Seong-Heon Kim

Urban air pollution, a significant environmental hazard, is linked to adverse health outcomes and increased mortality across various diseases. This study investigates the neurotoxic effects of particulate matter (PM), specifically PM2.5 and PM10, by examining their role in inducing oxidative stress and subsequent neuronal cell death. We highlight the novel finding that PM increases mitochondrial ROS production via stimulating NOX4 activity, not through its expression level in Neuro-2A cells. Additionally, PMs provoke ROS production via increasing the expression and activity of NOX2 in SH-SY5Y human neuroblastoma cells, implying differential regulation of NOX proteins. This increase in mitochondrial ROS triggers the opening of the mitochondrial permeability transition pore (mPTP), leading to apoptosis through key mediators, including caspase3, BAX, and Bcl2. Notably, the voltage-dependent anion-selective channel 1 (VDAC1) increases at 1 µg/mL of PM2.5, while PM10 triggers an increase from 10 µg/mL. At the same concentration (100 µg/mL), PM2.5 causes 1.4 times higher ROS production and 2.4 times higher NOX4 activity than PM10. The cytotoxic effects induced by PMs were alleviated by NOX inhibitors GKT137831 and Apocynin. In SH-SY5Y cells, both PM types increase ROS and NOX2 levels, leading to cell death, which Apocynin rescues. Variability in NADPH oxidase sources underscores the complexity of PM-induced neurotoxicity. Our findings highlight NOX4-driven ROS and mitochondrial dysfunction, suggesting a potential therapeutic approach for mitigating PM-induced neurotoxicity.

Atmospheric particulate matter (PM) contains different components that can elicit varying adverse health effects in humans and animals. Studies on PM toxicity and its underlying mechanisms in the middle ear are limited, and they generally use a PM standard. However, as PM composition varies temporally and geographically, it is crucial to identify the toxic PM constituents according to season and region and investigate their associated health effects. Thus, we sought to determine whether PM induces cytotoxicity and inflammatory factor and reactive oxygen species (ROS) generation in human middle ear epithelial cells obtained from patients with otitis media. The cells were treated with both standard urban PM and PM directly captured from the atmosphere in Wonju City. The association between mitochondrial dysfunction and PM was investigated. PM exposure significantly increased COX-2 and TNF-α mRNA expression, increased ROS generation, induced inflammatory responses, and caused abnormalities in mitochondrial motility and function. Furthermore, PM induced cell apoptosis, which consequently reduced cell survival, particularly at the concentration of 100 μg/mL. Overall, our study provides new insights into the toxic effects of standard and atmospheric PM on middle ear cell line.

Seoul, the capital city of South Korea, is the social, political, and economic center of the country. Significant levels of PM₁₀-bound As metalloid and metals have been found in the city, which poses possible adverse health risks to the residents from inhalation exposure. Therefore, this study focuses on the health risk assessment of age-dependent cancer and non-cancer using exposure pathway and human respiratory tract (HRT) mass deposition models. In the case of non-cancer risks, the hazard quotient (HQ) of As via ingestion exposure and the hazard index (HI) was found to be significant (> 1) for the children. The cancer risks through ingestion pathway (CR_ing) were estimated in the order of 10⁻⁴ and 10⁻⁵ for children and adult groups, respectively. The overall CR_ing levels for children were estimated slightly higher than the acceptable level of cancer risk (1 × 10⁻⁴) at all locations throughout the study area. Moreover, the risks of cancer through the inhalation (CR_inh) and incremental lifetime cancer risks (ILCR) due to HRT mass deposition were found to be significant (> 10⁻⁶) and with very small discrepancy in risk levels for both age groups. Furthermore, possible sources of the PM₁₀-bound metalloid (As) and metals were predicted through correlation, principal component, and enrichment factor analysis. The results of source apportionment study indicated the local anthropogenic emission sources (vehicular, biomass/coal/oil combustion, industrial), road dust re-suspension, and trans-boundary sources were responsible for the pollution levels in Seoul, South Korea. The health risks can be minimized by reducing the pollution levels of particulate matter at source.