Pubdate: Tue, 14 Apr 2009
Source: Canadian Medical Association Journal (Canada)
Copyright: 2009 Canadian Medical Association
Contact:  http://www.cmaj.ca/
Details: http://www.mapinc.org/media/754
Referenced: http://www.mapinc.org/drugnews/v09/n430/a02.html
Bookmark: http://www.mapinc.org/pot.htm (Cannabis)
Author: Donald P. Tashkin, MD
Note: MAP recommends reading the commentary at
http://www.cmaj.ca/cgi/content/full/180/8/797
Note: Donald Tashkin is with the Division of Pulmonary and Critical 
Care Medicine, David Geffen School of Medicine, University of 
California Los Angeles (UCLA), Los Angeles, USA.

DOES SMOKING MARIJUANA INCREASE THE RISK OF CHRONIC OBSTRUCTIVE 
PULMONARY DISEASE?

Correspondence to: Dr. Donald P. Tashkin, Department of Medicine, 
David Geffen School of Medicine, University of California Los Angeles 
(UCLA), 10833 Le Conte Ave., Los Angeles CA 90095-1690, USA; fax 310 
206-5088; Marijuana is the second most commonly smoked substance worldwide 
after tobacco.1 The constituents of marijuana smoke are qualitatively 
and, to a large extent, quantitatively similar to those of tobacco 
smoke, with the exceptions of 9-tetrahydrocannabinol (THC), found 
only in marijuana, and nicotine, found only in tobacco. Given these 
similarities, there is concern that the health risks of regular 
marijuana smoking may be similar to those of habitual tobacco 
smoking. Chronic obstructive pulmonary disease (COPD), which is 
associated with high morbidity and mortality, is among those risks.

Over the past 2 decades, studies have addressed the possible relation 
between smoking marijuana and COPD by systematically assessing 
respiratory symptoms and measuring lung function in smokers and 
nonsmokers of marijuana or tobacco.2-8 These cross-sectional2,3,6 and 
longitudinal4,5,7 studies have used convenience sampling, random or 
stratified random sampling or birth cohorts from the general 
community. One study examined lung structure using thoracic 
high-resolution computed tomography to identify macroscopic emphysema.8

In this issue of CMAJ, Tan and colleagues report the findings of a 
cross-sectional population-based study of the possible association 
between smoking marijuana and risk of COPD.9 Whereas previous studies 
have consistently reported an association between use of marijuana 
and chronic respiratory symptoms even in the absence of concomitant 
use of tobacco,2,3,6,8 Tan and colleagues did not report a similar 
finding for marijuana only. However, they found that the concurrent 
use of marijuana and tobacco appeared to synergistically increase 
respiratory symptoms and risk of COPD.

An association between using marijuana and COPD has been suggested by 
evidence of proximal airway injury (i.e., increased erythema, edema 
and mucous secretions) observed during bronchoscopy in both 
marijuana-only and tobacco smokers.10 Such an association has also 
been suggested by histopathologic evidence of goblet cell metaplasia, 
loss of ciliated columnar epithelial cells and inflammatory changes 
in the bronchial mucosa of smokers of marijuana and smokers of both 
marijuana and tobacco.10,11

The evidence for an association between use of marijuana and 
abnormalities in lung function, however, is inconsistent. In a 
convenience sample of young men (mean age 33 years) in Los Angeles, 
United States, who were habitual, heavy smokers of marijuana or 
tobacco and nonsmoking controls (n = 446), smoking only marijuana was 
not associated with abnormalities in forced expiratory volume in 1 
second (FEV1), forced vital capacity (FVC), ratio of FEV1 to FVC, 
various measures of small airway function or single-breath diffusing 
capacity for carbon monoxide.2 However, a modest decrease in specific 
airway conductance was observed in those who smoked only marijuana. 
This decrease was consistent with endoscopic observations of slight 
narrowing of the central airways and edematous changes in the 
tracheobronchial mucosa in this subgroup.10 An 8-year longitudinal 
extension of this study did not show an age-related accelerated 
decline in FEV1 among participants who smoked only marijuana compared 
with participants who did not smoke marijuana or tobacco. There was a 
significant accelerated decline among those who smoked tobacco.5

By contrast, an epidemiologic study in Tucson, United States, 
involving participants aged 15-40 years (n = 585) found a slight but 
significant decrease in the ratio of FEV1 to FVC and in a measure of 
obstruction of the small airways among participants who used 
marijuana independent of tobacco.3 A related longitudinal study in 
Tucson involving 856 participants aged 15-60 years showed slight 
decreases in FEV1 and in the ratio of FEV1 to FVC among those who had 
previously smoked marijuana but not among those who currently smoked 
marijuana.4 In a birth cohort of 1037 participants aged 21 years in 
Dunedin, New Zealand, a reduced ratio of FEV1 to FVC (using a 
threshold of ( 80%) was found in a significantly higher percentage of 
participants who showed signs of marijuana dependency and did not 
smoke tobacco than in participants who smoked neither marijuana nor 
tobacco (36% v. 20%) (p 0.04).6 In the same cohort, longitudinal 
observations of participants up to 26 years of age showed a 
nonsignificant trend toward a dose-dependent relation between 
cumulative use of marijuana and a decreased ratio of FEV1 to slow 
vital capacity after adjustment for smoking tobacco and other 
covariates (p = 0.082).7 The results of this study also suggested an 
additive influence of marijuana and daily use of tobacco.

In a convenience sample of 339 residents of Wellington, New Zealand, 
aged 18-70 years (mean age 43.4) comprising nonsmokers and smokers of 
either marijuana only, tobacco only or both substances, the authors 
reported that there was no association between use of marijuana and 
abnormalities in lung function (including lung volume and diffusing 
capacity).8 However, regression analyses with marijuana as a 
continuous variable showed significant associations between lifetime 
cumulative use of marijuana and airflow obstruction (measured by both 
the ratio of FEV1 to FVC and specific airway conductance) and between 
use of marijuana and hyperinflation (measured by total lung 
capacity). The same study did not show an association between smoking 
marijuana and evidence of macroscopic emphysema, as shown by 
high-resolution computed tomography.

These studies, involving mainly younger individuals, have provided 
inconsistent but suggestive evidence that smoking marijuana only may 
lead to modest airflow obstruction and hyperinflation that could 
predispose the individual to COPD later in life. The findings of Tan 
and colleagues9 add to the limited evidence of an association between 
use of marijuana and COPD because their study focuses on an older 
population (aged 40 or older) that is at greater risk of COPD. Their 
finding that concurrent smoking of marijuana and tobacco is 
associated with a greater likelihood of COPD than smoking only 
tobacco implies a possible additive effect of the 2 substances on 
lung health. An additive effect was also suggested by Taylor and 
colleagues,7 whose study involved a younger population. By contrast, 
Aldington and colleagues8 concluded that concurrent smoking of 
marijuana and tobacco attenuated the association between smoking 
tobacco and a reduced ratio of FEV1 to FVC and respiratory symptoms.

Firm conclusions cannot be drawn about the association between use of 
marijuana and COPD based on the limited and inconsistent data 
available. The studies that address this topic are limited by their 
small numbers of participants and by the uncertain accuracy of 
self-reported use of marijuana, particularly in view of its 
illegality and the difficulty of accurately recalling amounts 
previously used. Some of these studies are also limited by their 
cross-sectional design, and most are limited by the young age (40 
years or younger) of participants. Nevertheless, the consistency of 
some aspects of the available data allows us to more firmly conclude 
that smoking marijuana by itself can lead to respiratory symptoms 
because of injurious effects of the smoke on larger airways. Given 
the consistently reported absence of an association between use of 
marijuana and abnormal diffusing capacity or signs of macroscopic 
emphysema, we can be close to concluding that smoking marijuana by 
itself does not lead to COPD.

See related research paper by Tan and colleagues, page 814: 
http://www.cmaj.ca/cgi/content/full/cmaj;180/8/814

Key points

Given the increased risk of chronic obstructive pulmonary disease 
(COPD) among smokers of tobacco, there is concern that a similar risk 
may exist among smokers of marijuana.

A limited body of evidence suggests an association between regular 
marijuana smoking and adverse effects on respiratory health. Studies 
that address this possibility have many limitations, however.

The finding by Tan and colleagues that smoking both marijuana and 
tobacco is associated with a greater risk of COPD than smoking only 
tobacco suggests an additive effect of the 2 substances on lung 
health. This study involved an older population that is more at risk of COPD.

Marijuana smoking by itself probably does not lead to COPD.

Footnotes

Competing interests: None declared.

REFERENCES

1. World drug report 2006. New York (NY): United Nations Office on 
Drugs and Crime; 2006. Available: 
www.unodc.org/pdf/WDR_2006/wdr2006_volume1.pdf (accessed 2009 Mar. 18)

2. Tashkin DP, Coulson AH, Clark VA, et al. Respiratory symptoms and 
lung function in habitual, heavy smokers of marijuana alone, smokers 
of marijuana and tobacco, smokers of tobacco alone, and nonsmokers. 
Am Rev Respir Dis 1987;135:209-16.

3. Bloom JW, Kaltenborn WT, Paoletti P, et al. Respiratory effects of 
non-tobacco cigarettes. BMJ 1987;295:1516-8.

4. Sherrill DL, Krzyzanowski M, Bloom JW, et al. Respiratory effects 
of non-tobacco cigarettes: a longitudinal study in general 
population. Int J Epidemiol 1991;20:132-7.

5. Tashkin DP, Simmons MS, Sherrill DL, et al. Heavy habitual 
marijuana smoking does not cause an accelerated decline in FEV1 with 
age. Am J Respir Crit Care Med 1997;155:141-8.

6. Taylor DR, Poulton R, Moffitt TE, et al. The respiratory effects 
of cannabis dependence in young adults. Addiction 2000;95:1669-77.

7. Taylor DR, Fergusson DM, Milne BJ, et al. A longitudinal study of 
the effects of tobacco and cannabis exposure on lung function in 
young adults. Addiction 2002;97:1055-61.

8. Aldington S, Williams M, Nowitz M, et al. Effects of cannabis on 
pulmonary structure, function and symptoms. Thorax 2007;62:1058-63.

9. Tan WC, Lo C, Jong A, et al.; for the Vancouver Burden of 
Obstructive Lung Disease (BOLD) Research Group. Marijuana and chronic 
obstructive lung disease: a population-based study. CMAJ 2009;180:814-20.

10. Roth MD, Arora A, Barsky SH, et al. Airway inflammation in young 
marijuana and tobacco smokers. Am J Respir Crit Care Med 1998;157:928-37.

11. Fligiel SE, Roth MD, Kleerup EC, et al. Tracheobronchial 
histopathology in habitual smokers of cocaine, marijuana, and/or 
tobacco. Chest 1997;112:319-26.

Related Articles

Highlights

Can. Med. Assoc. J. 2009 180: 789.

Marijuana and chronic obstructive lung disease: a population-based study

Wan C. Tan, Christine Lo, Aimee Jong, Li Xing, Mark J. FitzGerald, 
William M. Vollmer, Sonia A. Buist, Don D. Sin for the Vancouver 
Burden of Obstructive Lung Disease (BOLD) Research Group Can. Med. 
Assoc. J. 2009 180: 814-820.
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MAP posted-by: Jay Bergstrom