Impact of acute exposure to tobacco smoke on gelatinases in the bronchoalveolar space.

Clinical studies have indicated increased gelatinase activity in the airways of patients suffering from chronic obstructive pulmonary disease caused by tobacco smoke. The present study aimed to determine whether acute exposure to tobacco smoke per se causes a substantial and lasting impact on gelatinases and their inhibitors in the peripheral airways of atopic and nonatopic human subjects. Bronchoscopy with bronchoalveolar lavage (BAL) was performed on occasional smokers with and without atopy before and after smoking 10 cigarettes over a 48-h period. Samples from a group of never-smokers not exposed to tobacco smoke served as controls. Gelatinase identity and activity were measured using zymography, and gelatinase activity assay and concentrations of matrix metalloproteinase (MMP)-2, MMP-9, tissue inhibitor of MMP (TIMP)-1 and TIMP-2 were measured using ELISA. The results revealed no pronounced changes in identity, net activity or concentration of the gelatinases or changes in concentrations of TIMP-1 and TIMP-2 in BAL fluid before and after acute exposure to tobacco smoke. In conclusion, the present experimental study indicates that acute exposure to tobacco smoke does not cause any substantial impact on gelatinases or their inhibitors in the peripheral airways, irrespective of atopy status, a finding that is compatible with the fact that it takes many years of tobacco smoking to establish chronic obstructive pulmonary disease.

High-resolution computed tomography in healthy smokers and never-smokers: a 6-year follow-up study of men born in 1933.

PURPOSE: To elucidate whether emphysematous lesions and other high-resolution computed tomography (HRCT) findings considered associated with smoking are part of a progressive process, and to measure the extent to which similar changes are found in never-smokers. MATERIAL AND METHODS: Healthy smokers and never-smokers were recruited from a randomized epidemiological study and investigated with a 6-year interval. Emphysema, parenchymal and subpleural nodules, ground-glass opacities, bronchial alterations, and septal lines were evaluated in 66 subjects (40 smokers, 11 of whom had stopped smoking in the interval, and 26 never-smokers). Lung function was tested. RESULTS: All except emphysematous lesions were present to some extent in never-smokers. Emphysema, parenchymal nodules, and septal lines occurred significantly more in current smokers, and a progression in extent of emphysema, ground-glass opacities, bronchial alterations and septal lines was seen. There was no significant change among those who stopped and never-smokers except for bronchial alterations, which progressed in never-smokers. CONCLUSION: In healthy, elderly never-smokers a low extent of various HRCT findings has to be considered normal. Emphysema, parenchymal nodules, and ground-glass opacities are indicative of smoking-induced disease. Further progress may cease if smoking is stopped.