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Dying for a Cigarette?

Cigarette smoking has been unquestionably linked to fatal respiratory disease. Seventy percent of all person s who die of respiratory disease are smokers. Although many of these people die of lung cancer or emphysema, infectious pulmonary disease commonly develops because of the physiological changes that accompany long term inhalation of smoke. The following cigarette induced physiological changes contribute to high mortality among smokers and to some extent, nonsmokers who breathe air contaminated with cigarette smoke.
·         Chronic cough: smoking irritates the membranes of the lyrnx and trachea, triggering vigorous coughing. The violent inhalations that accompany coughing spasms encourage the aspiration of microbe-laden droplets and particles, which may inoculate the lower airways with opportunistic pathogens.
·         Increased mucus:  inhaled smoke stimulates the respiratory mucous glands to overproduce mucus. So much mucus accumulates along the respiratory epithelium that it can no longer be elevated by the action of cilia. Instead of being carried out of the respiratory tract, trapped particles descend by gravity deep into the lower airways and lung.
·         Saturation: smoke is an air borne suspension of carbon particles. Each lungful of inhaled smoke coats the alveoli with these particles, which are phagocytized by protective alveolar macrophages (dust cell). Unfortunately there are a finite number of dust cells available and these can be rendered ineffective by the task of engulfing an overwhelming number of smoke particles. A few opportunistic pathogens inevitably escape destruction by this saturated line of defense.

·         Paralysis of ciliated mucosa: nicotine has been associated with temporary loss of ciliary function along the respiratory tract. The mobility of the mucous blanket is eventually recovered in most persons who quit smoking.
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