Global_Environmental_Research_Vol.27No.1
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2. Effects of PM on COVID-19 eosinophils, lymphocytes, neutrophils and macrophages in BALF and accelerated eosinophilic inflammation, antibody production and mucus production via IL-5, eotaxin, antigen-specific IgG and IgE, IL-13, muc5AC and TSLP (He et al., 2015; He et al., 2017; Liu et al., 2017: Liu et al., 2022). As underlying mechanisms, PM2.5 can activate the TLR2/TLR4/MyD88 signaling pathway (He et al., 2017), JAK-STAT6 signaling pathway (Yang et al., 2020) and notch signaling pathway (Liu et al., 2022). PM2.5-induced airway hyper-responsiveness is involved in the kallikrein-bradykinin pathway (Cao et al., 2020), and activation of bromodomain-containing protein 4 (Lu et al., 2021) and TRPA1/TRPV1 (Wang et al., 2019). In some in vitro studies, DEP, PM2.5, or its extracts increased CD86 expression in antigen-presenting cells (Honda et al., 2021), antigen-presenting activity for ovalbumin-specific T cell proliferation (Koike and Kobayashi, splenocyte proliferation (Honda et al., 2017) and mast cell degradation (Devouassoux et al., 2002). These reactions involving the eosinophils, antigen-presenting cells, T cells and mast cells can act in concert like an orchestra and aggravate allergic inflammation in the lungs. 2005), TCR Studies have also been conducted to narrow down the health-impacting and endotoxin/β-glucan were identified by analyzing in vitro biological responses and components of PM2.5 collected from Asia with relatively high positive correlations (Onishi et al., 2018; Chowdhury et al., 2019). Detection of Ti and TiO2 in the atmosphere from e-waste recycling facilities and high traffic roads has also been reported (Yasar et al., 2021; Gallego-Hernández et al., 2020). Sagawa et al., (2021) revealed that TiO2 is taken up by alveolar macrophages and that the necroptosis of alveolar macrophages that phagocytose TiO2 particles is involved in acute lung inflammation. Endotoxins and β-glucans as biological influence exacerbation of asthma (He et al., 2017; Zheng et al., 2020). Moreover, aromatic hydrocarbons (PAHs), quinone alone or combined exposure to quinones and particles in PM2.5 have induced cell death or reduced viability of airway epithelial cells (Honda et al. 2022, 2023). Benzo[a]pyrene disrupts immune response via an increase of CD86 expression on antigen-presenting cells (Chowdhury et al., 2007) in addition to being carcinogenic (Moorthy et al., 2015). Levoglucosan, mannosan and galactosan are characteristic components of open-burning plants, with a positive correlation with mutagenicity (Van Den Heuvel et al., 2018), however, few studies have focused on the relationship between the PM2.5 components of open burning and health effects. Future research should clarify the components that determine the health effects of PM arising from open burning. components of PM2.5. Ti components of PM2.5 among expression, can polycyclic Mechanisms by which PM worsens respiratory disease Coronavirus disease 2019 There are several explanations for these results, including to airborne particles, such as PM, and is transported and diffused that way (Liu et al., 2020; Nor et al., 2021) and the theory that exposure to ambient PM may also reduce resistance to infection in the population (Maleki et al., 2021). However, the exact mechanism is unknown. Upon SARS-CoV-2 entry into cells, the spike protein (S-protein) on the viral surface binds to the receptor protein (ACE2) expressed on the host cell. Subsequently, the S-protein is degraded through the action of proteolytic enzyme transmembrane protease 2 (TMPRSS2), exposing the fusion active domain within the S-protein, which fuses the viral membrane to the host cell membrane and allows the viral genome to enter the cell (Hoffmann et al., 2020; Jackson et al., 2022). Variations in the expression of ACE2 and TMPRSS2 are thought to influence the development of COVID-19 and other diseases (Saheb Sharif-Askari et al., 2020), and increased expression of ACE2 and TMPRSS2 in the lungs has been reported in smokers, who have a higher incidence of severe COVID-19 (Chakladar et al., 2020). Moreover, smoke exposure increases the expression of ACE2 in the airways in animal models (Yilin et al., 2015). This means that the expression of ACE2 and TMPRSS2 varies depending on environmental factors. Thus, we hypothesized that PM might be involved in the pathogenesis of COVID-19 by affecting the expression of ACE2 and TMPRSS2 and verified this hypothesis in animal studies (Sagawa et al., 2021). Mice from the Male Institute of Cancer Research were intratracheally administered 500 µg of PM particles (PM fine: 0.3 to 2.4 µm particle size, PM coarse: >2.4 µm particle size) collected in Yokohama, Japan, and dispersed in phosphate-buffered saline (PBS). Twenty-four hours later, their lung tissues were collected and immuno- stained for ACE2 and TMPRSS2. The results showed that compared to those in the PBS control group, the number the theory that SARS-CoV-2 adheres angiotensin-converting (COVID-19) is an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and is a major public health concern on a global scale. Epidemiological studies suggesting a link between COVID-19 and air pollution have been reported from around the world. Specifically, it has been noted that exposure to wildfire smoke may promote COVID-19 morbidity (Centers for Disease Control and Prevention, 2023), and exposure to PM2.5 and PM10 concentrations in the air are positively correlated with the number of COVID-19 cases, the severity of cases and deaths, whether short-term on the order of days or long-term on the order of years (Fattorini and Regoli, 2020; Yao et al., 2020; Prinz and Richter, 2022; Shao et al., 2022; Xu et al., 2022). enzyme 2 23

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