Pratiti H. Chowdhury1, Akiko Honda 1, Sho Ito1, Hitoshi Okano1, Toshinori Onishi1,2, Makoto Higashihara1, Tomoaki Okuda3, Toshio Tanaka4, Seitarou Hirai4, Hirohisa Takano1

Environmental Health Division, Department of Environmental Engineering, Graduate School of Engineering, Kyoto University, Kyoto 606-8501, Japan
Department of Otolaryngology-Head and Neck Surgery, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan
Department of Applied Chemistry, Faculty of Science and Technology, Keio University, Kanagawa 223-8522, Japan
Technology and Innovation Centre, Daikin Industries, Ltd., Osaka 566-8585, Japan

Received: February 17, 2019
Revised: April 29, 2019
Accepted: June 2, 2019
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Cite this article:
Chowdhury, P.H., Honda, A., Ito, S., Okano, H., Onishi, T., Higashihara, M., Okuda, T., Tanaka, T., Hirai, S. and Takano, H. (2019). Effects of Ambient PM2.5 Collected Using Cyclonic Separator from Asian Cities on Human Airway Epithelial Cells. Aerosol Air Qual. Res. 19: 1808-1819.


  • PM2.5 collected from Japan, Thailand and Taiwan are potentially toxic in airway.
  • PAH, microbial factor, metal, and EC/OC in PM2.5 can induce inflammation.
  • Cyclone technique is advantageous to collect PM2.5 for in vitro exposure study.


Recent studies have shown that air pollution is intense and hazardous in Asia compared to other parts of the world due to the late and poor implementation of updated technology in automobiles and industry as well as to the high population density. Respiratory disease, including asthma, is exacerbated by air pollution. However, the effects of PM2.5, especially on respiratory allergies in Asian cities, have not yet been examined in detail. In this study, airway epithelial cells were exposed to crude PM2.5 particles collected by cyclonic separation from three different Asian cities, namely, Sakai, Bangkok, and Taipei. We compared the cytotoxicity and inflammatory potential of the PM2.5 from these cities by measuring IL-6 and IL-8. The samples from Sakai and Bangkok caused cytotoxic effects at a dose of 75 µg mL–1 and, moreover, induced the release of IL-6 and IL-8 even at low doses. The release of these two interleukins was highly associated with fluoranthene derivatives, microbial factors (endotoxin and β-glucan), metals (e.g., Ti), and organic (OC2 and OC3) and elemental carbon (EC1) in the PM2.5. Thus, these components potentially contribute to cellular damage and a pro-inflammatory response in the airway epithelial cells, and the effect depends on PM2.5 sources in the locations.

Keywords: Crude PM2.5; Cyclone sampler; Cytotoxicity; Pro-inflammatory response


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