| Objective To study the mechanism of the airway inflammationinduced by the particles with an aerodynamic diameter of less than 10μm( PM10 ) , and to observe the effect of high-risk team injured by differentsources of PM10. Methods Collected particles at kitchen, smoking-room,roadside and community were analyzed by plasm atomic emissionspectrometry. Make suspension of PM10 and create PM10- treat model ofrats including heated oil smoke group, cigarette smoke group, road dustgroup, and community group. On 22nd day, the counts of total leukocyteand neutrophils in bronchoalveolar lavage fluid (BALF) and superoxidedismutase (SOD) , glutathion peroxidase (GSH-Px) , malondiadehyde(MDA), Cytokin-induced neutrophil chemotactics (CINC) in lunghomogenate were measured. Analyze lung tissue histopathology. ResultsThe concentration of collected dust particles is the most, those ofcommunity air particles is the lest. The number of collected particles in2-5μm in the cigarette smoke group is more than those in heated oil smokegroup and the most in four groups. The counts of total leukocyte,macrophage and neutrophils in PM10- treat groups and the count ofeosinophilia in road dust group were increased significantly than those incommunity group P<0.05. MDA and CINC in heated oil smoke group,cigarette smoke group and road dust group were increased, SOD andGSH-Px in those groups were decreased compared with community groupsignificantly P<0.05. The pathological changes of PM10- treat groupsindicated that PM10 can cause airway injury. Conclusions Themechanism of the airway inflammation by PM10 is complicated. Theterminal way is inflammation reaction by inflammation cell and cell factor .The effect of particles with an aerodynamic diameter of less than 2.5μmwould not be ignored.
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