A review paper prepared for DrugScope's submission to the Home Affairs
Drawn extensively from a technical paper by John Witton,
National Addiction Centre.
Headlines | Introduction
| Short-term effects of cannabis | Long-term
effects of cannabis | References
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.).
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
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 where appropriate.
Interpreting the evidence base
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:
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
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
prohibited status of cannabis has made the collection of epidemiological
is a lack of controlled long-term studies
cannabis use is intermittent and time-limited, with most users
stopping in their mid to late twenties.
SHORT-TERM EFFECTS OF CANNABIS
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% 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).
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).
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).
effects and driving
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.
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% and
0.10%. 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% 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).
EFFECTS OF CANNABIS
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).
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).
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-
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).
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).
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).
Cannabis may have behavioural and developmental effects on infants
exposed in utero during the first few months after birth. Between
the ages of 4 and 9 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 significance 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).
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).
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
and mental health issues
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).
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 Solowij1998). Overall, those people with schizophrenia
or a family history of schizophrenia are at a greater risk for adverse
effects from the use of cannabis (McGuire 1995).
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 4 days. However,
there are still methodological problems to be addressed in measuring
the severity of these withdrawal symptoms (Smith in press).
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 ten of those who ever use cannabis become dependent
on it during the 4-5 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 Solowij1998; 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
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.
and adolescent development
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).
Impact of increased potency of cannabis
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).
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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