Abstract:Ultrafine particles (UFPs) are aerosols with an aerodynamic diameter of 0.1 µm (100 nm) or less. There is a growing concern in the public health community about the contribution of UFPs to human health. Despite their modest mass and size, they dominate in terms of the number of particles in the ambient air. A particular concern about UFPs is their ability to reach the most distal lung regions (alveoli) and circumvent primary airway defenses. Moreover, UFPs have a high surface area and a capacity to adsorb a su… Show more
“…These particles can also accumulate in air due to their long suspension time. Reprinted with permission of Springer Nature from Kwon et al ( 2020 ) Fig. 3 Predicted fractional depositions of inhaled particles in the human respiratory tract during nose breathing, based on data from the International Commission on Radiological Protection (ICRP 1994).…”
Section: Introductionmentioning
confidence: 99%
“…These particles can also accumulate in air due to their long suspension time. Reprinted with permission of Springer Nature from Kwon et al ( 2020 )…”
The relationship between outdoor atmospheric pollution by particulate matter and the morbidity and mortality of coronavirus disease 2019 (COVID-19) infections was recently disclosed, yet the role of indoor aerosols is poorly known. Since people spend most of their time indoor, indoor aerosols are closer to human occupants than outdoors, thus favoring airborne transmission of COVID-19. Therefore, here we review the characteristics of aerosol particles emitted from indoor sources, and how exposure to particles affects human respiratory infections and transport of airborne pathogens. We found that tobacco smoking, cooking, vacuum cleaning, laser printing, burning candles, mosquito coils and incenses generate large quantities of particles, mostly in the ultrafine range below 100 nm. These tiny particles stay airborne, are deposited in the deeper regions of human airways and are difficult to be removed by the respiratory system. As a consequence, adverse effects can be induced by inhaled aerosol particles via oxidative stress and inflammation. Early epidemiological evidence and animal studies have revealed the adverse effects of particle exposure in respiratory infections. In particular, inhaled particles can impair human respiratory systems and immune functions, and induce the upregulation of angiotensin-converting enzyme 2, thus inducing higher vulnerability to COVID-19 infection. Moreover, co-production of inflammation mediators by COVID-19 infection and particle exposure magnifies the cytokine storm and aggravates symptoms in patients. We also discuss the role of indoor aerosol particles as virus carriers. Although many hypotheses were proposed, there is still few knowledge on interactions between aerosol articles and virus-laden droplets or droplet nuclei.
“…These particles can also accumulate in air due to their long suspension time. Reprinted with permission of Springer Nature from Kwon et al ( 2020 ) Fig. 3 Predicted fractional depositions of inhaled particles in the human respiratory tract during nose breathing, based on data from the International Commission on Radiological Protection (ICRP 1994).…”
Section: Introductionmentioning
confidence: 99%
“…These particles can also accumulate in air due to their long suspension time. Reprinted with permission of Springer Nature from Kwon et al ( 2020 )…”
The relationship between outdoor atmospheric pollution by particulate matter and the morbidity and mortality of coronavirus disease 2019 (COVID-19) infections was recently disclosed, yet the role of indoor aerosols is poorly known. Since people spend most of their time indoor, indoor aerosols are closer to human occupants than outdoors, thus favoring airborne transmission of COVID-19. Therefore, here we review the characteristics of aerosol particles emitted from indoor sources, and how exposure to particles affects human respiratory infections and transport of airborne pathogens. We found that tobacco smoking, cooking, vacuum cleaning, laser printing, burning candles, mosquito coils and incenses generate large quantities of particles, mostly in the ultrafine range below 100 nm. These tiny particles stay airborne, are deposited in the deeper regions of human airways and are difficult to be removed by the respiratory system. As a consequence, adverse effects can be induced by inhaled aerosol particles via oxidative stress and inflammation. Early epidemiological evidence and animal studies have revealed the adverse effects of particle exposure in respiratory infections. In particular, inhaled particles can impair human respiratory systems and immune functions, and induce the upregulation of angiotensin-converting enzyme 2, thus inducing higher vulnerability to COVID-19 infection. Moreover, co-production of inflammation mediators by COVID-19 infection and particle exposure magnifies the cytokine storm and aggravates symptoms in patients. We also discuss the role of indoor aerosol particles as virus carriers. Although many hypotheses were proposed, there is still few knowledge on interactions between aerosol articles and virus-laden droplets or droplet nuclei.
“…Ultrafine particles (UPFs) generally refer to particles smaller than 100 nm [13] and account for most of the particle number (PN) concentration measured by a Scanning Mobility Particle Sizer (SMPS) device. Road vehicles are the primary source of UFP emissions in urban pollution hotspots [14].…”
Highway toll booth workers have been reported to be at an increased risk of occupational lung cancer. Moreover, insufficient studies have been performed on exposure assessment of workers at highway toll booths. Elemental carbon (EC), black carbon (BC), and respirable crystalline silica (RCS) concentrations were measured at highway toll booths in Gyeongsangbuk-do (Republic of Korea). The particle number (PN) concentration and size distribution of ultrafine particle were measured using three SMPS devices. The average concentration of the EC inside the booth was 3.3 μg/m 3 , with the maximum being 5.8 μg/m 3. The concentrations of EC were highest for booths that operated exclusively for trucks. The average PN concentration inside the booth was 3.54 × 10 4 cm-3 , approximately 5-fold higher than the reference indoor background. The average BC concentration in the booths were approximately 8 μg/m 3 , and the instantaneous peak concentration was 271 μg/m 3. The RCS was below the detection limit in all samples. This study revealed that toll workers were most frequently exposed to diesel engine particle less than 100 nm, with an extremely high respiratory deposition rate. Therefore, a respiratory protection program is necessary to safeguard these workers against vehicle-related pollutants.
“…To a certain extent, fine particulate matter, also known as ultrafine particles (UFPs), comprises all particles with a diameter of less than 1 μm. UFPs in air pollutants are primary pathogenic factors because of their high numbers, and they possess a large surface area, allowing a substantial amount of toxic chemicals to be adsorbed [6,7]. UFPs can pass through the respiratory tract to the alveoli with high efficiency.…”
Background: Air pollution is a growing public health burden associated with several negative health effects, especially cardiovascular disease. Shenlian extract (SL), a traditional Chinese medicine, has the effects of clearing heat-toxin and promoting blood circulation for removing blood stasis, and it has long been used to treat cardiovascular diseases and atherosclerosis. This study explored the underlying action mechanism of SL against ultrafine particle-induced myocardial ischemic injury (UFP-MI) through network pharmacology prediction and experimental verification. Methods: Male Sprague-Dawley rats with UFP-MI were pre-treated with SL intragastrically for 7 days, all the animals were randomly divided into five groups: Sham, Model (UFP+MI), SLL( 31.08mg/ kg×d) + UFP+ MI, SLM (62.16 mg/ kg×d) + UFP+MI, and SLH (124.32 mg/ kg×d) + UFP+ MI. SL or saline was administrated 7 days before UFP instillation (100 μg/kg), followed by 24 h of ischemia. Inflammatory cytokine detection and histopathological analysis were performed to assess the protective effects of SL. For the mechanism study, differentially expressed genes were identified in UFP-MI rats treated with SL through transcriptomic analysis. Subsequently, in combination with network pharmacology, potential pathways involved in the effects of SL treatment were identified using the Internet-based Computation Platform (www.tcmip.cn) and Cytoscape 3.6.0. Further validation experiments were performed to reveal the mechanism of the therapeutic effects of SL on UFP-MI.Results: In pharmacodynamics experiments, SL significantly suppressed inflammatory cell infiltration into myocardial tissue and exhibited significant anti -inflammatory activity. Transcriptomic analysis revealed that the differentially expressed genes after SL treatment had significant anti-inflammatory, immunomodulatory, and anti-viral activities. Network pharmacology analysis illustrated that the targets of SL participate in the inflammatory response, apoptotic process, innate immune response, platelet activation, and other processes. By combining transcriptomic and network pharmacology data, we found that SL may exert anti-inflammatory effects by acting on the NOD-like signaling pathway to regulate immune response activation and inhibit systemic inflammation. Verification experiments revealed that SL suppressed NLRP3 inflammasome active and inflammasomes are cytosolic protein complexes that stimulate the activation of Caspase-1, which in turn induces the secretion of the inflammatory cytokines Interleukin-1 (IL-1), Interleukin-18(IL-18) and Interleukin-33(IL-33) Conclusion: UFP can induce the activation of NLRP3 inflammasome, leading to the release of downstream the inflammatory cytokines, aggravate the pathological conditions of inflammatory infiltration, and further aggravate the myocardial ischemic injury. Experimental verification indicated that SL can directly inhibit the activation of NLRP3 inflammasomes in the NOD-like signaling pathway and reduce cytokines release. In conclusion, our results confirmed that SL may prevent UFP-MI by acting on the NOD-like signaling pathway.
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