Pulmonary toxicity of actual alveolar deposition concentrations of ultrafine particulate matters in human normal bronchial epithelial cell

Air pollution is a major worldwide concern, and exposure to particulate matter (PM) can increase the risks of pulmonary diseases. Normal human bronchial epithelial cells were applied to clarify the role of ultrafine PM (UFPM) in the pathogenesis of pulmonary toxic effects with realistic alveolar deposition doses. The UFPM used in this research originated from vehicular emissions and coal combustion. UFPM exposure of up to 72 h was found to induce significant time- and concentration-dependent decreases in cell viability. Exposure to UFPM increased reactive oxygen species (ROS) accumulation through heme oxygenase-1 (HO-1) inhibition and induced massive oxidative stress that increased the interleukin-8 (IL-8) expression. UFPM also reduced the pulmonary trans-epithelial electrical resistance through the depletion of zonula occludens (ZO) proteins. Finally, UFPM decreased the alpha 1-antitrypsin (A1AT) expression, which implies high risk of chronic obstructive pulmonary disease (COPD). The evidence demonstrates that exposure to UFPM, even at very low concentrations, may affect the functions of the respiratory system.

Automated summary

This study found that exposure to ultrafine particulate matter (UFPM) can lead to decreased cell viability, increased oxidative stress, and upregulated expression of interleukin-8 (IL-8). Additionally, UFPM can reduce pulmonary trans-epithelial electrical resistance by depleting zonula occludens (ZO) proteins. Furthermore, UFPM was shown to decrease the expression of alpha 1-antitrypsin (A1AT), indicating a higher risk of chronic obstructive pulmonary disease (COPD).