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

Abstract

Introduction: 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.