Effects of reactive oxygen species generation induced by Wonju City particulate matter on mitochondrial dysfunction in human middle ear cell

• Published in: Environmental science and pollution research international 2021-09, Vol.28 (35), p.49244-49257
• Main Authors: Lee, Su Hoon, Ha, Sun Mok, Jeong, Min Jae, Park, Dong Jun, Polo, Carlos Noriega, Seo, Young Joon, Kim, Seong Heon
• Format: Article
• Language: English
• Subjects: Abnormalities; Air pollution; Apoptosis; Aquatic Pollution; Atmospheric Protection/Air Quality Control/Air Pollution; Cell survival; Cyclooxygenase-2; Cytotoxicity; Ear diseases; Earth and Environmental Science; Ecotoxicology; Environment; Environmental Chemistry; Environmental Health; Environmental science; Epithelial cells; Epithelium; Gene expression; Health risks; Hypoxia; Inflammation; Investigations; Middle ear; Mitochondria; Molecular weight; Otitis media; Otolaryngology; Outdoor air quality; Oxidative stress; Particulate emissions; Particulate matter; Reactive oxygen species; Research Article; Toxicity; Tumor necrosis factor-TNF; Tumor necrosis factor-α; Waste Water Technology; Water Management; Water Pollution Control; Winter
• ISSN: 0944-1344; 1614-7499
• DOI: 10.1007/s11356-021-14216-7

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.