Alcohol-induced bronchospasm in an asthmatic patient: pharmacologic evaluation of the mechanism.

A 23-year-old Asian with histamine-reactive asthma complained of recurrent chest tightness, nasal congestion and flushing immediately after drinking minimal amounts of alcoholic beverages. He was extensively studied to determine the possible mechanism of his alcohol-induced respiratory symptoms. Drinking of either beer or 95 percent ethanol in apple juice immediately provoked vasomotor signs and moderately severe bronchospasm (54 percent and 73 percent decreases in specific airway conductance, respectively), which spontaneously improved over 30 minutes and two hours, respectively. Intravenous and inhaled ethanol caused less bronchospasm than observed with oral ethanol, and recovery was rapid. Pretreatment with cromolyn sodium (inhaled or oral) and isoproterenol had no inhibitory effect on the alcohol-induced bronchoconstriction, whereas atropine, acetylsalicylic acid, cyproheptadine, and chlorpheniramine appeared to have a partial inhibitory effect. Approximately 70 percent inhibition was observed after chlorpheniramine. Observations in this patient suggest that the bronchoconstriction induced by alcoholic beverages is related to their ethanol content and may be related to formation or release of one or more bronchoconstrictor and vasoactive compounds, including a stimulant of histamine1-receptors. The route of ethanol administration may also influence the bronchospastic response.

Respiratory status of seventy-four habitual marijuana smokers.

Previous studies of the long-term effects of habitual marijuana smoking on respiratory status and lung function have yielded conflicting results. In the present study, lung function tests obtained in 74 regular marijuana smokers (duration of smoking > two-five years; frequency of smoking three days/week to several times/day) who denied intravenous narcotic drug abuse were compared with similar tests performed in two groups of control subjects. One group consisted of individuals tested in a mobile laboratory who were computer-matched to the marijuana smokers for anthropometric characteristics and quantity and duration of tobacco smoking; the other group was comprised of 41 nonsmokers of marijuana who were tested in the same laboratory as the marijuana smokers. Paired and unpaired t analyses revealed lower values for specific airway conductance (-0.07 to -0.08 +/- 0.02; P < 0.001) in the marijuana smokers compared with either group of control subjects, but no differences in spirometric indices, closing volume or delta N2 750-1250. When non-tobacco smoking marijuana users (n = 50) were matched with either non-tobacco smoking or tobacco smoking control subjects, significant differences were again noted in specific airway conductance (P < 0.001) but not in spirometric tests, closing volume or delta N2 750-1250. These results suggest that habitual smoking of marijuana may cause mild, but significant, functional impairment predominantly involving large airways which is not detectable in individuals of the same age who regularly smoke tobacco. The clinical implications of these findings await further study.