PMID: 

Sci Total Environ. 2018 Aug 1 ;631-632:47-55. Epub 2018 Mar 7. PMID: 29524902

Abstract Title: 

Ambient air pollutants are associated with newly diagnosed tuberculosis: A time-series study in Chengdu, China.

Abstract: 

Although a few studies have analyzed the associations between ambient air pollutants and the development of tuberculosis (TB), most have been conducted in the core countries with inconsistent results. In this study, we used a distributed lag non-linear model to investigate the associations between the newly diagnosed TB cases and daily exposure to particulate matter with an aerodynamic diameter of

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PMID: 

BMC Public Health. 2019 Oct 21 ;19(1):1319. Epub 2019 Oct 21. PMID: 31638933

Abstract Title: 

The short-term effects of air pollutants on influenza-like illness in Jinan, China.

Abstract: 

BACKGROUND: There is valid evidence that air pollution is associated with respiratory disease. However, few studies have quantified the short-term effects of six air pollutants on influenza-like illness (ILI). This study explores the potential relationship between air pollutants and ILI in Jinan, China.METHODS: Daily data on the concentration of particulate matters

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PMID: 

Int J Biometeorol. 2019 Jan ;63(1):51-60. Epub 2018 Oct 31. PMID: 30382350

Abstract Title: 

Effects of air pollutants on occurrences of influenza-like illness and laboratory-confirmed influenza in Hefei, China.

Abstract: 

Accumulating evidence suggests that air pollution is a risk factor for adverse respiratory and cardiovascular health outcomes. However, the different impacts of exposure to air pollutants on influenza virus activity and influenza-like illness (ILI) have not been well documented in epidemiological studies. We examined the association between air pollutants of particular matters

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PMID: 

Biochem Biophys Res Commun. 2017 11 18 ;493(2):1122-1128. Epub 2017 Sep 5. PMID: 28887033

Abstract Title: 

Long-term exposure to PM2.5 lowers influenza virus resistance via down-regulating pulmonary macrophage Kdm6a and mediates histones modification in IL-6 and IFN-β promoter regions.

Abstract: 

Atmospheric particulates, especially PM2.5, not only damage the respiratory system, but also play important roles in pulmonary immunity. China is influenced by atmospheric diffusion conditions, industrial manufacturers, and heating and discharging. PM2.5 levels in the air rise substantially in the winter, which is also a period of flu high-incidence. Although an epidemiological link exists between PM2.5 and flu, we do not understand how long-term PM2.5 inhalation affects pulmonary immunity and the influenza virus response. Our study has prepared an in vivo PM2.5 mouse pharyngeal wall drop-in model and has found that PM2.5 exposure leads to mouse inflammatory injuries and furthers influenza A infection. Our results suggest that short-term exposure to PM2.5 significantly enhances the survival rate of influenza A-contaminated mice, while long-termPM2.5 inhalation lowers the capacity of pulmonary macrophages to secrete IL-6 and IFN-β. A disorder in the pulmonary innate defense system results in increased death rates following influenza infection. On a macromolecular level, this mechamism involves Kdm6a down-regulation after long-term exposure to PM 2.5 and a resultant increase in H3K4 and H3K9 methylation in IL-6 and IFN-β promoter regions. In summary, PM2.5 causes injuries of lung tissue cells and downregulates immune defense mechanisms in the lung.

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PMID: 

Int J Toxicol. 2017 Mar/Apr;36(2):165-173. Epub 2016 Dec 29. PMID: 28033732

Abstract Title: 

Fine Particulate Matter and Sulfur Dioxide Coexposures Induce Rat Lung Pathological Injury and Inflammatory Responses Via TLR4/p38/NF-κB Pathway.

Abstract: 

Fine particulate matter (PM) and sulfur dioxide (SO) are 2 common air pollutants, but their toxicological effects of coexposure are still not fully clear. In this study, SOexposure (5.6 mg/m) couldn't cause obvious inflammatory responses in rat lungs. The PMexposure (1.5 mg/kg body weight) increased inflammatory cell counts in bronchoalveolar lavage fluid (BALF) and some inflammation damage. Importantly, SOand PM(1.5, 6.0, and 24.0 mg/kg) coexposure induced pathological and ultrastructural damage and raised inflammatory cells in BALF compared with the control. Also, they significantly elevated the levels of pro-inflammatory cytokines, adhesion molecule, and nitric oxide (NO) and promoted the gene expression of nuclear factor kappa B (NF-κB), phosphorylated p38 (p-p38), and Toll-like receptor 4 (TLR4) in rat lungs treated with higher dose of PM(6.0 and 24.0 mg/kg) plus SOrelative to the control or SOgroup, along with the decreased inhibitor of NF-κBα and increased inhibitor of NF-κB kinase β expressions. The changes in the inflammatory markers in the presence of PMplus SOwere not significant compared with the PMgroup. The results indicated that inflammatory injury and pathological and ultrastructural damage in rat lungs exposed to PMplus SOwere involved in TLR4/p38/NF-κB pathway activation accompanied by oversecretion of pro-inflammatory cytokine, adhesion molecule, and NO. It provides more useful evidence to understand the possible toxicological mechanism that PMand SOcopollution exacerbate lung disease.

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PMID: 

Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2018 Apr 8 ;34(4):299-303 317. PMID: 30788935

Abstract Title: 

[Effect of particulate matter 2.5 at urban centre of Hangzhou on lung impairment in rats].

Abstract: 

OBJECTIVE: To explore the effect of ambient particle matter 2.5 (PM2.5) collected in the urban center of Hangzhou on the lung injury of rats and on the activating of endoplasmic reticulum pathway.METHODS: PM2.5 samples were collected on quartz fiber filters using a PM2.5 high-volume air sampler in the urban area of Hangzhou. The collected PM2.5 particles were extracted in ultrapure water and concentrated by vacuum freeze-drying. Twenty-four male Sprague-Dawly (SD) rats were randomly divided into 3 groups:saline control group, low dose PM2.5 exposure group (5 mg/kg BW) and high dose PM2.5 exposure groups (25 mg/kg BW). Each group received intratracheal instillation of PM2.5, once a week for 4 weeks. Twenty-four hours after the last exposure, the rats were narcotized and sacrificed, left lung was isolated and fixed with 4% paraformaldehyde for histopathological detection. The bronchoalveolar lavage fluid (BALF) was collected from the right lung. The total antioxidant capacity (T-AOC) level, the activities of superoxide dismutase (SOD) and lactic dehydrogenase (LDH) in BALF were detected by chemical colorimetry. The level of tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β) and interleukin-6 (IL-6) cytokines in BALF was measured by enzyme linked immunosorbent assay (ELISA). And the protein expressions of glucose-regulated protein 78 (GRP78), phosphorylated protein kinase receptor-like endoplasmic reticulum kinase (p-PERK), phosphorylated eukaryotic translation initiation factor (p-eIF2α), transcription factors C/EBP homologue protein (CHOP), inositol-requiring enzyme 1α (IRE1α) and X-box binding protein 1 (XBP1) in lung tissue were determined by Western blotting.RESULTS: Compared with control group, rats in both low dose (5 mg/kg) and high dose (25 mg/kg) PM2.5-treated groups showed obviously dose-dependent pulmonary toxicity including thickening of alveolar walls, narrowing of alveolar space, interstitial hyperplasia and inflammatory cell infiltration. Compared with control group, T-AOC level and the SOD activity in BALF in both PM2.5-treated groups were decreased dose-dependently (

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PMID: 

Toxicol Lett. 2013 Nov 25 ;223(2):146-53. Epub 2013 Sep 14. PMID: 24045146

Abstract Title: 

Beijing ambient particle exposure accelerates atherosclerosis in ApoE knockout mice.

Abstract: 

BACKGROUND: Air pollution is associated with significant adverse health effects including increased cardiovascular morbidity and mortality. However research on the cardiovascular effect of"real-world"exposure to ambient particulate matter (PM) in susceptible animal model is very limited. In this study, we aimed to investigate the association between Beijing ambient particle exposure and the atherosclerosis development in the apolipoprotein E knockout mice (ApoE(-/-) mice).METHODS: Two parallel exposure chambers were used for whole body exposure among ApoE knockout mice. One of the chambers was supplied with untreated ambient air (PM group) and the other chamber was treated with ambient air filtered by high-efficiency particulate air (HEPA) filter (FA group). Twenty mice were divided into two groups and exposed to ambient PM (n=10 for PM group) or filtered air (n=10 for FA group) for two months from January 18th to March 18th, 2010. During the exposure, the mass concentrations of PM2.5 and PM10 in the two chambers were continuously monitored. Additionally, a receptor source apportionment model of chemical mass balance using 19 organic tracers was applied to determine the contributions of sources on the PM2.5 in terms of natural gas, diesel vehicle, gasoline vehicle, coal burning, vegetable debris, biomass burning and cooking. At the end of the two-month exposure, biomarkers of oxidative stress, inflammation and lipid metabolism in bronchoalveolar lavage fluid (BAL) and blood samples were determined and the plaque area on the aortic endothelium was quantified.RESULTS: In the experiment, the concentrations of PM10 and PM2.5 in PM chamber were 99.45μg/m(3) and 61.0μg/m(3) respectively, while PM2.5 in FA chamber was 17.6μg/m(3). Source apportionment analysis by organic tracers showed that gasoline vehicle (39.9%) and coal burning (24.3%) emission were the two major sources contributing to the mass concentration of PM2.5 in Beijing. Among theApoE knockout mice, the PM group were significantly higher than the FA group in terms of serum total cholesterol, low-density lipoprotein, tumor necrosis factor-alpha (TNF-alpha) and C-reactive protein as well as TNF-alpha and interleukin-6 in BAL. Also the total antioxidant capacity and oxidized low-density lipoprotein were significantly different between the two groups. In addition, pathological analysis of aortic arch reveals that the plaques area in the PM group increased significantly compared to the FA group.CONCLUSIONS: Our results demonstrated that ambient PM exposure could induce considerable oxidative stress and systemic inflammation in ApoE knockout mice and contribute to the progression of atherosclerosis.

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PMID: 

Toxicol Sci. 2004 Feb ;77(2):263-71. Epub 2003 Dec 2. PMID: 14657513

Abstract Title: 

Suppression of cell-mediated immune responses to listeria infection by repeated exposure to diesel exhaust particles in brown Norway rats.

Abstract: 

Diesel exhaust particles (DEP) have been shown to alter pulmonary immune responses to bacterial infection. Exposure of rats to 100 mg/m(3) DEP for 4 h was found to aggravate Listeria monocytogenes(Listeria) infection at 3 days postinfection, but the bacteria were largely cleared at 7 days postinfection due to the development of a strong T cell-mediated immunity. In the present study, we examined the effects of repeated DEP exposure at lower doses on pulmonary responses to bacterial infection. Brown Norway rats were exposed to DEP by inhalation at 20.62 +/- 1.31 mg/m 3 for 4 h/day for 5 days, followed by intratracheal inoculation with 100,000 Listeria at 2 h after the last DEP exposure. DEP-exposed rats showed a significant increase in lung bacterial load at both 3 and 7 days postinfection. The repeated DEP exposure was shown to suppress both the innate, orchestrated by alveolar macrophages (AM), and T cell-mediated responses to Listeria. DEP inhibited AM production of interleukin- (IL-) 1beta, tumor necrosis factor- (TNF-) alpha, and IL-12 but enhanced Listeria-induced AM production of IL-10, which has been shown to prolong the survival of intracellular pathogens such as Listeria. DEP exposure also suppressed the development of bacteria-specific lymphocytes from lung-draining lymph nodes, as indicated by the decreased numbers of T lymphocytes and their CD4(+) and CD8(+) subsets. Furthermore, the DEP exposure markedly inhibited the Listeria-induced lymphocyte secretion of IL-2 at day 7, IL-10 at days 3 and 7, and interferon- (IFN-) gamma at days 3 to 10 postinfection when compared to air-exposed controls. These results show a sustained pattern of downregulation of T cell-mediated immune responses by repeated low-dose DEP exposure, which is different from the results of a single high-dose exposure where the acute effect of DEP aggravated bacteria infection but triggered a strong T cell-mediated immunity.

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PMID: 

Environ Res. 2011 Apr ;111(3):348-55. Epub 2011 Jan 21. PMID: 21256479

Abstract Title: 

PM 2.5 collected in a residential area induced Th1-type inflammatory responses with oxidative stress in mice.

Abstract: 

Epidemiologists have tried to establish an association between human health and exposure to particulate matter (PM). In addition, many researchers have investigated the adverse effects of PM as a trigger of cardiovascular and pulmonary diseases. It is known that a number of environmental contaminants are attached to PM and the toxicity of PM may depend on the sources. We investigated the effects of PM collected in a residential area of Seoul on the immunotoxic responses including cytokine production in BAL fluid and in blood after a single intratracheal instillation in mice with the characterization of physico-chemical properties of PM 2.5 samples. As results, pro-inflammatory cytokines (IL-1, TNF-α, and IL-6), Th0-type cytokine (IL-2), and Th1-type cytokines (IL-12 and IFN-γ) were increased by a dose-dependent manner. Cell infiltration in the alveolar area and phagocytosis by macrophage was observed until day 28 after instillation. The expressions of oxidative stress-related genes (HSP 1a,HSP 8, and SOD) and tissue damage-related genes (MMP-15, -19, and Slpi) were time-dependently increased. PM 2.5 also induced an increase of T cell distribution in lymphocyte and decreased the CD4+/CD8+ ratio. Based on the results, we suggest that PM 2.5 collected in a residential area of Seoul mayinduce Th1 type-inflammatory responses with oxidative stress and trigger adverse effects in human health.

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PMID: 

Am J Physiol Lung Cell Mol Physiol. 2008 Jul ;295(1):L79-85. Epub 2008 May 9. PMID: 18469117

Abstract Title: 

Particulate matter exposure induces persistent lung inflammation and endothelial dysfunction.

Abstract: 

Epidemiologic and animal studies have shown that exposure to particulate matter air pollution (PM) is a risk factor for the development of atherosclerosis. Whether PM-induced lung and systemic inflammation is involved in this process is not clear. We hypothesized that PM exposure causes lung and systemic inflammation, which in turn leads to vascular endothelial dysfunction, a key step in the initiation and progression of atherosclerosis. New Zealand White rabbits were exposed for 5 days (acute, total dose 8 mg) and 4 wk (chronic, total dose 16 mg) to either PM smaller than 10 mum (PM(10)) or saline intratracheally. Lung inflammation was quantified by morphometry; systemic inflammation was assessed by white blood cell and platelet counts and serum interleukin (IL)-6, nitric oxide, and endothelin levels. Endothelial dysfunction was assessed by vascular response to acetylcholine (ACh) and sodium nitroprusside (SNP). PM(10) exposure increased lung macrophages (P

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