摘要
Background Airborne fine particulate matter （PM） can induce pulmonary inflammation which may adversely affect human health, but very few reports about its effect on the neonate rats are available. This study aimed to observe the potential impact and toxicity of fine PMs on the airway in neonate rats.Methods Pulmonary inflammation, cytotoxicity, histopathology, and antioxidants as well as oxidant products were assessed 24 hours after intratracheal instillation of fine PM consecutively for 3 days. Cytotoxicity of fine PM was measured in Hep-2 cells.Results Rats treated with high dose fine PM developed significant pulmonary inflammation characterized by neutrophiland macrophage infiltration. The inflammatory process was related to elevated level of TNF-α and prooxidant/antioxidant imbalance in the lung. Cytotoxicity studies performed in human epithelial cells indicated that high dose fine PM significantly reduced cell viability.Conclusion The study demonstrated acute exposure to fine PM induced airway inflammation as well as increased oxidative stress in addition to its direct toxic effect on airway epithelium cells.
Background Airborne fine particulate matter （PM） can induce pulmonary inflammation which may adversely affect human health, but very few reports about its effect on the neonate rats are available. This study aimed to observe the potential impact and toxicity of fine PMs on the airway in neonate rats.Methods Pulmonary inflammation, cytotoxicity, histopathology, and antioxidants as well as oxidant products were assessed 24 hours after intratracheal instillation of fine PM consecutively for 3 days. Cytotoxicity of fine PM was measured in Hep-2 cells.Results Rats treated with high dose fine PM developed significant pulmonary inflammation characterized by neutrophiland macrophage infiltration. The inflammatory process was related to elevated level of TNF-α and prooxidant/antioxidant imbalance in the lung. Cytotoxicity studies performed in human epithelial cells indicated that high dose fine PM significantly reduced cell viability.Conclusion The study demonstrated acute exposure to fine PM induced airway inflammation as well as increased oxidative stress in addition to its direct toxic effect on airway epithelium cells.
基金
This study was supported by grants from Natural Science Foundation of Zhejiang Province （No.Y2080323）, Zhejiang Provincial Science and Technology Administration （No. 2009R100310）, and Health Department of Zhejiang Province （No. 2009QN010）.
