Ambient particulate matter compositions and increased oxidative stress: Exposure-response analysis among high-level exposed population

Hu, Wei; Wang, Yanhua; Wang, Ting; Ji, Qianpeng; Jia, Qiang; Meng, Tao; Ma, Stefan; Zhang, Zhihu; Li, Yanbo; Chen, Rui; Dai, Yufei; Luan, Yang; Sun, Zhiwei; Leng, Shuguang; Duan, Huawei; Zheng, Yuxin

doi:10.1016/j.envint.2020.106341

Cited by 51 publications

(27 citation statements)

References 56 publications

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“…Some heavy metals, such as arsenic, copper, cobalt, and chromium, can generate ROS through Fenton reaction. The generation of ROS can cause oxidative damage to biological macromolecules such as lipids, DNA, and proteins in the body [ 48 – 53 ]. Many studies have suggested that the pathological mechanism of the increase of mortality caused by PM2.5 is mainly reflected in the following aspects: (1) PM2.5 and oxidative stress; (2) PM2.5 and inflammatory injury; (3) PM2.5 and nucleic acid repair; and (4) PM2.5 and immune reaction [ 54 ].…”

Section: Discussionmentioning

confidence: 99%

Tissue-Protective Effect of Erdosteine on Multiple-Organ Injuries Induced by Fine Particulate Matter

et al. 2021

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Background Fine particulate matter (PM2.5) is the air pollutant that most threatens global public health. The purpose of this study was to observe the inflammatory and oxidative stress injury of multiple organs induced by PM2.5 in rats and to explore the tissue-protective effect of erdosteine. Material/Methods We randomly divided 40 male Wistar rats into a blank control group, a saline group, a PM2.5 exposure group, and an erdosteine intervention group. We assessed changes in organs tissue homogenate and biomarkers of inflammation and oxidative stress in serum and bronchoalveolar lavage fluid (BALF). Results (1) The expressions of IL-6, IL-1β, TNF-α, 8-OHdG, 4-HNE, and PCC in serum and BALF of the PM2.5 exposure group increased, but decreased after treatment with erdosteine, suggesting that erdosteine treatment attenuates inflammatory and oxidative stress injury. (2) The expression of γ-GCS in serum and lungs in the PM2.5 exposure group increased, but did not change significantly after treatment with erdosteine. This suggests that PM2.5 upregulates the level of γ-GCS, while erdosteine does not affect this protective response. (3) The expression of T-AOC in serum, lungs, spleens, and kidneys of the PM2.5 exposure group decreased, but increased after treatment with erdosteine. Our results suggest that PM2.5 can cause imbalance of oxidation/anti-oxidation in multiple organs, and erdosteine can alleviate this imbalance. Conclusions PM2.5 exposure can lead to inflammatory and oxidative stress damage in serum and organ tissues of rats. Erdosteine may be an effective anti-inflammatory and antioxidant that can reduce this injury.

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Section: Discussionmentioning

confidence: 99%

Tissue-Protective Effect of Erdosteine on Multiple-Organ Injuries Induced by Fine Particulate Matter

et al. 2021

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“…Previous reports also stated that PM exposure induced oxidative injury, which further activates the inflammatory response [ 84 , 85 , 86 ]. These findings suggest that anti-inflammatory and antioxidant agents may help prevent the adverse effects of PM on the prothrombotic state.…”

Section: In Vitro Interventional Reports On the Effects Of Particulat...mentioning

confidence: 99%

Effects of Particulate Matter on Inflammation and Thrombosis: Past Evidence for Future Prevention

Hantrakool

Kumfu

Chattipakorn

et al. 2022

IJERPH

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Ambient air pollution has become a common problem worldwide. Exposure to pollutant particles causes many health conditions, having a particular impact on pulmonary and cardiovascular disease. Increased understanding of the pathological processes related to these conditions may facilitate the prevention of the adverse impact of air pollution on our physical health. Evidence from in vitro, in vivo, and clinical studies has consistently shown that exposure to particulate matter could induce the inflammatory responses such as IL-6, TNF-α, IL-1β, as well as enhancing the oxidative stress. These result in vascular injury, adhesion molecule release, platelet activation, and thrombin generation, ultimately leading to a prothrombotic state. In this review, evidence on the effects of particulate matter on inflammation, oxidative stress, adhesion molecules, and coagulation pathways in enhancing the risk of thrombosis is comprehensively summarized and discussed. The currently available outcomes of interventional studies at a cellular level and clinical reports are also presented and discussed.

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“…Wang et al (45) demonstrated that PM exposure increased the levels of inflammatory cytokines and pro-inflammatory cytokines through ROS-mediated activation of MAPK and downstream NF-κB pathways. Hu et al (46) showed that environmental levels of both PM 2.5 and total PAHs were significantly correlated with increased PAH metabolite levels in the urine of human subjects, while urinary metal metabolite levels were significantly correlated with oxidative stress biomarkers, suggesting a dose-dependent relationship between exposure to metal components and oxidative stress. In the study, PM 2.5 bound PAHs and metals showed significant exposure-response relationship with markers of oxidative stress, and it was illustrated that the levels of urinary metal metabolites such as 8-OHdG, 8-iso-PGF2α and MDA gradually elevated with increasing environmental PM 2.5 exposure.…”

Section: Oxidative Stress and Inflammationmentioning

confidence: 99%

Narrative review: association between lung cancer development and ambient particulate matter in never-smokers

Lim¹,

Yoon²

2022

J Thorac Dis

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Objective: To review the association and pathophysiological link between lung cancer in never smokers and ambient particulate matter (PM).Background: Although the association between exposure to PM and lung cancer development is well known, the pathophysiological background is yet to be studied in depth. Never smokers comprise a large proportion of newly diagnosed lung cancer cases and account for 25% of all cases. Considering the carcinogenic nature of ambient PM and the fact that many patients with lung cancer are never smokers, it is necessary to evaluate the interrelation and possible clinical background, in order to effectively prevent lung cancer development in this subgroup.Methods: An online search of literature was conducted. The National Center for Biotechnology Information (NCBI), PubMed, Google Scholar, Cochrane Library and EMBASE were searched. Conclusions:In never smokers, the risk of lung cancer was dose-dependent with the concentration of ambient air pollutants. Regarding the pathophysiological link, involvement of epithelial mesenchymal transition (EMT) and chronic inflammation has been mentioned, but further studies are necessary to enable therapeutic interventions to prevent cancer development. Considering the significant burden of PM on lung cancer development, both public and clinical approaches to cancer prevention are essential. To prevent lung cancer more effectively, clinicians should develop a more individualized approach in patients, focusing on gender and genetic background.

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Ambient particulate matter compositions and increased oxidative stress: Exposure-response analysis among high-level exposed population

Cited by 51 publications

References 56 publications

Tissue-Protective Effect of Erdosteine on Multiple-Organ Injuries Induced by Fine Particulate Matter

Tissue-Protective Effect of Erdosteine on Multiple-Organ Injuries Induced by Fine Particulate Matter

Effects of Particulate Matter on Inflammation and Thrombosis: Past Evidence for Future Prevention

Narrative review: association between lung cancer development and ambient particulate matter in never-smokers

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