Airway hyperresponsiveness development and the toxicity of PM2.5

• Published in: Environmental science and pollution research international Vol. 28; no. 6; pp. 6374 - 6391
• Main Authors: Lu, Xi, Li, Rongqin, Yan, Xixin
• Format: Journal Article
• Language: English
• Published: Berlin/Heidelberg Springer Berlin Heidelberg 01-02-2021; Springer Nature B.V
• Subjects: Air pollution; Air Pollution - adverse effects; Air pollution effects; Apoptosis; Aquatic Pollution; Asthma; Atmospheric Protection/Air Quality Control/Air Pollution; Autophagy; Bronchoconstriction; Contraction; Earth and Environmental Science; Ecotoxicology; Environment; Environmental Chemistry; Environmental Health; Environmental science; Genotoxicity; Helper cells; Humans; Inflammation; Inflammatory response; Lung; Lymphocytes T; Molecular modelling; Morbidity; Muscle contraction; Muscles; Oxidative stress; Particulate emissions; Particulate matter; Particulate Matter - toxicity; Phagocytosis; Respiratory Hypersensitivity; Respiratory system; Respiratory tract; Review Article; Smooth muscle; Stenosis; Toxicity; Waste Water Technology; Water Management; Water Pollution Control; Inflammatory responses; Oxidative stress; Cell cycle alteration; Epigenetic alterations; Immune system imbalances; Cytoplasmic calcium concentration Apoptosis; Fine particulate matter (PM2.5); Autophagy; Airway hyperresponsiveness; Asthma
• ISSN: 0944-1344; 1614-7499
• DOI: 10.1007/s11356-020-12051-w

Airway hyperresponsiveness (AHR) is characterized by excessive bronchoconstriction in response to nonspecific stimuli, thereby leading to airway stenosis and increased airway resistance. AHR is recognized as a key characteristic of asthma and is associated with significant morbidity. At present, many studies on the molecular mechanisms of AHR have mainly focused on the imbalance in Th1
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Th2 cell function and the abnormal contraction of airway smooth muscle cells. However, the specific mechanisms of AHR remain unclear and need to be systematically elaborated. In addition, the effect of air pollution on the respiratory system has become a worldwide concern. To date, numerous studies have indicated that certain concentrations of fine particulate matter (PM2.5) can increase airway responsiveness and induce acute exacerbation of asthma. Of note, the concentration of PM2.5 does correlate with the degree of AHR. Numerous studies exploring the toxicity of PM2.5 have mainly focused on the inflammatory response, oxidative stress, genotoxicity, apoptosis, autophagy, and so on. However, there have been few reviews systematically elaborating the molecular mechanisms by which PM2.5 induces AHR. The present review separately sheds light on the underlying molecular mechanisms of AHR and PM2.5-induced AHR.