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Table 1.  

Study (year) Study
design
Subjects
(n)
Results Ref.
Hancox et al.
(2010)
Observational
cohort
919 Increased lung capacity and airway
resistance in marijuana smokers. No
evidence of airway obstruction, gas
trapping or impaired gas transfer
[18]
Tan et al.
(2009)
Observational
cohort
878 Marijuana smoking not associated
with increased bronchitic symptoms
and COPD.
[17]
Sherrill et al.
(1991)
Observational
cohort
856 Pulmonary function was reduced
in subjects reporting
marijuana smoking
[50]
Tashkin et al.
(1997)
Observational
cohort
394 No effect of marijuana smoking on
FEV1 decline
[51]
Aldington
et al. 2007
Cross-
sectional
339 Marijuana associated with airflow
obstruction, hyperinflation and
large airways impairment
[11]
Bloom et al.
(1987)
Cross-
sectional
990 No effect of marijuana on FEV1
or FVC
[45]
Cruickshank
(1976)
Cross-
sectional
60 No difference between marijuana
smokers and controls
[46]
Hernandez
et al. (1981)
Cross-
sectional
23 Normal spirometry in
marijuana smokers
[47]
Moore et al.
(2005)
Cross-
sectional
6728 marijuana use not associated with
decreased FEV/FVC ratio
[48]
Sherman
et al. (1991)
Cross-
sectional
63 No significant difference in
FEV/FVC and DLco in marijuana
smokers and nonsmokers
[49]
Tashkin et al.
(1980)
Cross-
sectional
189 Marijuana smokers had lower sGaw
compared with controls (p < 0.001)
[21]
Tashkin et al.
(1993)
Cross-
sectional
542 Marijuana smoking associated with
airway hyper-responsiveness with
lose-dose methacholine
[52]
Tilles et al.
(1986)
Cross-
sectional
68 Marijuana smoking regardless of
tobacco smoking, resulted in
reduction of single breath DLco
compared with nonsmokers
[53]
Tashkin et al.
(1987)
Cross-
sectional
446 Male marijuana smokers had
reduced sGaw compared with male
tobacco smokers. No difference
in DLco.
[20]
Total:   12,613  

Epidemiological Associations Between Cannabis Use and Lung Function.

Taylor et al. performed two studies (2000 [8] and 2002 [19]) on the same cohort that have been superseded by Hancox et al. 2010 [18].
COPD: Chronic obstructive pulmonary diease; DLco: Diffusing capacity for carbon monoxide; FEV1: Forced expiratory volume; FVC: Forced vital capacity; sGaw: Specific airway conductance.

Table 2.  

Study
(year)
Pateints
(n)
Mean
age
(years)
Mean
joint-years
Results Ref.
Beshay et al.
(2007)
17 27 53 Upper lobe predominance
with bullae ranging from 0.3
to 12 cm
[23]
Johnson
et al. (2000)
4 38 NS All had upper lobe bullae
and normal lower lobes.
[40]
Gao et al.
(2010)
1 23 NS Bilateral upper lobe bullae,
more prominent on the right
[41]
Hii et al.
(2008)
10 41 74 Upper and mid-zone
emphysematous bullae
[42]
Phan et al.
(2005)
1 26 >10 Extensive cystic and bullous
lung changes primarily
affecting lower lobes
[43]
Thompson
et al. (2002)
3 39 NS Large apical lung bullae [44]

Reports of Bullous Lung Disease in Cannabis Users.

NS: Not stated.

Table 3.  

Measure Cannabis Tobacco
FEV1 ↔/↓
FVC ↑↑
FEV/FVC ratio ↓↓
TLC ↑↑ ↔/↑
RV ↑↑ ↑↑
DL
co
↓↓
sGaw ↔/↓↓

Differences in Lung Function Associated With Cannabis and Tobacco Use.

: No association; : Increase; : Decrease; DLco: Diffusing capacity for carbon
monoxide; FEV1: Forced expiratory volume; FVC: Forced vital capacity;
RV: Residual volume; sGaw: Specific airway conductance; TLC: Total
lung capacity.
Data taken from [18].

CME

Effects of Smoking Cannabis on Lung Function

  • Authors: Robert J. Hancox, MD; Marcus H.S. Lee, MD
  • CME Released: 8/22/2011
  • THIS ACTIVITY HAS EXPIRED
  • Valid for credit through: 8/22/2012
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Target Audience and Goal Statement

This activity is intended for primary care physicians, pulmonary medicine specialists, and other physicians who care for individuals who use cannabis.

The goal of this activity is to evaluate the effects of cannabis on lung function and the risk for cancer.

Upon completion of this activity, participants will be able to:

  1. Distinguish short-term effects of smoking cannabis on lung function
  2. Evaluate the long-term effects of cannabis use on lung function
  3. Describe the effects of cannabis use in promoting emphysema and lung bullae
  4. Analyze the effects of cannabis use on the risk for cancer


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Author(s)

  • Robert J. Hancox, MD

    Department of Respiratory Medicine, Waikato Hospital, Hamilton, New Zealand; Department Preventive & Social Medicine, University of Otago, Dunedin, New Zealand

    Disclosures

    Disclosure: Robert J. Hancox, MD, has disclosed no relevant financial relationships.

  • Marcus H.S. Lee, MD

    Department of Respiratory Medicine, Waikato Hospital, Hamilton, New Zealand

    Disclosures

    Disclosure: Marcus H.S. Lee, MD, has disclosed no relevant financial relationships.

Editor(s)

  • Elisa Manzotti

    Editorial Director, Future Science Group, London, United Kingdom

    Disclosures

    Disclosure: Elisa Manzotti has disclosed no relevant financial relationships.

CME Author(s)

  • Charles P. Vega, MD

    Associate Professor; Residency Director, Department of Family Medicine, University of California, Irvine

    Disclosures

    Disclosure: Charles P. Vega, MD, has disclosed no relevant financial relationships.

CME Reviewer(s)

  • Nafeez Zawahir, MD

    CME Clinical Director, Medscape, LLC

    Disclosures

    Disclosure: Nafeez Zawahir, MD, has disclosed no relevant financial relationships.

  • Sarah Fleischman

    CME Program Manager, Medscape, LLC

    Disclosures

    Disclosure: Sarah Fleischman has disclosed no relevant financial relationships.


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CME

Effects of Smoking Cannabis on Lung Function: Emphysema & Bullous Disease

processing....

Emphysema & Bullous Disease

There are now at least 36 case reports of bullous lung disease attributable to heavy cannabis smoking in English literature. These cases consistently report upper lobe predominance with relatively preserved lower lung parenchyma ( Table 2 ). Despite the presence of bullae on high resolution CT scans, lung function tests and chest x-ray appearances have largely been unremarkable in these patients. Most of these cases have been reported in young adults under the age of 45 years. This age distribution may reflect the fact that older generations may not have smoked much cannabis or may be owing to a reporting bias. How cannabis might cause such severe lung damage is not clear. It has been postulated that the methods of inhalation of cannabis smoke may cause significant barotrauma. Cannabis smokers tend to hold their breath for up to four-times longer than cigarette smokers, with a nearly 70% increase in inspiratory volume.[22] This high lung volume and breath holding results in the prolonged exposure to inhaled particulates at very high temperatures, which in turn may be responsible for epithelial injury and inflammation.

Currently, the evidence that smoking cannabis causes emphysema and bullae is limited to these case reports and therefore remains anecdotal. Although Tashkin et al. demonstrated modest short-term decreases in gas transfer (DLco) among 30 men allowed to smoke cannabis ad libitum for 94 days,[15] none of the population-based studies have been able to confirm that cannabis consumption is associated with persistent impairment of DLco.[11,15,16] This is in stark contrast to tobacco smoking, for which a reduction in DLco is probably the most sensitive indicator of parenchymal lung damage. In Aldington’s cross-sectional study, exclusive smokers of cannabis were much less likely to show evidence of emphysema on high-resolution CT scans than tobacco smokers, suggesting that macroscopic emphysema is not a common consequence of cannabis use.[11]

Even though cannabis smoking is infrequently associated with emphysema in population-based studies, two studies have found a trend towards increased static lung volumes among cannabis users. Both the cohort study by Hancox et al.[18] and the cross-sectional study by Aldington et al.[11] found greater total lung capacities among cannabis users, while Aldington also found evidence that cannabis was associated with hyperinflation on high-resolution CT scans. This is consistent with other studies demonstrating that cannabis is associated with statistically significant increases in FVC on spirometry.[17] It is difficult to interpret the significance of these increases in static and dynamic lung volumes: whereas hyperinflation is usually a feature of emphysema, this seems to be unlikely without evidence that cannabis causes either airflow obstruction (measured by FEV1/FVC ratios), impaired gas transfer (DLco), or parenchymal destruction on high-resolution CT scans.

There are at least two reasons why these observational studies conflict with numerous case reports of severe emphysematous bullae among cannabis smokers. Perhaps the most likely explanation relates to the dose of cannabis smoked. Most of the reported cases of bullous emphysema have been in very heavy cannabis smokers. For example, in the largest series of patients (n = 17) the mean lifetime consumption of cannabis was 54 joint-years.[23] Although cannabis use is very common, such prolonged heavy use is not. Even in large population-based studies there may only be a small number of heavy cannabis users. Indeed, in the cohort study by Hancox et al., none of the participants had accumulated more than a 30 joint-year history by the age of 32 (Hancox, Unpublished data). Purposeful samples, such as that used by Aldington, may be more likely to identify such heavy users, but it is important to note that Aldington et al. applied very strict exclusion criteria to their sample to exclude the possibility of respiratory effects owing to other illicit drugs. This may have also excluded the heaviest users of cannabis. The only exclusive cannabis smoker with macroscopic emphysema on high-resolution CT scanning in their study had a 437 joint-year history.[11]

The other reason why systematic studies have failed to identify the lung function changes reported in individual case reports may be that bullous lung disease is a rare complication. The number of cases reported in the literature is small in relation to the widespread use of cannabis. It is possible that, when compared to tobacco, only a relatively small proportion of people are susceptible to developing parenchymal lung damage from cannabis smoke and even then, only if they smoke a very large amount. Hence, impairment of gas transfer and macroscopic evidence of emphysema are unlikely to be detected among general population samples. This explanation would require parenchymal lung damage to be caused by a process distinct from the central inflammation that is observed in most regular cannabis users.

In summary, the existing data are unable to confirm a definite link between cannabis and bullous emphysema. However, the case reports support the likelihood that at least occasional heavy cannabis smokers are susceptible to this disease. Further evidence from systematic observational studies is required to confirm this.

Different to Tobacco?

The findings previously summarized suggest that smoking cannabis does have adverse effects on respiratory function, but contrary to what is often assumed, the pattern of damage in cannabis smokers is different from that associated with tobacco. There is now clear evidence that smoking cannabis causes inflammatory changes in the central bronchi and a consistent trend to increased airway resistance (or reduced conductance). Surprisingly, this does not appear to have a great impact on the FEV1. Trends to lower FEV1/FVC ratios have also been observed in several studies, but this seems to be owing to an increase in the FVC, rather than a reduction in FEV1. The higher FVC observed among cannabis users is consistent with evidence of hyperinflation seen on plethysmography and on CT scans. The patterns of effects associated with tobacco and cannabis smoking in a cohort of 32 year olds are compared in Table 3 .

Why cannabis and tobacco should have different effects on the lungs is not clear. As noted, other than nicotine and cannabinoids, smoke from the two substances contains a similar mix of chemicals. It is possible that tetrahydrocannibinol, a known short-term bronchodilator,[10] has long-lasting effects on lung function (although the short-term bronchodilator effect seen in single-dose studies does not persist during continued use[15]). It is also possible that differences in the concentration of some unidentified substance in the smoke results in these differences. However, it seems more likely that the different methods of smoking cannabis compared to smoking tobacco are responsible for the different effects on lung function. Cannabis is usually smoked unfiltered and the smoke from cannabis is hotter compared to filtered tobacco smoking.[22] Cannabis smokers also tend to take much deeper breaths and employ breath-holding techniques to increase the absorption of tetrahydrocannabinol as bioavailability ranges from 18 to 50%, depending on the volume of air inhaled, the depth of inhalation and the duration of retention of smoke in the alveoli.[24,25] It is possible that by using Valsalva maneuvres to increase the uptake of tetrahydrocannabinol, smokers also subject themselves to hyperexpansion of the chest and the potential for barotrauma. Interestingly, although prolonged breath-holding and Valsalva maneuvres appear to be widely used by cannabis smokers, studies indicate that is not necessary to perform these maneuvres because the psychoactive effects of cannabis are similar if it is smoked normally.[26,27]

Cannabis can also be taken in a variety of ways: either rolled and smoked like cigarettes, inhaled through specialized devices that use water filtration, bongs or such as vaporisers, and can also be consumed in cakes, beverages and oils. To date, we are not aware of any research looking specifically at the methods of cannabis delivery to the lungs and their long-term impact on lung function.

Importantly, whether cannabis and tobacco have synergistic effects on lung function is a question that remains unanswered. Most cannabis smokers also smoke tobacco and it seems likely that they would be predisposed to a combination of effects. Tan et al. found that although cannabis smoking alone was not associated with an increased risk of COPD in their sample of older adults, it appeared to increase the risk among those who also smoked tobacco.[17] However, other studies have found little evidence that cannabis modifies the effects of tobacco on lung function. Rather, the pattern of abnormalities found in those who smoke both substances suggests an additive effect or a combination of the different tobacco and cannabis effects, rather than synergistic action.[11,12,18,19]

The fact that there appears to be a difference in the pattern of lung function abnormalities associated with tobacco and cannabis does not necessarily mean that cannabis will not have a similar effect to tobacco for lung cancer and other health problems. However, conflicting reports published in recent years have also been unable to resolve the issue of whether cannabis smoking causes lung malignancies.

While it has been found that cannabis condensates are more cytotoxic, mutagenic and have a greater tendency to induce chromosomal damage and in a more erratic fashion compared with tobacco,[28] a systematic review of the evidence by Mehra et al. in 2006 failed to demonstrate a clear increased risk of lung cancer among cannabis smokers after accounting for tobacco use. They cite methodological deficiencies in the observational studies that they reviewed and a lack of adjustment for tobacco smoking as the main reason they were unable to reach the conclusion that cannabis is a cause of lung cancer.[29] The evidence that cannabis smoking causes lung cancer remains elusive.[30] For example, a large American cohort study found no evidence of an increase in overall cancer risk, and no increased risk of lung cancer in particular among cannabis smokers.[31]

Recently, a New Zealand case–control study of 79 cases of lung cancer showed a trend towards an increased risk of lung cancer of about 8% for each joint-year smoked (compared with a 7% increase in risk for each pack-year of cigarette smoking). This increase in risk was only evident for the heaviest tertile (>10.5 joint-years) of cannabis smokers who had a relative risk of 5.7 (95% CI: 1.5–21.6) after adjusting for cigarette smoking and other potential confounding variables.[32] By contrast, a larger case–control study of 2252 subjects in Los Angeles (CA, USA) did not find an increased risk of lung cancer nor for oropharyngeal cancers in cannabis smokers despite some subjects smoking very large amounts of cannabis (in excess of 60 joint-years).[33] Possible reasons for the differences between these findings include differences in study design and the selection of controls, selection bias of the cases, difficulty in quantifying cannabis use, and the difficulty in separating the effects of tobacco from those of cannabis in people who smoke both.[29,30,32] Further data are urgently required to resolve this issue.

The continuing uncertainty about the risk of lung cancer associated with cannabis highlights the problems associated with studying the effects of an illegal and unstandardized substance such as cannabis. On the other hand, these conflicting epidemiological findings are matched by contradictory biological data from in vitro studies which have found that that cannabinoids have both antineoplastic effects[34] and can also stimulate growth of lung cancer cells.[35] In fact, despite the similarities in chemical properties, the pharmacological effects of cannabis and tobacco smoke differ substantially and this may influence the carcinogenic potential of the smoke.[36]