We examined the impact of marijuana smoking in a population-based sample by quantifying the association between marijuana smoking and COPD using 3 definitions: as defined by spirometric testing, by self-report of a physician’s diagnosis and by self-report of respiratory symptoms. Smoking only tobacco was associated with an increased risk of COPD, as defined in all 3 ways. Smokers who reported using both marijuana and tobacco were almost 2.5 times more likely than nonsmokers to have respiratory symptoms and nearly 3 times more likely than nonsmokers to have COPD as defined by spirometric testing. These effects persisted even after we adjusted for potential confounders, such as age, sex, asthma and other comorbidities, and comparable tobacco exposure (in pack-years).
A dose-related effect of marijuana was suggested by our finding that a self-reported lifetime exposure to marijuana of at least 50 marijuana cigarettes was strongly associated with an increased risk of COPD. The significant interaction term suggested that the effects of marijuana and cigarette smoking were synergistic. We were unable to rule out clinically important respiratory effects of smoking only marijuana, because of insufficient statistical power. A much larger study is needed to address this critically important question.
Both the demographic characteristics of the study population (older adults in Vancouver) and the prevalence of smoking in our study differed from those in the published literature. Participants in our study were older than those in other studies to date.4,10,13,18
The prevalence of tobacco smoking in our study was comparatively lower. Marijuana use was as prevalent as tobacco use and was much higher than that previously reported for marijuana in the United States and Canada.3,19,20
Although studies have consistently linked long-term marijuana use to increased respiratory symptoms, studies examining the role of marijuana smoking in the development of COPD have reported conflicting results.8,10,11,13,21,22
The lack of an association between smoking only marijuana and COPD in our study is similar to that reported in the cross-sectional United States National Health and Nutrition Examination Survey. That survey studied a younger population and defined marijuana smoking as a history of at least 100 instances of marijuana use.4
Our findings also concur with those of a longitudinal study of a convenience sample of adults in Los Angeles, United States, who smoked marijuana heavily (i.e., had a mean dose of more than 3–5 marijuana cigarettes per day).11
However, our results differ from those of a longitudinal population-based study involving adults in Tucson, United States, in which nontobacco smoking (assumed to be marijuana smoking) was associated with reductions in FEV1
and in the ratio of FEV1
Our findings also differ from those of a recent case–control study involving mostly male volunteers that linked a lifetime marijuana exposure of at least 5 joint-years (1825 marijuana cigarettes) with COPD.12
Our study had several limitations. We lacked data on possible variations in the potency of marijuana smoked over a participant’s lifetime, on individual differences in method of inhalation used by smokers of only tobacco and by smokers of both tobacco and marijuana, on the proportion of smokers who combine marijuana and tobacco in the same cigarette and on the concomitant use of other illegal drugs. Our study had insufficient power to detect a modest association between smoking only marijuana and increased risk of COPD. However, we were able to detect a significant synergistic effect between marijuana smoking and tobacco smoking. This effect suggests that smoking marijuana (at least in relatively low doses) may act as a primer, or sensitizer, in the airways to amplify the adverse effects of tobacco on respiratory health. Further studies are needed to test this hypothesis.