Association of long-term PM2.5 exposure with traditional and novel lipid measures related to cardiovascular disease risk

McGuinn, Laura A.; Schneider, Alexandra; McGarrah, Robert W.; Ward‐Caviness, Cavin; Neas, Lucas M.; Di, Qian; Schwartz, Joel; Hauser, Elizabeth R.; Kraus, William E.; Cascio, Wayne E.; Díaz-Sánchez, David; Devlin, Robert B.

doi:10.1016/j.envint.2018.11.001

Cited by 111 publications

(63 citation statements)

References 34 publications

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“…Severe air pollution is a major health risk and can lead to large premature mortality (Schraufnagel et al, 2019). Previous studies have shown that PM 2.5 has an adverse impact on human health and long-term exposure to high PM 2.5 concentration environment will lead to various respiratory diseases because -PM 2.5 carries lots of harmful matters and viruses and can go directly into our lungs (Hayes et al, 2019;McGuinn et al, 2019). As reported in the 6 th Edition of COVID-19 Treatment Regimen (Trial Implementation) published by the National Health Commission of the People's Republic of China, COVID-19 is mainly transmitted by direct contact and droplet transmission, and aerosol transmission is also a potential way (Wang and Du, 2020).…”

Section: Introductionmentioning

confidence: 99%

Influence of COVID-19 Event on Air Quality and their Association in Mainland China

Chen

Huang

Yuan

et al. 2020

Aerosol Air Qual. Res.

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The outbreak of 2019 novel coronavirus (COVID-19) has hugely impacted the world and becomes a global public threat. To prevent the spread of COVID-19, human activities are largely restricted in China in early February, 2020. The influence of strict COVID-19 control policies on air quality and the potential influence of particulate matter concentration on COVID-19 infection in China are of great interest. This study analyzes the concentrations of six major air pollutants in 366 urban areas across mainland China during January 1 to April 30 in 2017-2020. Results show that strict COVID-19 control policies have significantly improved the air quality in many provinces. Compared to 2019, national mean concentrations of PM 2.5 , PM 10 , SO 2 , NO 2 and CO in 2020 decrease by 14%, 15%, 12%, 16% and 12%, respectively, while the concentration of O 3 increases by 9%. Generally, the diurnal variation of PM 2.5 and PM 10 concentrations remains unchanged during COVID-19 and their concentrations are high in the morning and evening while low in the afternoon. Correlation analysis shows that daily COVID-19 infections are positively correlated with PM 2.5 concentration in many provinces, indicating a potential risk of aerosol transmission in high PM 2.5 environment. Thus it is suggested to stay at home in highly polluted days and go out in the afternoon to reduce the risk of infection due to aerosol transmission.

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Section: Introductionmentioning

confidence: 99%

Influence of COVID-19 Event on Air Quality and their Association in Mainland China

Chen

Huang

Yuan

et al. 2020

Aerosol Air Qual. Res.

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“…Exposure to respirable urban air particles poses a serious threat to human health across the world (Englert, 2004; Brook et al, 2010; Schneider et al, 2010; Zheng et al, 2015; McGuinn et al, 2019). The toxic effects of particulate matters (PMs) are mainly related to their particle size, and particulate matters with diameter of less than 2.5 µm (PM2.5) can penetrate deeper into the respiratory tract and about 50% of them are retained in the lung parenchyma, causing respiratory infection, cardiovascular disease, and systemic inflammation (Clifford et al, 2018; Nhung et al, 2018; Pope et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

Ma Xing Shi Gan Decoction Attenuates PM2.5 Induced Lung Injury via Inhibiting HMGB1/TLR4/NFκB Signal Pathway in Rat

et al. 2019

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Ma Xing Shi Gan Decoction (MXD), a classical traditional Chinese medicine prescription, is widely used for the treatment of upper respiratory tract infection. However, the effect of MXD against particulate matters with diameter of less than 2.5 μm (PM2.5) induced lung injury remains to be elucidated. In this study, rats were stimulated with PM2.5 to induce lung injury. MXD was given orally once daily for five days. Lung tissues were harvested to assess pathological changes and edema. Myeloperoxidase (MPO) activity and malonaldehyde (MDA) content in lung were determined to evaluate the degree of injury. To assess the barrier disruption, the bronchoalveolar lavage fluid (BALF) was collected to determine the total protein content and count the number of neutrophils and macrophages. For evaluating the activation of macrophage in lung tissue, CD68 was detected using immunohistochemistry (IHC). The levels of inflammatory factors including tumor necrosis factor-alpha (TNF-α), interleukin-1beta (IL-1β), and interleukin-6 (IL-6) in BALF and serum were measured. In vitro, a PM2.5-activated RAW 264.7 macrophages inflammatory model was introduced. To evaluate the protective effect of MXD-medicated serum, the cell viability and the release of inflammatory factors were measured. The effects of MXD on the High mobility group box-1/Toll-like receptor 4/Nuclear factor-kappa B (HMGB1/TLR4/NFκB) pathway in lung tissue and RAW 264.7 cells were assessed by Western blot. For further confirming the protective effect of MXD was mediated by inhibiting the HMGB1/TLR4/NFκB pathway, RAW 264.7 cells were incubated with MXD-medicated serum alone or MXD-medicated serum plus recombinant HMGB1 (rHMGB1). MXD significantly ameliorated the lung injury in rats, as evidenced by decreases in the pathological score, lung edema, MPO activity, MDA content, CD68 positive macrophages number, disruption of alveolar capillary barrier and the levels of inflammatory factors. In vitro, MXD-medicated serum increased cell viability and inhibited the release of inflammatory cytokines. Furthermore, MXD treatment was found to inhibit HMGB1/TLR4/NFκB signal pathway both in vivo and in vitro. Moreover, the protection of MXD could be reversed by rHMGB1 in RAW 264.7. Taken together, these results suggest MXD protects rats from PM2.5 induced acute lung injury, possibly through the modulation of HMGB1/TLR4/NFκB pathway and inflammatory responses.

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“…A number of studies have found elevated PM exposure to be negatively correlated with the level of HDL-C [28,32,[37][38][39][40][41][42][43]. However, the literature is somewhat inconsistent on this issue, as some studies find exposure to PM associated with an increase in HDL-C [44][45][46], while others find no statistical Studies are shown in chronological order based on the year of publication association [47][48][49][50]. Various studies have shown a significant increased incidence of atherosclerosis in individuals despite elevated levels of HDL-C [51].…”

Section: Hdl Functionalitymentioning

confidence: 99%

Effects of particulate matter on atherosclerosis: a link via high-density lipoprotein (HDL) functionality?

et al. 2020

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Background: Exposure to air pollution has been associated with adverse effects on human health, and ultimately increased morbidity and mortality. This is predominantly due to hazardous effects on the cardiovascular system. Exposure to particulate matter (PM) is considered to be responsible for the most severe effects. Main body: Here we summarize current knowledge from existing epidemiological, clinical and animal studies on the influence of PM exposure on high-density lipoprotein (HDL) functionality and the potential initiation and progression of atherosclerosis. We highlight experimental studies that bring support to the causality and point to possible mechanistic links. Recent studies indicate that the functional properties of HDL are more important than the levels per se. Fine (PM 2.5-0.1) and ultrafine (UFP) PM are composed of chemicals as well as biological elements that are redox-active and may trigger pro-inflammatory responses. Experimental studies indicate that these properties and responses may promote HDL dysfunction via oxidative pathways. By affecting protein and lipid components of the HDL particle, its anti-atherosclerotic characteristics including cholesterol efflux capacity, as well as other anti-oxidative and anti-inflammatory features might be impaired. Conclusion: Current literature suggests that PM promotes HDL dysfunction via oxidative pathways. However, as relatively few studies so far have evaluated the impact of particulate air pollution on HDL functionality, more human epidemiological as well as experimental studies are needed to strengthen any possible causal relationship and determine any relevance to atherosclerosis.

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Association of long-term PM2.5 exposure with traditional and novel lipid measures related to cardiovascular disease risk

Cited by 111 publications

References 34 publications

Influence of COVID-19 Event on Air Quality and their Association in Mainland China

Influence of COVID-19 Event on Air Quality and their Association in Mainland China

Ma Xing Shi Gan Decoction Attenuates PM2.5 Induced Lung Injury via Inhibiting HMGB1/TLR4/NFκB Signal Pathway in Rat

Effects of particulate matter on atherosclerosis: a link via high-density lipoprotein (HDL) functionality?

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