Epithelial permeability, inflammation, and oxidant stress in the air spaces of smokers

The mechanism responsible for the increased air-space permeability in cigar ette smokers is unknown. The aim of this study was to assess the acute and chronic effects of cigarette smoking on epithelial permeability, inflammati on, and oxidant stress in the air spaces of smokers. Fourteen cigarette smo kers underwent Tc-99m-diethylenetriamine pentaacetic acid (Tc-99m-DTPA) lun g scans after abstaining from smoking for 12 h (chronic smoking) and 1 h af ter smoking two cigarettes (acute smoking). Each smoker also underwent bron choscopy and bronchoalveolar lavage (BAL) after either chronic (n = 8) or a cute smoking (n = 7). Seven nonsmokers also underwent bronchoscopy and BAL. The time to 50% clearance of Tc-99m-DTPA (t(50)) after chronic smoking was 16.7 +/- 1.3 min (mean +/- SE), and was further reduced after acute smokin g to 14.8 +/- 1.0 min (p < 0.01). Neutrophil numbers were increased in bron choalveolar lavage fluid (BALF) in the acute smoking group as compared with the nonsmokers (p < 0.05). Superoxide release from mixed BAL leukocytes wa s increased after chronic (p < 0.01) and acute (p < 0.001) smoking, as were thiobarbituric acid-reactive species (TBARS), providing evidence of lipid peroxidation in plasma (chronic, p < 0.05; acute, p < 0.05). Trolox equival ent antioxidant capacity (TEAC) was reduced in plasma (p < 0.001) and incre ased in BALF (p < 0.05) in both smoking groups. The study therefore showed an acute increase in epithelial permeability and an increase in the number of neutrophils in the air spaces of cigarette smokers concomitant with evid ence of increased oxidant stress.