Previous data suggest that regular tobacco smoking may lead to nonspecific airway hyperresponsiveness (AHR) independent of airway obstruction, possibly because of effects on bronchial inflammation or mucosal permeability. Little is known concerning the effects on AHR of other widely smoked substances besides tobacco such as marijuana or cocaine. The smoke of both marijuana and cocaine contains respiratory irritants that elicit cough and produce abnormalities in airway dynamics and bronchial mucosal histopathology in habitual smokers. Therefore, regular smoking of one or both of these illicit substances could cause AHR or augment the AHR associated with tobacco smoking. The present study examined the influence of habitual smoking of marijuana, cocaine, and/or tobacco on nonspecific AHR in 542 (456 male) healthy participants (mean age, 34.8 ± 6.8 SD yr) in an ongoing cohort study of the pulmonary effects of habitual smoking of illicit substances. Subjects with a history of intravenous drug abuse, significant occupational exposures, asthma, or recent upper respiratory tract infection were excluded. Inhalation challenge studies were performed using solutions of diluent and methacholine chloride (1.25 to 25 mg/ml) aerosolized by a DeVilbiss no. 646 nebulizer attached to a breath-activated dosimeter inhaled by three to five inspiratory capacity breaths. Positive responses to methacholine were defined by ⩾ 20% or ⩾ 10% declines in FEV1 from the postdiluent control value after inhalation of each concentration of methacholine. Participants were categorized by smoking status (nonsmoking and smoking of marijuana, cocaine, and/or tobacco alone and in combination); most analyses were performed in men and women separately. No significant differences in prevalence of positive responses (declines in FEV1 of ⩾ 20% or ⩾ 10%) to any concentration of methacholine were found between nonsmokers and smokers of marijuana and/or cocaine without tobacco in either sex. However, logistic regression revealed significant associations between marijuana smoking and positive responses to some concentrations of methacholine (⩽ 10 mg/ml) in both men and women. A relationship between heavier and/or longer exposure to tobacco and AHR was suggested by a significant positive correlation between the slope of the methacholine dose-response curve and cumulative lifetime amount of tobacco in men, as well as by a significant association (logistic regression) between current daily amount of tobacco and positive responses to methacholine in both men and women, independent of baseline lung function. In contrast, no dose-response relationship was found between AHR and either the current weekly or cumulative lifetime amount of either marijuana or cocaine smoking. In addition, no evidence of an additive or potentiating influence of marijuana and/or cocaine on the association between tobacco and airway responsiveness could be demonstrated in either sex. We conclude that habitual cocaine smoking has no demonstrable influence on nonspecific AHR, whereas heavy, habitual marijuana smoking appears to have an inconsistent effect and tobacco smoking a dose-dependent effect on AHR in both men and women, independent of the influence of lung function on AHR. Neither cocaine nor marijuana was found to potentiate the effect of each or of tobacco on methacholine responsiveness.
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Tashkin et al. (1993) studied this question.