Chemical Composition of Asian Dust in Daejeon, Korea, during the Spring Season

Dasari, K. B.; Cho, Hanna; Jačimović, Radojko; Sun, Gwang Min; Yim, Yong‐Hyeon

doi:10.1021/acsearthspacechem.9b00327

Cited by 15 publications

(8 citation statements)

References 40 publications

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“…Air pollutants such as yellow and fine dust, have become a critical social issue and are life-threatening to patients with respiratory diseases. Several studies [ 1 , 2 , 3 , 4 ] have particularly reported that titanium dioxide nanoparticles (TiO 2 NPs), components of Asian dust and air pollutants, exacerbate respiratory distress [ 1 , 2 , 3 , 4 ]. Moreover, TiO 2 NPs induce an intensive inflammatory response by triggering inflammatory cell migration and pro-inflammatory cytokine secretion, consequently contributing to the development and exacerbation of respiratory diseases [ 5 , 6 ].…”

Section: Introductionmentioning

confidence: 99%

Titanium Dioxide Nanoparticles Exacerbate Allergic Airway Inflammation via TXNIP Upregulation in a Mouse Model of Asthma

Lim

Lee

Kim

et al. 2021

IJMS

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Titanium dioxide nanoparticles (TiO2NPs) are widely used in industrial and medicinal fields and in various consumer products, and their increasing use has led to an increase in the number of toxicity studies; however, studies investigating the underlying toxicity mechanism have been rare. In this study, we evaluated potential toxic effects of TiO2NPs exposure on lungs as well as the development of asthma through the ovalbumin (OVA)-induced mouse model of asthma. Furthermore, we also investigated the associated toxic mechanism. TiO2NPs caused pulmonary toxicity by exacerbating the inflammatory response, indicated by an increase in the number and level of inflammatory cells and mediators, respectively. OVA-induced asthma exposed mice to TiO2NPs led to significant increases in inflammatory mediators, cytokines, and airway hyperresponsiveness compared with those in non-exposed asthmatic mice. This was also accompanied by increased inflammatory cell infiltration and mucus production in the lung tissues. Additionally, TiO2NPs decreased the expression of B-cell lymphoma 2 (Bcl2) and the expressions of thioredoxin-interacting protein (TXNIP), phospho-apoptosis signal-regulating kinase 1, Bcl2-associated X, and cleaved-caspase 3 were escalated in the lungs of asthmatic mice compared with those in non-exposed asthmatic mice. These responses were consistent with in vitro results obtained using human airway epithelial cells. TiO2NPs treated cells exhibited an increase in the mRNA and protein expression of interleukin (IL)-1β, IL-6, and tumor necrosis factor-α with an elevation of TXNIP signaling compared to non-treated cells. Moreover, pathophysiological changes induced by TiO2NP treatment were significantly decreased by TXNIP knockdown in airway epithelial cells. Overall, TiO2NP exposure induced toxicological changes in the respiratory tract and exacerbated the development of asthma via activation of the TXNIP-apoptosis pathway. These results provide insights into the underlying mechanism of TiO2NP-mediated respiratory toxicity.

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Section: Introductionmentioning

confidence: 99%

Titanium Dioxide Nanoparticles Exacerbate Allergic Airway Inflammation via TXNIP Upregulation in a Mouse Model of Asthma

Lim

Lee

Kim

et al. 2021

IJMS

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“…The elemental mass fraction values labeled # in Table 2 represent non-accredited activities, in accordance with LP-090, beyond the scope of the range of testing or the specified uncertainty. All details of uncertainty evaluation of k0-INAA method is explained in our previous studies [13,38] and the literature [32]. The expanded uncertainties for mass fraction values represented in Table 1 and Table 2 have a coverage factor k = 2 at 95% confidence level.…”

Section: Validation Of the K 0 -Inaa Methods Using Nist Srm 1648a Urban Pmmentioning

confidence: 99%

“…However, the contribution of fission of 235 U may be ignored if only a low amount of U is present in the sample, which is not the case of NIST SRM 1648a. All details of uncertainty evaluation of k 0 -INAA method is explained in our previous studies [13,38] and the literature [32]. The expanded uncertainties for mass fraction values represented in Tables 1 and 2 have a coverage factor k = 2 at 95% confidence level.…”

Section: Validation Of the K 0 -Inaa Methods Using Nist Srm 1648a Urban Pmmentioning

confidence: 99%

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Application of k0-INAA Method in Preliminary Characterization of KRISS Urban Airborne Particulate Matter Certified Reference Material

et al. 2020

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We report comprehensive elemental composition studies on the average urban airborne particulate matters (PMs) collected in the Greater Seoul area, Korea, in 2019 to identify regional and chronological characteristics of the sample as a candidate for certified reference material (CRM), using k0-based single comparator instrumental neutron activation analysis (k0-INAA). The method was successfully validated by comparing the analysis result of a similar matrix CRM (SRM 1648a urban particulate matter) of National Institute of Standards and Technology, USA, with corresponding certified values. The same methodology was applied to determine various elements in candidate environmental materials for future CRM development, including the urban PMs and incineration ashes, to investigate the possibility of using k0-INAA for certification of relevant reference materials. In total, 46 elements in the urban PM sample were analyzed and their concentration levels were compared with the urban PMs collected in the 1970s in St. Louis, USA. Urban PMs of Korea Research Institute of Standards and Science in 2019 contain significantly lower levels of hazardous elements, such as As, Cd, Cr, Hg, and Pb, as compared to those of the 1970s, which can be attributed to the reduced air pollution by environmental regulation and technological innovation. The potential major source of urban airborne PMs was also discussed.

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“…Air pollutants, such as yellow dust and ne dust, have become a critical social issue and are lifethreatening to patients with respiratory diseases. In particular, titanium dioxide nanoparticles (TiO 2 NPs), a component of Asian dust and air pollutants, have been reported to exacerbate respiratory distress in several studies [1][2][3][4]. Moreover, TiO 2 NPs induce an intensive in ammatory response by triggering in ammatory cell migration and pro-in ammatory cytokine secretion, and consequently, contributing to the development and exacerbation of respiratory diseases [5,6].…”

Section: Introductionmentioning

confidence: 99%

Titanium dioxide nanoparticles exacerbate allergic airway inflammation via TXNIP upregulation in a mouse model of asthma

Lim

Lee

Kim

et al. 2021

Preprint

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Background Titanium dioxide nanoparticles (TiO2NPs) are widely used in the fields of industry and medicine and in various consumer products. With the increasing use of TiO2NPs, there has been an increase in the number of toxicity studies; however, studies investigating the mechanism underlying its toxicity are very rare. In this study, we evaluated the potential toxic effects of TiO2NPs exposure on the lungs as well as the development of asthma in ovalbumin (OVA)-induced mouse model of asthma. We also investigated the related toxic mechanism. Results TiO2NPs caused pulmonary toxicity by exacerbating the inflammatory response, indicated by an increase in the number of inflammatory cells and levels of inflammatory mediators. Exposure of mice with OVA-induced asthma to TiO2NPs led to significant increases in inflammatory mediators, cytokines, and airway hyperresponsiveness compared with non-exposed mice with asthma. This was also accompanied by an increase in inflammatory cell infiltration and mucus production in the lung tissues. TiO2NPs also decreased the expression of B-cell lymphoma 2 (Bcl2) and increased the expression of thioredoxin-interacting protein (TXNIP), phospho-apoptosis signal-regulating kinase 1, Bcl2-associated X, and cleaved-caspase 3 in the lungs of asthmatic mice compared with those of non-exposed asthmatic mice. These responses were consistent with in vitro results obtained using human airway epithelial cells. TiO2NPs treated cells exhibited an increase in the mRNA and protein expression of IL-1β, IL-6, and TNF-α with an elevation of TXNIP signaling compared to non-treated cells. Moreover, pathophysiological changes induced by TiO2NPs treatment were significantly decreased by TXNIP knockdown in the airway epithelial cells. Conclusion Taken together, TiO2NPs exposure induced toxicological changes in the respiratory tract and exacerbated the development of asthma via activation of the TXNIP-apoptosis pathway. These results provide insights into the mechanism underlying TiO2NPs-mediated respiratory toxicity.

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Chemical Composition of Asian Dust in Daejeon, Korea, during the Spring Season

Cited by 15 publications

References 40 publications

Titanium Dioxide Nanoparticles Exacerbate Allergic Airway Inflammation via TXNIP Upregulation in a Mouse Model of Asthma

Titanium Dioxide Nanoparticles Exacerbate Allergic Airway Inflammation via TXNIP Upregulation in a Mouse Model of Asthma

Application of k0-INAA Method in Preliminary Characterization of KRISS Urban Airborne Particulate Matter Certified Reference Material

Titanium dioxide nanoparticles exacerbate allergic airway inflammation via TXNIP upregulation in a mouse model of asthma

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