CANNABIS-RELATED HEALTH RISKS DRAWN EXTENSIVELY
FROM A TECHNICAL PAPER BY JOHN WITTON, NATIONAL ADDICTION CENTRE
Any review of the possible health implications
of cannabis needs to be placed in the comparative perspective
of what is known about alcohol and tobacco, two other widely used
psychoactive drugs. Cannabis shares with tobacco, smoking as the
usual route of administration and resembles alcohol in being used
for intoxicating and euphoric effects. The comparison serves the
useful purpose of reminding us of the risks we currently tolerate
with our most widely used psychoactive drugs (Hall, W et al, 1996.).
Cannabis is not a harm-free drug.
It is important to look at cannabis
in the context of the risks society already accepts.
The primary health problems associated
with the drug are the possibility of respiratory disorders similar
to those experienced by tobacco smokers.
Cannabis use may also exacerbate
existing mental health problems.
Many of the other possible risks
from using cannabis remain unproven or inconclusive.
Due to the nature of the evidence
it is important that policy makers assess the likely health impact
on the greatest number, rather than extrapolating from individual
case studies or those involving surveys with only small samples.
In relation to the millions of individuals
who have been exposed to the drug in this country since the late
1960s, cannabis compares favourably (in terms of health implications)
with legal drugs widely used such as alcohol and tobacco.
1. This paper summarises the best currently
available evidence for the adverse effects of cannabis use. The
evidence is predominantly drawn from studies involving humans.
There is inconclusive evidence available in a number of areas
and this will be indicated where appropriate.
2. This paper is based in a number of authoritative
major reviews of the cannabis research literature conducted in
the last decade and supplemented by more recent research reports
3. Much of the research evidence reviewed
derives from American studies, although there is increasing evidence
emerging from Australian research. There are a number of difficulties
in assessing the value of this evidence:
the main psychoactive component of
cannabis is tetrahydrocannabinol (THC) and apart from laboratory
studies, it is difficult to ascertain the amount of THC consumed
by cannabis users.
cannabis is often used with other
substances, most commonly alcohol and tobacco, which may also
have adverse effects on health and make it difficult to distinguish
the effects of cannabis from those of these substances
the prohibited status of cannabis
has made the collection of epidemiological evidence difficult
there is a lack of controlled long-term
most cannabis use is intermittent
and time-limited, with most users stopping in their mid to late
4. The reported effects of cannabis use
are a sense of euphoria and relaxation, perceptual distortions,
time distortion and the intensification of sensory experiences
such as listening to music. Cannabis use in social settings can
lead to increased talkativeness and infectious laughter followed
by states of introspection and dreaminess. The user typically
has a feeling of greater emotional and physical sensitivity that
can include greater interpersonal empathy. Short-term memory and
attention are also impaired. (Hall 1998; Joy et al. 1999).
5. Cannabis use can increase the heart rate
by 20-100 per cent above baseline. This increase is greatest in
the first 10 to 20 minutes then decreases rapidly thereafter.
The rate of decrease depends on whether smoked or oral cannabis
is used, lasting three hours in the former and five hours in the
latter (Graham 1986; Hall et al. 1994; Joy et al. 1999). Blood
pressure is increased while the person is sitting and decreased
while standing. The change from sitting to standing can cause
faintness and dizziness due to the change in blood pressure. These
cardiovascular effects are of negligible clinical significance
because most cannabis users are young and healthy and develop
tolerance to these effects (Hall 1994; 1998; Joy et al. 1999).
6. Adverse mood effects can occur, particularly
in inexperienced users, after large doses of cannabis. Anxiety
and paranoia are the most common of these effects and others include
panic, depression, delusions and hallucinations. These effects
normally disappear after a few hours after cessation of use and
are responsive to reassurance and a supportive environment (Adams
and Martin 1996; Joy et al. 1999).
7. The acute toxicity of cannabis is very
low and there is no overdose risk from cannabis. There are no
confirmed published cases of human deaths related to cannabis
poisoning (Hall 1998).
8. Cannabis produces dose-related impairments
in a wide range of behavioural and cognitive functions. These
include slowing reaction time and information processing, and
impairing perceptual and motor performance, tracking behaviour
and time perception. These effects can increase with the dose
of THC and are larger and more persistent with tasks that require
sustained attention (Chait and Pierri 1992). These effects may
have implications for accidents if the users drive or operate
machinery while intoxicated.
9. Laboratory driving simulator and standardised
road studies have found impairments in driving skills after cannabis
use, similar to those effects when blood alcohol levels are between
0.07 per cent and 0.10 per cent. However more realistic on-road
and simulator studies have found that cannabis drivers tend to
be more cautious and drive more slowly, compared to alcohol-intoxicated
drivers. This may be because they are aware of their intoxication
and take appropriate precautions (Hall et al 1994; Smiley 1998).
10. Epidemiological evidence for the role
of cannabis in road accidents is equivocal. UK studies have found
traces of illicit drugs in 18 per cent of those killed in fatal
accidents, with cannabis constituting around two thirds of the
drugs found (Sexton et al 2001). However, because traces of cannabis
can remain in the body system for up to 28 days the presence of
cannabinoids in the blood of accident victims cannot be taken
to indicate that the driver was intoxicated at the time of the
accident. Many drivers in accidents also have a high blood alcohol
level at the time of their accident. Two studies with drivers
who had only used cannabis found that there was no increased culpability
of accidents amongst this group (Chesher 1995).
11. Cannabis smoke contains many of the
same components as tobacco smoke. As much as four times the amount
of tar can be deposited on the lungs of cannabis smokers as cigarette
smokers if a cigarette of comparable weight is smoked. This difference
is probably the result of differences in administration. Cannabis
cigarettes usually do not have filters and cannabis smokers usually
develop a larger puff volume, inhale more deeply and hold their
breath several times longer than tobacco smokers (Joy et al 1999).
12. Chronic smoking effects are similar
to those of tobacco smoking. Chronic heavy use of cannabis is
associated with increased symptoms of chronic bronchitis such
as coughing and wheezing. Lung function is impaired and there
are greater abnormalities in the large airways of cannabis smokers
than non-smokers. Cannabis smoking is associated with changes
in bronchial tissue. Many cannabis smokers have erythema (increased
redness of airway tissues) and edema (swelling of the airway tissues).
(Joy et al 1999). Studies have shown that people who are regular
users of cannabis but not tobacco have more symptoms of chronic
bronchitis than non-smokers (Hall 2001).
13. There is no conclusive evidence that
cannabis causes cancer in humans including those cancers associated
with tobacco use. However, cellular, genetic and human studies
suggest that cannabis smoke may be an important risk factor for
the development of respiratory cancer. There is not yet any evidence
from controlled studies showing a higher rate of respiratory cancers
among chronic cannabis smokers. However there is evidence of an
additive effect of cannabis and tobacco smoking on abnormalities
in lung tissue, similar to those that precede lung cancer in tobacco
smokers (Joy et al, 1999; Tashkin, 1999; Hall, 2001). These effects
are related to the amount of cannabis smoked and it has been argued
that cannabis smokers will not smoke as much as tobacco smokers
or smoke as long in their lives. Most cannabis users have stopped
using cannabis by their mid- to late-twenties.
14. There have been case reports of cancers
in the digestive tract of young adults with a history of heavy
cannabis use. These findings are significant because these kinds
of cancers are rarely found in the adults under the age of 60,
even among those who smoke tobacco and drink alcohol. This suggests
that cannabis smoking may potentate the effects of other risk
factors such as tobacco smoking and is a more important risk factor
than tobacco and alcohol use in the early development of respiratory
cancers (Sridhar 1994; Joy et al 1999; Hall 2001).
15. THC has been found to inhibit reproductive
function in the few human studies reported although these studies
have yielded inconsistent evidence. On the basis of research on
animals it has been argued that cannabis would probably decrease
fertility for both men and women in the short term (Hall et al
1994; Joy et al 1999). It has been suggested that in this respect
the possible effects of cannabis use may be most significant for
those males whose fertility is already impaired, for example those
with a low sperm count (Hall et al 1994).
16. The results of research studies on the
effects of prenatal cannabis use and birth outcome have been small
and inconsistent. Some studies have suggested that cannabis smoking
in pregnancy may reduce birthweight. A controlled study has found
this relation has remained after controlling for any confounding
variables but this relation has not been found in other studies
(Zuckerman et al 1989; Hall and Solowij 1998; Joy et al 1999).
The effects of cannabis smoking where the study has found an association
has been small compared to tobacco (Fried 1998). There is little
evidence that gestation is shorter except for adolescent mothers
(Cornelius et al 1995). Large well-controlled epidemiological
studies have found no evidence that cannabis causes birth defects
(Zuckerman et al 1989).
17. Cannabis may have behavioural and developmental
effects on infants exposed in utero during the first few months
after birth. Between the ages of four and nine children who have
been exposed to cannabis in utero have shown deficits in sustained
attention, memory and cognitive functioning. However the effects
were small compared to tobacco and their clinical significant
is unclear. The underlying causes might be the cannabis exposure
or might be more closely related to the reasons underlying the
mothers' use of cannabis during pregnancy (Fried 1998; Hall and
Solowij 1998; Joy et al 1999).
18. Recent case studies have found an increased
risk of child cancers in children born to mothers who reported
using cannabis during their pregnancies. However cannabis was
one amongst several factors considered in the analysis of the
data from these studies and this area requires further study (Hall
and Solowij 1998).
19. There is no conclusive evidence that
cannabis impairs immune function to any significant extent. The
few studies that have suggested that cannabis has an adverse effect
on the immune system have not been replicated.
20. There is evidence that large doses of
THC can produce an acute psychosis marked by confusion, amnesia,
delusions, hallucinations, anxiety, and agitation. Such reactions
are rare and occur usually after heavy cannabis use, or in some
instances, after acute cannabis use by sensitive/vulnerable individuals.
These effects abate rapidly after discontinuing cannabis use.
There is little evidence that cannabis alone produces a psychosis
that persists after the period of intoxication (Hollister 1986;
Hall 1998; Joy et al 1999).
21. A Swedish study found an association
between cannabis use and schizophrenia. In this prospective study
of 50,000 Swedish conscripts a dose response relation was found
between the frequency of cannabis use and the risk of a diagnosis
of schizophrenia over the next 15 years (Andreasson et al. 1987).
Although the value of this study has been debated (Negrete 1989;
Hall 1998), it has been suggested that cannabis use may exacerbate
the symptoms of schizophrenia and a prospective study has found
that continued cannabis use predicts more psychotic symptoms in
people with schizophrenia (Linszen et al. 1990). However, the
incidence of schizophrenia has decreased in recent years whilst
the use of cannabis has increased. Hall suggests that, this may
indicate that cannabis use is unlikely to have caused cases of
schizophrenia that might not have otherwise occurred. Chronic
cannabis use may precipitate cannabis in vulnerable individuals
but not cause the underlying psychotic disorder, an effect that
would not change reported incidence (Hall and Solowij 1998). Overall,
those people with schizophrenia or a family history of schizophrenia
are at a greater risk for adverse effects from the use of cannabis
22. Heavy smokers of cannabis develop tolerance
to the subjective and cardiovascular effects of cannabis. Some
users report a withdrawal syndrome on cessation of use with symptoms
that may include restlessness, irritability, mild agitation, insomnia,
sleep disturbance, nausea and cramping. Controlled laboratory
studies have observed withdrawal symptoms which were short lived
and abated after four days. However, there are still methodological
problems to be addressed in measuring the severity of these withdrawal
symptoms (Smith in press).
23. There is some evidence that a cannabis
dependence syndrome occurs with heavy cannabis use marked by difficulty
in controlling use and continued use despite experiencing adverse
personal consequences (Stephens et al 1993; Swift et al 1999).
American studies have found that about one in 10 of those who
ever use cannabis become dependent on it during the four-five
years of heaviest use (Anthony et al 1994). However, the risk
of dependence is more like that for alcohol, than tobacco and
opioids (Hall and Solowij 1998; Joy et al 1999). This may be due
to differences in drug effects, its availability or the penalties
associated with the use of the drug or some combination of these.
24. Studies have shown that cannabis can
produce a subtle impairment of attention, memory and the organisation
and integration of complex information (Block and Ghoneim 1993;
Joy et al 1999). The longer the cannabis use the more pronounced
the impairment. These impairments are subtle and it remains unclear
whether these effects are reversed after an extended period of
abstinence or what implications they may have for everyday functioning
(Hall and Solowij 1998; Solowij 1998). In addition, researching
this complex area is difficult: for example there has been criticism
of the adequacy of matching cannabis uses with control subjects
in those studies on cognitive deficits in heavy cannabis users
(Joy et al 1999). There is no evidence for the scale of severe
or debilitating impairment of memory, cognitive function and attention
found with chronic heavy alcohol use. There is no evidence that
cannabis causes structural brain damage in humans.
25. There is no evidence to support a causal
relationship between cannabis use and those behavioural characteristics
which have been described as an amotivational syndrome (Joy et
al 1999). Studies have shown an association between heavy cannabis
use in adolescence and the risk of leaving school early and of
experiencing job instability in young adulthood. However, the
strength of these associations are reduced in longitudinal studies
when the low educational aspirations and poorer school performance
of heavy cannabis users before their cannabis use is taken into
account (Fergusson and Horwood 1997; Hall 1998). On balance the
evidence available suggests that daily or near daily cannabis
use does not improve the educational performance of those who
were performing poorly already (Lynskey and Hall 2000).
26. High THC-containing cannabis seems to
have become increasingly available although the published evidence
for this is scant (Hall and Swift 1999; Ashton 2001). This may
reflect an increased market for more potent cannabis amongst regular
users and improved methods of growing high potency cannabis. The
health implications of this development are unclear. Those who
use these high potency products may increase their risks of developing
dependence, having accidents while driving or experiencing psychotic
symptoms (Hall 1998). However, regular users may be able to titrate
their dose and decrease the risks of respiratory disease and naive
users who experience adverse effects may be deterred from further
cannabis use (Hall 1998).
27. Cannabis is not a harm-free drug. The
primary problems with the drug focus mainly on the possibility
of respiratory disorders similar to those experienced by tobacco
smokers and the risk of exacerbating existing mental health problems.
Many of the other possible risks from using cannabis remain unproven
or inconclusive. In using this data to help formulate policy that
will impact on many individuals, it is helpful to think of the
likely health impact on the greatest number, rather than extrapolating
from individual case studies or those involving surveys with only
small samples. In relation to the millions of individuals who
have been exposed to the drug in this country since the late 1960s,
cannabis compares favourably (in terms of health implications)
with legal drugs widely used such as alcohol and tobacco.
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