Pubdate: Tue, 14 Apr 2009
Source: Canadian Medical Association Journal (Canada)
Copyright: 2009 Canadian Medical Association
Contact: This e-mail address is being protected from spambots. You need JavaScript enabled to view it
Website: 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; This e-mail address is being protected from spambots. You need JavaScript enabled to view it

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.
__________________________________________________________________________
Distributed without profit to those who have expressed a prior interest in
receiving the included information for research and educational purposes.
---
MAP posted-by: Jay Bergstrom


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