Particulates induced lung inflammation and its consequences in the development of restrictive and obstructive lung diseases: a systematic review

Shamsollahi, Hamid Reza; Jahanbin, Behnaz; Rafieian, Shahab; Yunesian, Masud

doi:10.1007/s11356-021-13559-5

Cited by 14 publications

(8 citation statements)

References 58 publications

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“…PM 2.5 is considered to be the most harmful PM and is subject to several air pollution regulations [ 1 , 10 ]. PM 2.5 is a PM with an aerodynamic diameter of <2.5 μm [ 11 ] and includes several pollutants: heavy metals, PAHs, unburned or incompletely burned fuel gases, sulfur compounds, and nitric compounds [ 12 ]. PM 2.5 includes PMs that are directly produced by combustion (so-called ‘primary particulates’) and those that are produced, largely from primary pollutants, by chemical reactions in the atmosphere (known as ‘secondary particulates’).…”

Section: Ambient Pollution and Occupational Pollutionmentioning

confidence: 99%

The Impact of Ambient Environmental and Occupational Pollution on Respiratory Diseases

Nishida

Yatera

2022

IJERPH

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Ambient pollutants and occupational pollutants may cause and exacerbate various lung and respiratory diseases. This review describes lung and respiratory diseases in relation to ambient pollutants, particularly particulate matter (PM2.5), and occupational air pollutants, excluding communicable diseases and indoor pollutants, including tobacco smoke exposure. PM2.5 produced by combustion is an important ambient pollutant. PM2.5 can cause asthma attacks and exacerbations of chronic obstructive pulmonary disease in the short term. Further, it not only carries a risk of lung cancer and death, but also hinders the development of lung function in children in the long term. It has recently been suggested that air pollution, such as PM2.5, is a risk factor for severe coronavirus disease (COVID-19). Asbestos, which causes asbestosis, lung cancer, and malignant mesothelioma, and crystalline silica, which cause silicosis, are well-known traditional occupational pollutants leading to pneumoconiosis. While work-related asthma (WRA) is the most common occupational lung disease in recent years, many different agents cause WRA, including natural and synthetic chemicals and irritant gases. Primary preventive interventions that increase awareness of pollutants and reduce the development and exacerbation of diseases caused by air pollutants are paramount to addressing ambient and occupational pollution.

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Section: Ambient Pollution and Occupational Pollutionmentioning

confidence: 99%

The Impact of Ambient Environmental and Occupational Pollution on Respiratory Diseases

Nishida

Yatera

2022

IJERPH

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“…Pulmonary inflammation may play a critical role for the development of pulmonary dysfunction, ( Yao and Rahman, 2009 ) and PM 2.5 exposure is well known to induce pulmonary inflammation. ( Arias-Pérez et al, 2020 ; Shamsollahi et al, 2021 ) Therefore we performed histological analysis on the lungs and quantitated their inflammatory levels through calculating the inflammatory score as described in Method. Fig.…”

Section: Resultsmentioning

confidence: 99%

“…Fine particulate matters (PM 2.5 ) exposure is correlated with various adverse health effects including pulmonary dysfunction, non-alcoholic fatty liver disease, abnormal glucose metabolism and so forth. ( EPA, 2020 ) Numerous studies have demonstrated that PM 2.5 exposure provokes marked pulmonary inflammation, which is widely considered to be responsible for not only PM 2.5 exposure-induced pulmonary dysfunction ( Shamsollahi et al, 2021 ) but also various extra-pulmonary inflammations and dysfunctions. ( Arias-Pérez et al, 2020 ) Interlukin-6 (IL-6) is one of the best known pulmonary ( Hamanaka and Mutlu, 2018 ) and circulating ( Mutlu et al, 2007 ) inflammatory markers that are up-regulated by exposure to PM 2.5 .…”

Section: Introductionmentioning

confidence: 99%

Deficiency of interleukin-6 receptor ameliorates PM2.5 exposure-induced pulmonary dysfunction and inflammation but not abnormalities in glucose homeostasis

Peng

Yang

Shao

et al. 2022

Ecotoxicology and Environmental Safety

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“…Of these, approximately 2.1 million and 470,000 deaths were estimated to have been caused by ne particulate matter (PM) and ozone, respectively [14,15]. Many studies have reported that particulate matter exposure is the root cause of a variety of health problems, including premature death in patients with lung or heart disease, respiratory irritation, cough, breathing di culties, the acute exacerbation of asthma and chronic obstructive pulmonary disease, reduced lung function, heart attacks, and irregular heart rhythms [16,17]. Increases of 10 µg per cubic meter of PM2.5 and 10 ppb of ozone have been associated with a 7.3% and 1.1% increase in mortality rate, respectively.…”

Section: Discussionmentioning

confidence: 99%

Inhalation of Salvianolic acid B Prevents Fine Particulate Matter-Induced Acute Airway Inflammation and Oxidative Stress by Downregulating the LTR4/MyD88/NLRP3 Pathway

Li¹,

Kan²,

Xie³

2021

Preprint

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Background: Air pollution is a serious threat to human health. Inhaled fine particulate matter (PM2.5) can cause inflammation and oxidation in the airway; however, the mechanisms responsible for this effect have yet to be elucidated and there are no specific drugs that can prevent and treat this condition. In the present study, we investigated the effects and mechanisms underlying the inhalation of salvianolic acid B (SalB) on PM2.5-induced airway inflammation and oxidation.Methods: We used a PM2.5-induced mouse model of airway inflammation and oxidation, along with a human epithelial cell model, to study the action and mechanisms of SalB by histopathology, real-time quantitative polymerase chain reaction, enzyme-linked immunosorbent assays, flow cytometry, and western blotting. Results: SalB treatment markedly inhibited the PM2.5-induced increase in the number of neutrophils and macrophages in bronchoalveolar lavage fluid, improved the infiltration of inflammatory cells in lung tissue, and reduced injury in the alveolar septum. Furthermore, SalB reduced the mRNA and protein levels of interleukin (IL)-1β, tumor necrosis factor (TNF)-α, keratinocyte (KC), and transforming growth factor (TGF)-β1 in lung tissues, and the protein levels of IL-1β, TNF-α, IL-8, IL-6 and TGF-β1 in human epithelial cells. SalB treatment also significantly reversed the reduction of levels of superoxide dismutase, catalase, glutathione and glutathione peroxidase in lung tissue and reduced the levels of reactive oxygen species in human epithelial cells induced by PM2.5. Furthermore, SalB and the myeloid differentiation primary response 88 (MyD88) inhibitor ST2825, inhibited the expression levels of toll-like receptor 4 (TLR4), MyD88, tumor necrosis factor receptor associated factor 6 (TRAF-6), and NOD-like receptor protein 3 (NLRP3), as well as the phosphorylation of downstream signals extracellular signal regulated kinase 1/2 (Erk1/2) and P38 MAP kinase (P38) in lung tissue and epithelial cells.Conclusion: SalB protects against PM2.5-induced airway inflammation and oxidation in a manner that is associated with the inhibition of the TLR4/MyD88/TRAF-6/NLRP3 pathway and downstream signals ERK1/2 and P38.

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Particulates induced lung inflammation and its consequences in the development of restrictive and obstructive lung diseases: a systematic review

Cited by 14 publications

References 58 publications

The Impact of Ambient Environmental and Occupational Pollution on Respiratory Diseases

The Impact of Ambient Environmental and Occupational Pollution on Respiratory Diseases

Deficiency of interleukin-6 receptor ameliorates PM2.5 exposure-induced pulmonary dysfunction and inflammation but not abnormalities in glucose homeostasis

Inhalation of Salvianolic acid B Prevents Fine Particulate Matter-Induced Acute Airway Inflammation and Oxidative Stress by Downregulating the LTR4/MyD88/NLRP3 Pathway

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