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Conference Paper: Effects of fine particulate matter collected in Hong Kong in human airway epithelial cells

TitleEffects of fine particulate matter collected in Hong Kong in human airway epithelial cells
Authors
Issue Date2018
PublisherHong Kong Academy of Medicine Press. The Journal's web site is located at http://www.hkmj.org/
Citation
23rd Medical Research Conference, Department of Medicine, The University of Hong Kong, 20 January 2018. In Hong Kong Medical Journal, 2018, v. 24 n. 1, Suppl.1, p. 45, abstract no. 68 How to Cite?
AbstractIntroduction: Fine particulate matter (PM) of an aerodynamic diameter of <2.5 micrometre (PM2.5) is considered a significant contributor in air pollution, and associated with an increased risk of lung cancer, cardiovascular and respiratory deaths and hospital admissions. Due to diversity in the origin and composition of PM2.5, it is necessary to evaluate the complex mechanisms underlying local PM2.5-induced adverse effects in human airway epithelial cells. Methods: Atmospheric PM2.5 samples were collected by two 47-mm Teflon filter on parallel using Desert Research Institute portable mid-volume samplers in one of the general air-monitoring stations in Hong Kong. PM2.5 extracts were prepared by sonication with ultrapure 0.1 micrometre filtered water and vacuum-freeze drying. Particles were then suspended in certain amount of phosphate-buffered saline solution for further use. Human bronchial epithelial cell line (BEAS-2B) was cultured in the keratinocyte serum-free medium with essential supplements. Results: Total PM2.5 exposure caused cell morphology alterations in BEAS-2B cells, resulting in cell shrinkage and reduction in cell number after 24 or 48 hours’ exposure. Exposure to total PM2.5 (12.5-200 microgram/mL) caused elevations of pro-inflammatory cytokines interleukin-8 release in a dose-dependent manner. Conclusion: Exposure to PM2.5 collected in Hong Kong caused cellular toxicity and inflammatory response in human bronchial epithelial cell line BEAS-2B. Further study should be conducted to explore the underlying mechanisms of PM2.5 on the regulation of inflammatory response in the airways.
Persistent Identifierhttp://hdl.handle.net/10722/256187
ISSN
2015 Impact Factor: 0.887
2015 SCImago Journal Rankings: 0.279

 

DC FieldValueLanguage
dc.contributor.authorLiang, YM-
dc.contributor.authorTian, L-
dc.contributor.authorHo, KF-
dc.contributor.authorIp, MSM-
dc.contributor.authorMak, JCW-
dc.date.accessioned2018-07-20T06:30:39Z-
dc.date.available2018-07-20T06:30:39Z-
dc.date.issued2018-
dc.identifier.citation23rd Medical Research Conference, Department of Medicine, The University of Hong Kong, 20 January 2018. In Hong Kong Medical Journal, 2018, v. 24 n. 1, Suppl.1, p. 45, abstract no. 68-
dc.identifier.issn1024-2708-
dc.identifier.urihttp://hdl.handle.net/10722/256187-
dc.description.abstractIntroduction: Fine particulate matter (PM) of an aerodynamic diameter of <2.5 micrometre (PM2.5) is considered a significant contributor in air pollution, and associated with an increased risk of lung cancer, cardiovascular and respiratory deaths and hospital admissions. Due to diversity in the origin and composition of PM2.5, it is necessary to evaluate the complex mechanisms underlying local PM2.5-induced adverse effects in human airway epithelial cells. Methods: Atmospheric PM2.5 samples were collected by two 47-mm Teflon filter on parallel using Desert Research Institute portable mid-volume samplers in one of the general air-monitoring stations in Hong Kong. PM2.5 extracts were prepared by sonication with ultrapure 0.1 micrometre filtered water and vacuum-freeze drying. Particles were then suspended in certain amount of phosphate-buffered saline solution for further use. Human bronchial epithelial cell line (BEAS-2B) was cultured in the keratinocyte serum-free medium with essential supplements. Results: Total PM2.5 exposure caused cell morphology alterations in BEAS-2B cells, resulting in cell shrinkage and reduction in cell number after 24 or 48 hours’ exposure. Exposure to total PM2.5 (12.5-200 microgram/mL) caused elevations of pro-inflammatory cytokines interleukin-8 release in a dose-dependent manner. Conclusion: Exposure to PM2.5 collected in Hong Kong caused cellular toxicity and inflammatory response in human bronchial epithelial cell line BEAS-2B. Further study should be conducted to explore the underlying mechanisms of PM2.5 on the regulation of inflammatory response in the airways.-
dc.languageeng-
dc.publisherHong Kong Academy of Medicine Press. The Journal's web site is located at http://www.hkmj.org/-
dc.relation.ispartofHong Kong Medical Journal-
dc.relation.ispartof23rd Medical Research Conference, 2018-
dc.rightsHong Kong Medical Journal. Copyright © Hong Kong Academy of Medicine Press.-
dc.titleEffects of fine particulate matter collected in Hong Kong in human airway epithelial cells-
dc.typeConference_Paper-
dc.identifier.emailLiang, YM: winniell@hku.hk-
dc.identifier.emailTian, L: linweit@hku.hk-
dc.identifier.emailIp, MSM: msmip@hku.hk-
dc.identifier.emailMak, JCW: judithmak@hku.hk-
dc.identifier.authorityTian, L=rp01991-
dc.identifier.authorityIp, MSM=rp00347-
dc.identifier.authorityMak, JCW=rp00352-
dc.identifier.hkuros286327-
dc.identifier.volume24-
dc.identifier.issue1, Suppl.1-
dc.identifier.spage45-
dc.identifier.epage45-
dc.publisher.placeHong Kong-

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