Chemical identity and cardiovascular toxicity of hydrophobic organic components in PM2.5

Qi, Zenghua; Zhang, Yanhao; Chen, Zhi Feng; Yang, Chun; Liao, Xiaoliang; Li, Weiquan; Tsang, Suk Ying; Liu, Guoguang; Cai, Zongwei

doi:10.1016/j.ecoenv.2020.110827

Cited by 41 publications

(20 citation statements)

References 210 publications

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“…PAHs, which originate from various emission sources, are one of the most abundant organic components contributing to PM 2.5 ( Qi et al, 2020 ). Different PAH diagnostic ratios are commonly used to investigate possible sources of PAHs, and subsequently, PM 2.5 ( Dong et al, 2021 ; Gao and Ji, 2018 ; Yan et al, 2019 ).…”

Section: Resultsmentioning

confidence: 99%

“…PM 2.5 constituents were characterized according to a previously described methodology ( Qi et al, 2020 ; Zhang et al, 2019 ). Water soluble inorganic ions, 16 Environmental Protection Agency (EPA) polycyclic aromatic hydrocarbons (PAHs), crustal elements (CM), organic carbon (OC) and elemental carbon (EC) were measured in the collected PM 2.5 samples during the COVID-19 epidemic.…”

Section: Methodsmentioning

confidence: 99%

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Investigation of PM2.5 pollution during COVID-19 pandemic in Guangzhou, China

Wen

Yang

Liao

et al. 2022

Journal of Environmental Sciences

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The COVID-19 pandemic has raised awareness about various environmental issues, including PM 2.5 pollution. Here, PM 2.5 pollution during the COVID-19 lockdown was traced and analyzed to clarify the sources and factors influencing PM 2.5 in Guangzhou, with an emphasis on heavy pollution. The lockdown led to large reductions in industrial and traffic emissions, which significantly reduced PM 2.5 concentrations in Guangzhou. Interestingly, the trend of PM 2.5 concentrations was not consistent with traffic and industrial emissions, as minimum concentrations were observed in the fourth period (3/01-3/31, 22.45 μg•m −3 ) of the lockdown. However, the concentrations of other gaseous pollutants, e.g., SO 2 , NO 2 and CO, were correlated with industrial and traffic emissions, and the lowest values were noticed in the second period (1/24-2/03) of the lockdown. Meteorological correlation analysis revealed that the decreased PM 2.5 concentrations during COVID-19 can be mainly attributed to decreased industrial and traffic emissions rather than meteorological conditions. When meteorological factors were included in the PM 2.5 composition and backward trajectory analyses, we found that long-distance transportation and secondary pollution offset the reduction of primary emissions in the second and third stages of the pandemic. Notably, industrial PM 2.5 emissions from western, southern and southeastern Guangzhou play an important role in the formation of heavy pollution events. Our results not only verify the importance of controlling traffic and industrial emissions, but also provide targets for further improvements in PM 2.5 pollution.

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Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Investigation of PM2.5 pollution during COVID-19 pandemic in Guangzhou, China

Wen

Yang

Liao

et al. 2022

Journal of Environmental Sciences

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“…One major mechanism of PM 2.5 cardiotoxicity is mediated via oxidative stress. Previous studies have demonstrated that PM 2.5 exposure has toxic effects on the heart such as cardiomyopathy and coronary disease (Pope et al, 2016;Qi et al, 2020). Nrf2 deletion was found to be related to cardiac injury but there was no connection between the pathways affected in cardiac damage and pulmonary injury.…”

Section: Discussionmentioning

confidence: 87%

Effects of Real-Ambient PM2.5 Exposure on Lung Damage Modulated by Nrf2−/−

Ding

Jiang

et al. 2021

Front. Pharmacol.

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Previous studies have shown that long-term exposure to fine particulate matter (PM2.5) increases the morbidity and mortality of pulmonary diseases such as asthma, chronic obstructive pulmonary disease and pulmonary emphysema. Oxidative stress and inflammation play key roles in pulmonary damage caused by PM2.5. Nuclear factor erythroid 2-related factor 2 (Nrf2) could regulate the expression of antioxidant and anti-inflammatory genes and is pivotal for protection against PM2.5-induced oxidative stress. In this study, a real-ambient exposure system was constructed with the outdoor ambient air in north China. Wild-type (WT) and Nrf2−/− (KO) mice were exposed to the real-ambient system for six weeks. After PM2.5 exposure, our data showed that the levels of inflammatory factors and malondialdehyde were significantly increased in WT and KO mice. Moreover, the lung function and pathological phenotype of the WT mice were altered but there was no obvious change in the Nrf2−/− mice. To further explore the potential molecular mechanisms, we performed RNA-sequencing. The RNA-sequence analysis results showed that the CYP450 pathway in the first ten pathways of KEGG was related to the metabolism of PM2.5. In WT and KO mice, the expression of CYP2E1 in the CYP450 pathway showed opposite trends after PM2.5 exposure. The data showed that the expression of the CYP2E1 gene in WT-PM mice increased while it decreased in KO-PM; the expression of the CYP2E1 protein showed a similar trend. CYP2E1 is primarily distributed in the endoplasmic reticulum (ER) where it could metabolize various exogenous substances attached to PM2.5 and produce highly toxic oxidation products closely related to ER stress. Consistently, the expression level of GRP94, a biomarker of ER stress, was increased in WT mice and reduced in KO mice under PM2.5 exposure. Persistent ER stress is a mechanism that causes lung damage under PM2.5 exposure. Nrf2 facilitates lung injury during PM2.5 exposure and CYP2E1 metabolism is involved in this process.

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“…In our work, we are focusing on the evaluation of the impact of the inorganic fraction of PM (in particular redoxactive transition metal elements) on cells by using the standard reference material for urban air pollutants deprived of organic components. The toxicity of organic compounds is usually based on specific interaction with biomolecules and is widely described in the literature (Hanzalova et al, 2010;Oh et al, 2011;Falco et al, 2017;Qi et al, 2020;Wang et al, 2020b). Among the most hazardous chemical compounds are PAHs, which have carcinogenic, mutagenic, and/or teratogenic effects.…”

Section: Introductionmentioning

confidence: 99%

Variations in Reactive Oxygen Species Generation by Urban Airborne Particulate Matter in Lung Epithelial Cells—Impact of Inorganic Fraction

2020

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Air pollution is associated with numerous negative effects on human health. The toxicity of organic components of air pollution is well-recognized, while the impact of their inorganic counterparts in the overall toxicity is still a matter of various discussions. The influence of airborne particulate matter (PM) and their inorganic components on biological function of human alveolar-like epithelial cells (A549) was investigated in vitro. A novel treatment protocol based on covering culture plates with PM allowed increasing the studied pollutant concentrations and prolonging their incubation time without cell exposure on physical suffocation and mechanical disturbance. PM decreased the viability of A549 cells and disrupted their mitochondrial membrane potential and calcium homeostasis. For the first time, the difference in the reactive oxygen species (ROS) profiles generated by organic and inorganic counterparts of PM was shown. Singlet oxygen generation was observed only after treatment of cells with inorganic fraction of PM, while hydrogen peroxide, hydroxyl radical, and superoxide anion radical were induced after exposure of A549 cells to both PM and their inorganic fraction.

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Chemical identity and cardiovascular toxicity of hydrophobic organic components in PM2.5

Cited by 41 publications

References 210 publications

Investigation of PM2.5 pollution during COVID-19 pandemic in Guangzhou, China

Investigation of PM2.5 pollution during COVID-19 pandemic in Guangzhou, China

Effects of Real-Ambient PM2.5 Exposure on Lung Damage Modulated by Nrf2−/−

Variations in Reactive Oxygen Species Generation by Urban Airborne Particulate Matter in Lung Epithelial Cells—Impact of Inorganic Fraction

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