (OR = 1.52; 95% CI: 1.22, 1.89), first trimester (OR = 1.93; 95% CI: 1.55, 2.40), second trimester (OR = 1.67; 95% CI: 1.35, 2.08), third trimester (OR = 1.53; 95% CI: 1.24, 1.90), and whole pregnancy (OR = 1.92; 95% CI: 1.55, 2.37).ConclusionsDespite relatively low exposures, our results suggest a monotonic positive relationship between PM2.5 exposure during preconception and pregnancy and IUI. IUI may be a sensitive biomarker for assessing early biological effect of PM2.5 exposure on the developing fetus.CitationNachman RM, Mao G, Zhang X, Hong X, Chen Z, Soria CS, He H, Wang G, Caruso D, Pearson C, Biswal S, Zuckerman B, Wills-Karp M, Wang X. 2016. Intrauterine inflammation and maternal exposure to ambient PM2.5 during preconception and specific periods of pregnancy: the Boston Birth Cohort. Environ Health Perspect 124:1608-1615;?http://dx.doi.org/10.1289/EHP243.

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

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

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