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Tashkin DP. 
“Does cannabis use predispose to chronic airflow obstruction?”. 
Eur Respir J. 2010 Jan 01;35(1):3-5.
Cannabis (derived from the ubiquitous plant, Cannabis sativa, and also known as marijuana) is the most widely used illicit drug worldwide, as well as the second most commonly smoked substance after tobacco, with an estimated 166 million users (3.9% of 15–64 yr olds) 1. Its wide popularity is due to the euphoric effects of its major psychoactive ingredient, Δ9-tetrahydrocannabinol (THC). Since the gas and particulate phase constituents of the smoke of marijuana are at least qualitatively similar to those of tobacco, the major exception being the nicotine in tobacco and the ∼60 cannabinoid (THC-like) components in marijuana 2, 3, there has long been concern that regular smoking of marijuana might increase the risk of developing chronic airflow obstruction and chronic obstructive pulmonary disease (COPD), by analogy with the well-known detrimental effects of tobacco. Several studies have documented that smokers of marijuana, even in the absence of tobacco smoking, show a higher prevalence of symptoms of chronic bronchitis than nonsmokers 4–7. However, the association between marijuana smoking and airflow obstruction is less clear. Several groups of investigators have addressed the latter question by measuring lung function in convenience samples or stratified random population samples of users and nonusers of marijuana and/or tobacco both cross-sectionally 4–6, 8–10 and longitudinally 11–13. The most recent study of the possible association of marijuana use with lung function abnormality appears in this issue of the European Respiratory Journal 14.

Previously published studies have yielded conflicting results relating to marijuana use and lung function. An early cross-sectional study of 74 young (mean age 24 yrs) habitual marijuana smokers showed no differences in either spirometric indices or sensitive measures of small airways function (closing volume or percentage change in nitrogen concentration between 750 and 1,250 mL of expired volume (ΔN2750–1250)) among marijuana users compared with non-marijuana smoking controls matched on age and tobacco smoking 8. Interestingly, however, the 50 non-tobacco-smoking marijuana smokers (MSs) exhibited airway resistances (Raw) that were modestly (28%) but significantly (p< 0.001) higher than Raw among both nonsmoker (NS) and tobacco smoker (TS) controls; similar differences were noted for specific airway conductance (sGaw). These findings suggested that marijuana smoking may cause mild, but significant, narrowing of larger airways not detectable in similarly aged tobacco smokers, but no demonstrable abnormality involving the smaller airways. A later cross-sectional study by the same authors in a Los Angeles convenience sample of young (mean age 34 yrs) heavy MSs (n = 144), smokers of both marijuana and tobacco (MTSs; n = 135), TSs (n = 79) and NSs (n = 97) showed similar results 4, i.e. no abnormalities in spirometric or small airways indices (closing volume, ΔN2750–1250 or measures derived from flow–volume curves obtained with air and a helium–oxygen mixture) among the MSs in contrast to modest-but-significant abnormalities in the TSs and MTSs. In addition, in accord with the previous findings was a modest-but-significant increase in Raw and decrease in sGaw in the MSs but not the TSs compared to the NSs. A decrement in diffusing capacity was noted in the TSs but not the MSs.
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