Mitochondrial Toxicity of Fine Particulate Matter (PM2.5) Collected in Hong Kong in Human Airway Epithelial Cells

Abstract

Background: Air pollution is considered as a serious problem worldwide, posing harmful threat to public health. Fine particulate matter 2.5 (PM2.5), an aerodynamic diameter of which is less than 2.5 micrometer, is associated with higher risk of respiratory diseases like asthma and chronic obstructive pulmonary disease (COPD). Mitochondria are highly sensitive to environmental toxicants and their roles on respiratory diseases have been well-documented. However, studies on the relationship between PM2.5 and mitochondria in respiratory tract are limited. Thus, we aimed to study the effects of PM2.5 on mitochondrial function and dynamic in human bronchial epithelial cells. Methods: Atmospheric PM2.5 samples were collected by 47 mm Teflon filters using Desert Research Institute portable mid-volume samplers in Hong Kong. Human bronchial epithelial cell line BEAS-2B cells were cultured until 80% confluent. After cell arrest, cells were treated with different concentrations of PM2.5 samples. The viability of cells was assessed by MTT and LDH assays. Mitochondrial function was measured by JC-1 probe. Protein expressions were examined by Western blot analysis. Results: The survival rate of BEAS-2B cells declined in a PM2.5 concentration-dependent manner. PM2.5 exposure also caused loss of mitochondrial membrane potential in a concentration-dependent manner. PM2.5 exposure reduced the expression of specific mitochondrial fusion proteins (OPA1 and Mfn1) and elevated the expression of mitochondrial fission protein (Fis1). Conclusion: Current data showed that exposure to PM2.5 collected in Hong Kong caused mitochondrial toxicity by affecting mitochondrial function and dynamic in human bronchial epithelial cells. This provides further understanding on the detrimental effects of PM2.5 in airway injury.