PMID: 

J Thorac Dis. 2019 Jun ;11(6):2617-2627. PMID: 31372298

Abstract Title: 

Particulate matter disrupts airway epithelial barrier via oxidative stress to promoteinfection.

Abstract: 

Background: Airborne particulate matter (PM) is associated with increasing susceptibility to respiratory bacterial infection. Tight junctions (TJs) are protein complexes that form airway epithelial barrier against infection. This study aimed to investigate the effects of PM on the airway TJs in response to infection.Methods: The cytotoxicity of PM to BEAS-2B was evaluated. The reactive oxygen species (ROS) production was measured by the flow cytometry. Colony forming units (CFUs) assay and confocal microscopy were utilized to evaluate the number of bacteria. Immunofluorescence and western blot assay were conducted to detect the expressions of TJs proteins. Animal models were used to investigate the role of TJs in PM-induced lung injury upon bacterial infection.Results: , PM decreased cell viability, increased ROS production, and increased the number of intracellular bacteria accompanying by the degradation of TJs. N-acetylcysteine (NAC) significantly reversed the PM-induced bacterial invasion and PM-induced disruption of TJs., PM increases bacteria-infected lung injury, lung bacteria burden and blood bacterial dissemination, which was closely correlated to the degradation of TJs.Conclusions: PM disrupts TJs via oxidative stress to promote bacterial infection.

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Curcumin has proven anti-inflammatory effects, and new research confirms that curcumin supplementation is an effective tool for pain management in patients with knee osteoarthritis

PMID: 

Environ Pollut. 2019 Nov ;254(Pt A):112875. Epub 2019 Jul 17. PMID: 31377334

Abstract Title: 

miRNAs deregulation in serum of mice is associated with lung cancer related pathway deregulation induced by PM2.5.

Abstract: 

Ambient fine particulate matter (PM2.5) as an environmental pollution has been associated with the lung cancer. However, the mechanism of epigenetics such as miRNAs deregulation between PM2.5-exposure and lung cancer has not been elucidated clearly. Twenty C57BL/6 mice were divided randomly into 2 groups and exposed to the filtered air (FA) and the concentrated air (CA), respectively. The FA mice were exposed to filtered air in chambers with a high-efficient particulate air filter (HEPA-filter), and the CA mice were exposed to concentration ambient PM2.5. The total duration of exposure was performed 6 h per day from December 1st, 2017 to January 27th, 2018. The mice exposed 900.21 μg/mPM2.5 for 6 h per day in CA chamber, which was nearly equaled to 225.05 μg/mfor 24-h calculatingly. After exposure, the serum miRNAs levels were detected by microarray. Genetic and pathological alterations in lung of mice with/without PM2.5 exposure were detected. 38 differential miRNAs in serum of mice were found after PM2.5 exposure for 8 weeks. Among of them, 13 miRNAs related with lung cancer were consistent in serum and lung of mice. The target genes of 13 deregulated miRNAs including CRK, NR2F2, VIM, RASSF1, CCND2, PRKCA, SIRT1, CDK6, MAP3K7, HIF1A, UBE2V2, ATG10, BAX, E2F1, RASSF5 and CTNNB1, could involve in the pathway of lung cancer developing. Compared with the FA group, the significantly increases of histopathological changes, ROS and DNA damage were observed in lung of mice in CA group. Our study suggested that miRNAs in serum could be identified as candidate biomarkers to predict the lung cancer development during early PM2.5 exposure.

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PMID: 

J Exp Clin Cancer Res. 2019 Aug 16 ;38(1):359. Epub 2019 Aug 16. PMID: 31420013

Abstract Title: 

Ambient fine particulate matter inhibits 15-lipoxygenases to promote lung carcinogenesis.

Abstract: 

BACKGROUND: Epidemiological observations have demonstrated that ambient fine particulate matter with d 

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PMID: 

Oncol Lett. 2020 Jan ;19(1):725-734. Epub 2019 Nov 21. PMID: 31897188

Abstract Title: 

Activated macrophages are crucial during acute PM2.5 exposure-induced angiogenesis in lung cancer.

Abstract: 

The importance of ambient particulate matter (PM2.5) in lung cancer progression is well established; however, the precise mechanisms by which PM2.5 modulates lung cancer development have not yet been determined. The present study demonstrated increased mRNA and protein expression levels of vascular endothelial growth factor in PM2.5-induced macrophages. However, no significant changes to the expression levels of angiogenic cytokines (vascular endothelial growth factor A, matric metallopeptidase 9, basic fibroblast growth factor and platelet-derived growth factor) were observed in the Lewis lung carcinoma (LLC) cell line in response to acute PM2.5 exposure. PM2.5-induced activated macrophages were revealed to upregulate angiogenic cytokine expression following the acute exposure of LLC cells to PM2.5-induced macrophage supernatant., the pro-angiogenic and macrophage accumulation functions of PM2.5 were supported by the establishment of a polyvinyl alcohol sponge implantation mouse model. Furthermore, PM2.5 was demonstrated to increase angiogenesis and macrophage recruitment in mice that were subcutaneously injected with LLCs. These results indicated that PM2.5 increases angiogenesis, and macrophages are crucial mediators of PM2.5-induced angiogenesis in lung cancer. These findings may provide novel insights for the development of lung cancer treatment strategies.

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PMID: 

Int J Public Health. 2020 Jan 7. Epub 2020 Jan 7. PMID: 31912175

Abstract Title: 

Comparing the lung cancer burden of ambient particulate matter using scenarios of air quality standards versus acceptable risk levels.

Abstract: 

OBJECTIVES: Ambient particulate matter (PM) is regulated with science-based air quality standards, whereas carcinogens are regulated with a number of"acceptable"cases. Given that PM is also carcinogenic, we identify differences between approaches.METHODS: We assessed the lung cancer deaths for Switzerland attributable to exposure to PM up to 10 µm (PM) and to five particle-bound carcinogens. For PM, we used an epidemiological approach based on relative risks with four exposure scenarios compared to two counterfactual concentrations. For carcinogens, we used a toxicological approach based on unit risks with four exposure scenarios.RESULTS: The lung cancer burden using concentrations from 2010 was 10-14 times larger for PMthan for the five carcinogens. However, the burden depends on the underlying exposure scenarios, counterfactual concentrations and number of carcinogens. All scenarios of the toxicological approach for five carcinogens result in a lower burden than the epidemiological approach for PM.CONCLUSIONS: Air quality standards-promoted so far by the WHO Air Quality Guidelines-provide a more appealing framework to guide health risk-oriented clean air policymaking than frameworks based on a number of"acceptable"cases.

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PMID: 

Int J Hyg Environ Health. 2019 06 ;222(5):756-764. Epub 2019 May 16. PMID: 31103472

Abstract Title: 

Ambient particulate air pollution and circulating C-reactive protein level: A systematic review and meta-analysis.

Abstract: 

BACKGROUND: Ambient particulate air pollution is a major threat to the cardiovascular health of people. Inflammation is an important component of the pathophysiological process that links air pollution and cardiovascular disease (CVD). A classical marker of inflammation-C-reactive protein (CRP), has been recognized as an independent predictor of CVD risk. Exposure to ambient particulate matter (PM) may cause systemic inflammatory response but its association with CRP has been inconsistently reported.OBJECTIVES: To estimate the potential effects of short-term and long-term exposures to ambient particulate air pollution on circulating CRP level based on previous epidemiological studies.METHODS: A systematic literature search of PubMed, Web of Science, Embase, and Scopus databases for publications up to January 2018 was conducted for studies reporting the association between ambient PM (PMor PM, or both) and circulating CRP level. We performed a meta-analysis for the associations reported in individual studies using a random-effect model and evaluated the effect modification by major potential modifiers.RESULTS: This meta-analysis comprised data from 40 observational studies conducted on 244,681 participants. These included 32 (27 PMstudies and 13 PMstudies) and 11 (9 PMstudies and 5 PMstudies) studies that investigated the associations of CRP with short-term and long-term exposure to particulate air pollution, respectively. A 10μg/mincrease in short-term exposure to PMand PMwas associated with increases of 0.83 % (95% CI: 0.30%, 1.37%) and 0.39% (95% CI: -0.04%, 0.82%) in CRP level, respectively, and a 10μg/mincrease in long-term exposure to PMand PMwas associated with much higher increases of 18.01% (95% CI: 5.96%, 30.06%) and 5.61% (95% CI: 0.79%, 10.44%) in CRP level, respectively. The long-term exposure to particulate air pollution was more strongly associated with CRP level than short-term exposure and PMhad a greater effect on CRP level than PM.CONCLUSION: Exposure to ambient particulate air pollution is associated with elevated circulating CRP level suggesting an activated systemic inflammatory state upon exposure, which may explain the association between particulate air pollution and CVD risk.

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PMID: 

Environ Sci Pollut Res Int. 2019 Aug ;26(23):23603-23614. Epub 2019 Jun 15. PMID: 31203548

Abstract Title: 

Short-term exposure to ambient air pollution and daily atherosclerotic heart disease mortality in a cool climate.

Abstract: 

The associations between exposure to short-term ambient air pollution and daily atherosclerotic heart disease (ASHD) mortality in cool climate have not been established. We performed a time-series analysis in Shenyang, the largest city of Northeastern China. We identified 7659 ASHD deaths and obtained deaths, ambient air pollution levels, and meteorological data for Shenyang during 2014-2017. The impact of ambient air pollution on daily ASHD deaths was analyzed using generalized additive models (GAMs). Cumulative lag effects were investigated using distributed lag non-linear models (DLNM). We found ASHD deaths significantly increased during days with higher air pollution. Particulate matter with diameter

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PMID: 

Hypertension. 2019 08 ;74(2):384-390. Epub 2019 Jun 24. PMID: 31230552

Abstract Title: 

Differential Effect of Ambient Air Pollution Exposure on Risk of Gestational Hypertension and Preeclampsia.

Abstract: 

Although ambient air pollution may increase hypertension risk through endothelial damage and oxidative stress, evidence is inconsistent regarding its effect on hypertension in pregnancy. Prior research has evaluated a limited scope of pollution species and often not differentiated preeclampsia, which may have a placental origin, from gestational hypertension. Among 49 607 women with at least 2 singleton deliveries in the Eunice Kennedy Shriver National Institute of Child Health and Human Development Consecutive Pregnancies Study (2002-2010), we estimated criteria pollutant and volatile organic compound levels during pregnancy using Community Multiscale Air Quality models and abstracted gestational hypertension and preeclampsia diagnoses from medical records. Generalized estimating equations accounted for repeat pregnancies and adjusted for ambient temperature and maternal age, race/ethnicity, body mass index, smoking, alcohol, parity, insurance, maritalstatus, and asthma. Air pollution levels were low to moderate (eg, median 41.6 ppb [interquartile range, 38.9-43.7 ppb] for ozone and 35.1 ppb [28.9-40.3 ppb] for nitrogen oxides). Higher levels of most criteria pollutants during preconception and the first trimester were associated with lower preeclampsia risk, while higher second-trimester levels were associated with greater gestational hypertension risk. For example, an interquartile increase in first-trimester carbon monoxide was associated with a relative risk of 0.88 (95% CI, 0.81-0.95) for preeclampsia and second-trimester carbon monoxide a relative risk of 1.14 (95% CI, 1.07-1.22) for gestational hypertension. Volatile organic compounds, conversely, were not associated with gestational hypertension but consistently associated with higher preeclampsia risk. These findings further suggest air pollution may affect the development ofhypertension in pregnancy, although differing causes of preeclampsia and gestational hypertension may alter these relationships.

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PMID: 

Environ Res. 2019 Oct ;177:108587. Epub 2019 Jul 15. PMID: 31326714

Abstract Title: 

Long-term exposure to PMand stroke: A systematic review and meta-analysis of cohort studies.

Abstract: 

BACKGROUND: Stroke is one of the world's leading causes of death. Many studies have checked the relationship between short-term exposure to particulate matter (PM) and stroke, but few have focused on the effect of long-term exposure to PM(particulate matters with an aerodynamic diameter of≤2.5 μm). This study aimed to quantitatively examine the relationship of long-term exposure to PMwith stroke incidence and mortality.METHODS: We identified relevant studies by searching the PubMed, EMBASE and MEDLINE. After the systematical review of pertinent studies, random-effect meta-analysis was conducted to investigate the association between long-term exposure to PMand stroke.RESULTS: Our meta-analysis included 16 cohort studies with more than 2.2 million people and above 49 149 endpoint events (incident stroke and death from stroke). The pooled hazard ratio (HR) for each 5 μg/mincrement in PMwas 1.11 (95% CI: 1.05, 1.17) (CI for confidence interval) for incidence of stroke and 1.11 (95% CI:1.05, 1.17) for mortality of stroke. In the region-specific analysis, significant association between PMand incidence of stroke was found in North America (HR=1.09, 95% CI:1.05, 1.14) and Europe (HR=1.07, 95% CI:1.05, 1.10), while the pooled result of Asia showed no significance (HR=2.31, 95% CI:0.49, 10.95).CONCLUSIONS: Long-term exposure to PMis an important risk factor for stroke. Since air quality is intimately related to everyone, policies aimed at reducing particulate matters will benefit public health a lot.

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