Pulmonary Effects of Marijuana Inhalation

Megan L Howden; Matthew T Naughton


Expert Rev Resp Med. 2011;5(1):87-92. 

In This Article

Lung Function

Studies examining the effect of marijuana smoking on lung function have produced somewhat variable results. This is likely to be related to the difficulty in obtaining random samples of smokers and the potential for under-reporting of marijuana use due to its illegal status. In addition, correcting for variables such as tobacco smoking may be difficult or virtually impossible in the case of differences in smoking technique.

In the same study as mentioned earlier, Tashkin et al. compared a convenience sample of 144 heavy smokers of marijuana alone to nonsmokers, smokers of tobacco alone and smokers of both substances over an 8-year period.[14] This study involved subjects from the Los Angeles area (USA) who undertook detailed respiratory questionnaires and lung-function assessment. Smokers of marijuana had no significant difference in FEV1, FVC, FEV1/FVC or diffusion lung capacity for carbon monoxide (DLCO) compared with nonsmokers. These spirometry findings were similar in a number of other studies, both cross-sectional and longitudinal.[4,12,17] Interestingly, however, there was a modest but statistically significant increase in airway resistance and reduction in specific airway conductance in smokers of marijuana compared with both nonsmokers and tobacco smokers. The findings of Aldington et al. were similar in their study of a convenience sample of 339 subjects in the Greater Wellington region of New Zealand.[10] In this study, airway conductance was reduced in both marijuana and tobacco smokers compared with nonsmokers, although the significance was small in tobacco smokers. In addition to this, FEV1/FVC was reduced in marijuana smokers due to an increased FVC, although with only marginal significance. There was no significant difference in FEV1 alone. Of note, total lung capacity was marginally increased in marijuana but not tobacco smokers.

An early study by Tilles et al. involved the recruitment of 15 regular marijuana smokers who underwent assessment of spirometry as well as DLCO and lung volumes.[18] In this case, FEV1 and FVC were both increased in marijuana smokers compared with nonsmokers and tobacco-alone smokers, similar to the findings of Bloom et al.[19] and Tan et al..[2] Total lung capacity was also significantly elevated.

A small number of longitudinal studies have similarly revealed conflicting results. The longest of these involved a birth cohort of 1037 subjects born in New Zealand in 1972–1973.[12] Marijuana and tobacco use was reported at ages 18, 21, 26 and 32 years. Lung function tests were performed at 32 years of age. While FEV1 and DLCO were not significantly different in marijuana smokers compared with nonsmokers, FVC, total lung capacity, functional residual capacity and residual volume were all elevated. Similar to cross-sectional studies described previously,[10] there was also an increase in airway resistance in marijuana smokers. A second longitudinal study by Tashkin et al. also found little difference in FEV1 with marijuana smoking in 255 subjects over an 8-year period.[17]

By contrast, another longitudinal study found long-term marijuana smoking to be associated with reduced FEV1/FVC, FEV1 and maximal expiratory flow at 50% of FVC.[15]

Overall, the majority of studies suggest that marijuana smoking may be associated with elevated lung volumes and slightly greater airway resistance but no change, or an increase, in spirometry values. This all suggests that hyperinflation may be one of the primary physiological abnormalities in marijuana smokers. The increased airway resistance and reduced conductance is consistent with mucosal edema and inflammation, which has been observed in the large airways of marijuana smokers.[11] It is not clear whether this large airway pathology contributes to the observed effect of hyperinflation with marijuana smoking. Measures of small airway dysfunction (mid-expiratory flows) in a small number of studies again had varying results, with one showing a reduction in mean midexpiratory flow in tobacco but not marijuana smokers,[10] and the other indicating a drop in small airway function more apparent with marijuana than with tobacco use.[19]

Overall, these findings are obviously in contrast to those seen with prolonged tobacco exposure. Tobacco is known to cause chronic obstructive pulmonary disease primarily with an obstructive defect of spirometry with associated decline in gas transfer. Marijuana smoking does not appear to impair DLCO,[12,14] although a single study did suggest marijuana in combination with tobacco resulted in further impairment of gas transfer than seen with tobacco alone.[18] In addition, Tashkin et al. performed several different types of measurements of small airway function (including maximal mid-expiratory flow rates, closing volume, closing capacity and the change in nitrogen concentration per liter of exhaled air) and found that the mean values were normal in smokers of marijuana only but abnormal in smokers of tobacco.[14]

In addition to variable changes in lung function, there have been numerous case reports of an association between marijuana smoking and bullous lung disease in relatively young subjects.[20–25] Commonly, these bullae are located apically and appear to be associated with normal lung function in some cases, though severe impairment has also been noted. Subjects were mainly aged 20–45 years, although one subject was 19 years of age,[20] and another was 55.[21] Unfortunately, it is difficult to separate marijuana use from tobacco smoking which does confound these reports. Nevertheless, there appears to be an association between bullous disease and marijuana use in a subset of patients. Aldington et al. also found evidence of reduced lung density on high-resolution CT (HRCT) scanning in marijuana smokers, although in this case without macroscopic emphysema.[10] It is possible that these changes are in part responsible for the common presentation of spontaneous pneumothoraces in marijuana smokers,[20] although pneumothoraces are not at all uncommon in young, healthy nonsmokers. It has also been suggested that barotraumas associated with large pulmonary pressure swings seen with breath holding and deep inspiration may contribute to the risk of pneumothoraces.[24]

Gill reviewed the histopathological findings of ten cannabis smokers who presented with spontaneous pneumothoraces and subsequently underwent bullectomy with video-assisted thoracoscopic surgery.[26] The main findings were a predominance of intra-alveolar pigmented histiocytes. There was associated interstitial scarring and irregular bullae and blebs. This is in contrast to tobacco smokers who had a relatively minor accumulation of pigmented histiocytes. The authors suggested that it may be the pattern of inhalation common with marijuana smoking that is responsible for these findings.


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