NetWellness is a global, community service providing quality, unbiased health information from our partner university faculty. NetWellness is commercial-free and does not accept advertising.
Friday, April 18, 2014
Smoking and Tobacco
Tobacco and effects on airways
Tobacco-induced release of protease enzymes may destroy elastic fibers surrounding small noncartilagenous airways. How may this affect small airway diameter?
These elastic fibers help keep the small airways open, especially during expiration; when these fibers are destroyed, the airway diameter decreases. A recent article summarizes the changes in the lungs with prolonged smoking: `The pathophysiologic mechanisms responsible for chronic bronchitis are not well understood, but suggest a complex disease process. A number of toxic stimuli have been recognized and include inhalation of tobacco smoke, bacterial infection, viral infection, tuberculosis, allergy, and a variety of other causes that result in inflammation of the bronchial tree. These toxic stimuli have a number of detrimental effects, including initial inflammation followed by hypersecretion, ciliary dysfunction, and stimulation of vagal reflexes. The inflammation and hypersecretion leads to excessive bronchial secretions, which, when expectorated, are defined as sputum. These secretions are thicker, stickier, more elastic, and more profuse than normal bronchial mucus. Ciliary function is impaired, thus diminishing the clearance of the excessive and abnormal bronchial secretions. Obstruction of the bronchial lumen progresses further due to stimulation of the vagal reflexes. An enhanced cholinergic effect results in an increased bronchomotor tone of the smooth muscle of the bronchial wall. The collective occurrence of all the aforementioned events eventually promotes bacterial colonization and infection in the bronchial tree (ie, inhaled bacteria are not cleared). These processes can predispose the individual to emphysema.`
Jerry Friemoth, MD
College of Medicine
University of Cincinnati