Functions and Symptoms

This study has identified the nature and magnitude of the
effects of cannabis smoking on respiratory structure, function
and symptoms. There was a dose-response relationship of
cannabis smoking with airflow obstruction, impaired large
airways function and hyperinflation. For measures of airflow
obstruction, one joint of cannabis had a similar effect to that of
2.5–5 tobacco cigarettes. In contrast, cannabis smoking was
uncommonly associated with macroscopic emphysema, which
was present almost entirely in the tobacco smoking groups.
There are several methodological issues relevant to the
interpretation of the results. The first was the inability to
identify a sufficient number of cannabis smokers from the
random population sample. Despite starting with an initial
postal questionnaire of 3500 adults, only 19 met the criteria for
smoking at least 5 joint-years with no other illegal drug use and
no chronic respiratory disorder such as asthma in childhood. It
was apparent that it was not possible to use a random
population sample for a study of this nature and, as previously,6
a convenience sample was used. While this approach incurred
the risk of selection bias by preferentially attracting people
concerned about their respiratory health, this applies equally to
all subject groups. We applied strict exclusion criteria for other
illegal drug use due to their potential respiratory effects.18 This
meant that many potential participants were ineligible,
particularly the heaviest cannabis users who were more likely
to have used other drugs. As a result, these criteria preferentially
excluded such heavy users, suggesting that the effects
observed may represent a conservative estimate.
The requirement for tobacco smokers to have a history of at
least 1 pack-year was based on the data that tobacco smokers
need to smoke in excess of this amount to develop abnormal
lung function.19 The requirement for cannabis smokers to have
a history of at least 5 joint-years was based on the data that one
cannabis joint results in three to five times higher levels of
carbon monoxide and tar deposition, respectively,20 thereby
achieving an a priori equivalence between the lower limit of
cannabis and tobacco smoking levels. It also ensured that
tx77081 Module 1 Thorax 3/7/07 14:23:19
Table 4 Regression coefficients for association between
selected lung function variables and cannabis and tobacco
use
Lung function
variable
Cannabis association
per joint-year
OR (95% CI)
Tobacco association
per pack-year
OR (95% CI)
FEV1/FVC ratio –0.019 (–0.033 to –0.0048) –0.15 (–0.20 to –0.096)
sGaw (/s.kPa) –0.0017 (–0.0026 to –0.0009) –0.007 (–0.01 to –0.004)
FRC (l) 0.0013 (–0.00013 to 0.0027) 0.0057 (0.0005 to 0.0109)
TLC (l) 0.002 (0.0004 to 0.004) –0.0006 (–0.006 to 0.005)
FEV1, forced expiratory volume in 1 s; FRC, functional residual capacity; FVC, forced
vital capacity; sGaw, specific airways conductance; TLC, total lung capacity.
Pulmonary effects of cannabis 5
www.thoraxjnl.com
Downloaded from thorax.bmj.com on 13 October 2007
experimental users who did not smoke cannabis habitually
were excluded.
Cannabis remains illegal in New Zealand although participants
were willing to volunteer under the assurance of strict
confidentiality. All subjects in the groups with no cannabis or
no tobacco use had negative samples for THC or cotinine,
demonstrating the honest reporting of the subjects in this
regard. A further problem is that cannabis use is often difficult
to quantify precisely due to smokers sharing joints, different
inhalation techniques and different ways of smoking cannabis
including joints, pipes and bongs. In order to standardise use,
subjects were asked to estimate the ‘‘joint equivalent’’ used by
these methods to enable cannabis use to be expressed as jointyears
of use. In our community the median amount of cannabis
in a joint was 0.37 g, although there was considerable
variability in the amount of cannabis in joints prepared by
different subjects. By comparison, the average amount of
tobacco in a commercial cigarette of standard length is 1 g.
Although the calculation of joint-years was based on
subjects’ self-reports, there is evidence that cannabis use is
more accurately reported than other drugs21 and self-reports
have been shown to correlate well with urinary THC levels.22
Influential factors in increasing the validity of self-reported
drug use include privacy, anonymity and credibility of the
study. Every effort was made to create a relaxed and
confidential environment to increase the accuracy of reporting,
and all subjects gave informed consent.
The practice of combining cannabis and tobacco within a
joint is relatively uncommon in New Zealand.9 In our sample of
cannabis only smokers, 12% had combined their cannabis with
tobacco on some occasions although it was not routine practice
in any of these subjects. As a result, the small quantities of
tobacco used by cannabis only smokers were unlikely to
significantly affect the results.
As this study was exploratory, caution must be used in
interpreting the presence or absence of associations. In
particular, we analysed a number of measures of pulmonary
structure, function and symptoms without any adjustment for
the inflation of type I error that may ensue. For some variables
where we failed to find associations, this may reflect a relative
lack of statistical power for any individual analysis.
The most important finding was that one joint of cannabis
was similar to 2.5–5 tobacco cigarettes in terms of causing
airflow obstruction. This dose equivalence is consistent with the
reported 3–5-fold greater levels of carboxyhaemoglobin and tar
inhaled when smoking a cannabis joint compared with a
tobacco cigarette of the same size.20 This pattern is likely to
relate to the different characteristics of the cannabis joint and
the way in which it is smoked. Cannabis is usually smoked
without a filter23 and to a shorter butt length,24 and the smoke is
a higher temperature. Furthermore, cannabis smokers inhale
more deeply,20 hold their breath for longer20 and perform the
Valsalva manoeuvre at maximal breath hold.25
Our findings have extended previous observations that the
principal physiological impairment with long-term cannabis
smoking is on large airway function6 by demonstrating a doseresponse
relationship for sGaw. Similarly, a dose-response
relationship was observed with measures of airflow obstruction
and hyperinflation which are a consequence of the large
airways impairment. Previous research has shown that this
large airways impairment is probably due to the inflammation
and oedema that occurs in the tracheobronchial mucosa of
cannabis smokers,26 as well as mucus hypersecretion.27 It is well
recognised that an increase in airway resistance leads to
hyperinflation.28 These effects are also likely to contribute to
the increased prevalence of symptoms of wheezing, cough and
sputum production associated with cannabis smoking, resulting
in the twofold increased prevalence of chronic bronchitis.
These findings are unlikely to be due to pre-existing disease as
subjects were excluded if they had chronic lung disease
diagnosed by a doctor before the age of 16 years.
Another novel finding was the effect of cannabis smoking—
but not tobacco smoking—on lung density, which has been
proposed as a marker of emphysema.29 30 However, we and
others have observed that decreased lung density may not be
specific to emphysema10 31–34 and correlates more closely with
markers of airflow obstruction and hyperinflation.11 As a result,
we have interpreted our lung density findings as being
predominantly due to the effect of cannabis smoking on
airflow obstruction and hyperinflation rather than causing
emphysema. This interpretation is consistent with our finding
that macroscopic emphysema was present almost entirely in
the tobacco smoking groups. Furthermore, tobacco—but not
cannabis use—was associated with a significant reduction in
TLCO, the most specific lung function measure of emphysema in
subjects with airflow obstruction.35 Thus, while a case series has
shown that heavy cannabis smoking may cause macroscopic
emphysema at a young age with a characteristic apical
paraseptal pattern,8 our findings would suggest that this is
not a common complication with the amount of cannabis
smoked in New Zealand. Importantly, it suggests that cannabis
does not cause emphysema when smoked in sufficient
quantities to cause airflow obstruction, hyperinflation and
chronic bronchitis.
Finally, we observed that, whereas cannabis smokers used
similar amounts of cannabis whether or not they were tobacco
smokers as well, tobacco smokers who used cannabis smoked
less tobacco than those who smoked tobacco alone. Similarly, a
study from the USA reported that, whereas cannabis users
more often smoked tobacco, they were less likely than never
cannabis users to be heavy long-term users of tobacco, as
defined by a level of .30 pack-years.36 However, this lesser
amount of tobacco in combined users did not result in reduced
adverse respiratory effects compared with tobacco only smokers
because of the additional effects of the cannabis use.
In conclusion, these findings suggest that the predominant
effects of cannabis on pulmonary structure, function and
symptoms are in causing the symptoms of wheezing, cough,
chest tightness and sputum production, large airways obstruction
and hyperinflation, but not emphysema. The dose
equivalence of 1:2.5–5 between cannabis joints and tobacco
cigarettes in causing airflow obstruction is of major public
health significance.

ACKNOWLEDGEMENTS
The authors thank the subjects who participated in the study and
Denise Fabian, Avrille Holt, Patricia Heuser, Eleanor Chambers, Andrew
Kingzett-Taylor and the radiology and administrative staff of Pacific
Radiology Ltd for their contribution to this study.
Further data are given in fig E1 in the online
supplement available at http://thorax.bmj.com/
supplemental.
Authors’ affiliations
. . . . . . . . . . . . . . . . . . . . . . .
Sarah Aldington, Mathew Williams, Alison Pritchard, Amanda
McNaughton, Geoffrey Robinson, Richard Beasley, Medical Research
Institute of New Zealand, Wellington, New Zealand
Mike Nowitz, Pacific Radiology, Wakefield Hospital, Wellington, and
Wellington School of Medicine and Health Sciences, Wellington, New
Zealand
Mark Weatherall, Wellington School of Medicine and Health Sciences,
Wellington, New Zealand
tx77081 Module 1 Thorax 3/7/07 14:23:20
6 Aldington, Williams, Nowitz, et al

Source: www.thoraxjnl.com October 2007