Tashkin D P, Simmons M S, Chang P, Liu H, Coulson A H
Department of Medicine, UCLA School of Medicine and Public Health 90024-1690.
Am Rev Respir Dis. 1993 Jan;147(1):97-103. doi: 10.1164/ajrccm/147.1.97.
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 > or = 20% or > 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.(ABSTRACT TRUNCATED AT 250 WORDS)
既往数据表明,长期吸烟可能导致非特异性气道高反应性(AHR),且与气道阻塞无关,这可能是由于对支气管炎症或黏膜通透性的影响。除烟草外,其他广泛吸食的物质如大麻或可卡因对AHR的影响知之甚少。大麻和可卡因的烟雾均含有呼吸道刺激物,可引发咳嗽,并使习惯性吸烟者的气道动力学和支气管黏膜组织病理学出现异常。因此,长期吸食这两种非法物质中的一种或两种可能会导致AHR,或增强与吸烟相关的AHR。在一项正在进行的关于习惯性吸食非法物质对肺部影响的队列研究中,本研究检测了习惯性吸食大麻、可卡因和/或烟草对542名(456名男性)健康参与者(平均年龄34.8±6.8标准差岁)非特异性AHR的影响。排除有静脉药物滥用史、大量职业暴露史、哮喘或近期上呼吸道感染的受试者。使用由德维比斯646型雾化器雾化的稀释剂和氯化乙酰甲胆碱(1.25至25mg/ml)溶液进行吸入激发试验,该雾化器连接到一个呼吸激活剂量计上,通过三到五次吸气容量呼吸进行吸入。对乙酰甲胆碱的阳性反应定义为吸入每种浓度的乙酰甲胆碱后,FEV1较稀释剂后对照值下降≥20%或≥10%。参与者按吸烟状况分类(不吸烟、单独吸食大麻、可卡因和/或烟草以及联合吸食);大多数分析分别在男性和女性中进行。(摘要截断于250字)