The health and psychological consequences of cannabis use chapter 1
National Drug Strategy
Monograph Series No. 25
1. Summary of report
Introduction
This review of the literature on the health and psychological effects
of cannabis was undertaken at the initiative of the former Federal
Justice Minister, Senator Michael Tate, who requested a review of
knowledge relating to cannabis, to inform policy decisions. At Senator
Tate's urging, a National Task Force on Cannabis was established on 25
May 1992. The Task Force commissioned this review of the evidence on
the health and psychological effects of cannabis use. A new and
independent review was thought necessary because there has not been
any major international review of the literature on the health and
psychological effects of cannabis since 1981, when the Addiction
Research Foundation and World Health Organization jointly reviewed the
literature. The purpose of this review was to update the conclusions
of earlier reviews in the light of research undertaken during the past
decade.
Our approach to the literature
Our review of the literature was not intended to be as comprehensive
as the major review undertaken by the Addiction Research Foundation
and the World Health Organization. The literature is too large, and
the diversity of relevant disciplines represented in it beyond the
expertise we had available for the task. Unavoidably, we have relied
upon expert opinion in the areas that lie outside the authors'
collective expertise which is primarily in areas of epidemiology,
psychiatry, psychopharmacology, neurophysiology and neuropsychology.
In order to minimise the effects of our lack of expertise in certain
areas we have relied upon the consensus views expressed in the
literature by experts in the relevant fields. When there has been
controversy between the experts we have explicitly acknowledged areas
of disagreement. We have checked our understanding and representation
of these expert views by asking Australian and overseas researchers
with expertise in the relevant fields to critically review what we
have written.
Our approach to assessing the health effects of cannabis
The evaluation of the health hazards of any drug is difficult for a
number of reasons. First, causal inferences about the effects of drugs
on human health are difficult to make, especially when the interval
between use and alleged ill effects is a long one. It takes time for
adverse effects to develop and for research to identify such effects.
Second, in making causal inferences there is a tension between the
rigour and relevance of the evidence. The most rigorous evidence is
provided by laboratory investigations using animals or in vitro
preparations (e.g. cell preparations in a test tube) in which well
controlled drug doses are related to precisely specified biological
outcomes. The relevance of this evidence to human disease is
uncertain, however, because many inferences have to be made in linking
the occurrence of specific biological effects in laboratory animals to
the likely effects of human use. Epidemiological studies of
relationships between drug use and human disease are of greater
relevance to the appraisal of the health risks of human drug use, but
their relevance is purchased at the price of reduced rigour. Doses of
illicit drugs over periods of years are difficult to quantify because
of the varied dosages of blackmarket drugs and the stigma in admitting
to illicit drug use. Interpretation is further complicated by
correlations between cannabis use and alcohol, tobacco and other
illicit drug use.
Third, appraisals of the hazards of drug use are affected by the
social approval of the drugs in question. The countercultural
symbolism of cannabis use in the late 1960s has introduced an
unavoidable sociopolitical dimension to the debate about the severity
of its adverse health effects. Politically conservative opponents of
cannabis use justify continued prohibition by citing evidence of the
personal and social harms of cannabis use. When the evidence is
uncertain they resolve uncertainty by assuming that the drug is unsafe
until proven safe. Complementary behaviour is exhibited by proponents
of cannabis use. Evidence of harm is discounted and uncertainties
about the ill-effects of chronic cannabis use resolved by demanding
better evidence, arguing that until such evidence is available
individuals should be allowed to choose whether or not they use the
drug.
Such evidential standards are rarely applied consistently. The
politically conservative would reject a similar approach to the
appraisal of the health hazards of industrial processes. Similarly,
proponents of cannabis liberalisation rarely apply the principles used
in their risk assessment of cannabis to the appraisal of the health
effects of pharmaceutical drugs, industrial processes, and pesticides.
To guard against such double evidential standards we will be as
explicit as possible about the evidential standards we have used, and
attempt to be as even-handed as we can in their application.
Evidential desiderata
The burden of proof concerns who bears the responsibility for making a
case: those who make a claim of adverse health effects of cannabis, or
those who doubt it. If the burden falls on those who claim that it is
safe, uncertainty will be resolved by assuming that it is unsafe until
proved otherwise; conversely, if the burden falls on those who claim
that the drug is unsafe, then it will be assumed to be safe until
proven otherwise.
It is by no means agreed who bears the burden of proof in the debate
about the health effects of cannabis use. Proponents of continued
prohibition appeal to established practice, arguing that since the
drug is illegal the burden of proof falls upon those who want to
legalise it; opponents of existing policies argue that the burden of
proof falls upon those who wish to use the criminal law to prevent
adults from freely choosing to use a drug.
We will vary the burden of proof depending upon the state of the
evidence and argument. Once a prima facie case of harm has been made,
positive evidence of safety is required rather than the simple absence
of any evidence of ill effect. We will assume that a prima facie case
has been made when there is either direct evidence that the drug has
ill effects in humans or animals (e.g. from a case-control study), or
there is a compelling argument that it could, e.g. since tobacco
smoking causes lung cancer, and since cannabis and tobacco smoke are
similar in their constituents, it is probable that heavy cannabis
smoking also causes lung cancer.
Standard of proof reflects the degree of confidence required in an
inference that there is a causal connection between drug use and harm.
In courts of law, the standard of proof demanded depends upon the
seriousness of the offence at issue and the consequences of a verdict,
with a higher standard of proof, "beyond reasonable doubt", being
demanded in criminal cases, and the "balance of probabilities" being
acceptable in civil cases. Scientists generally require something
closer to the standard of "beyond reasonable doubt" than the balance
of probabilities before they draw confident conclusions of harm.
However, since there are few adverse health effects of cannabis use
which meet this standard, we will indicate when the evidence permits
an inference to be made on the balance of probabilities.
The criteria for causal inference that we will use are standard ones.
These are: (1) evidence that there is a relationship between cannabis
use and a health outcome provided by one of the accepted types of
research design (namely, case-control, cross-sectional, cohort, or
experiment); (2) evidence provided by a statistical test or confidence
interval that the relationship is unlikely to be due to chance; (3)
good evidence that drug use precedes the adverse effect (e.g. from a
cohort study); and (4) evidence either from experiment, or
observational studies with statistical or other form of control, which
makes it unlikely that the relationship is due to some other variable
which is related to both cannabis use and the adverse health effect.
In the trade-off between relevance and rigour, our preference will be
for human evidence, both experimental and epidemiological, over animal
and in vitro studies. In the absence of human evidence, in vitro and
animal experiments will be regarded as raising a suspicion that drug
use has an adverse effects on human health, with the degree of
suspicion being in proportion to the number of such studies, the
consistency of their results across different species and experimental
preparations, and the degree of expert consensus on the
trustworthiness of the inferences from effects in vitro and in vivo to
adverse effects on human health under existing patterns of usage.
Ideally, it would be desirable to quantify the magnitude of risk posed
by cannabis use by estimating both the relative and attributable risks
of specific health effects. However, since there is generally
insufficient evidence to estimate these risks for many putative
adverse effects of cannabis, the magnitude of a health risk posed by
cannabis use will be qualitatively assessed by a comparison of its
probable health effects with those of two other widely used
recreational drugs, alcohol and tobacco. The motive for such a
comparison is to minimise double standards in the appraisal of the
health effects of cannabis use by providing some kind of common
standard, however approximate, for making societal decisions about
cannabis use.
Cannabis the drug
Cannabis is a generic name for a variety of preparations derived from
the plant Cannabis sativa. A sticky resin which covers the flowering
tops and upper leaves, most abundantly in the female plant, contains
more than 60 cannabinoid substances. Laboratory research on animals
and humans has demonstrated that the primary psychoactive constituent
in cannabis is the cannabinoid, delta-9-tetrahydrocannabinol or THC.
The cannabinoid receptor
Cannabis resembles the opioid drugs in acting upon specific receptors
in the brain. In this respect it differs from alcohol, cocaine and
other illicit drugs which act by disrupting brain processes. The
determination and characterisation of a specific cannabinoid receptor
has made it possible to map its distribution in the brain, and to
demonstrate that its well-known psychoactive effects are receptor
mediated. Very recently an endogenous brain molecule has been
discovered which binds to the cannabinoid receptor and mimics the
action of cannabinoids. It has been called "anandamide", from the
Sanskrit word for bliss. Its discovery promises to stimulate a great
deal of research which will improve our understanding of the role
played by a cannabinoid-like system of the brain, and elucidate the
mechanism of action of cannabis.
Forms of cannabis
The concentration of THC varies between the three most common forms of
cannabis: marijuana, hashish and hash oil. Marijuana is prepared from
the dried flowering tops and leaves of the harvested plant. The
potency of the marijuana depends upon the growing conditions, the
genetic characteristics of the plant and the proportions of plant
matter. The flowering tops and bracts are highest in THC
concentration, with potency descending through the upper leaves, lower
leaves, stems and seeds. The concentration of THC in a batch of
marijuana containing mostly leaves and stems may range from 0.5-5 per
cent, while the "sinsemilla" variety with "heads" may have THC
concentrations of 7-14 per cent.
Hashish or hash consists of dried cannabis resin and compressed
flowers. The concentration of THC in hashish generally ranges from 2-8
per cent, although it can be as high as 10-20 per cent. Hash oil is a
highly potent and viscous substance obtained by extracting THC from
hashish (or marijuana) with an organic solvent, concentrating the
filtered extract, and in some cases subjecting it to further
purification. The concentration of the THC in hash oil is generally
between 15 per cent and 50 per cent.
Routes of administration
Almost all possible routes of administration have been used, but by
far the most common method is smoking (inhaling). Marijuana is most
often smoked as a hand-rolled "joint", the size of a cigarette or
larger. Tobacco is often added to assist burning, and a filter is
sometimes inserted. Hashish may also be mixed with tobacco and smoked
as a joint, but it is probably more frequently smoked through a pipe,
with or without tobacco. A water pipe known as a "bong" is a popular
implement for all cannabis preparations because the water cools the
hot smoke before it is inhaled and there is little loss of the drug
through sidestream smoke. Hash oil is used sparingly because of its
extremely high psychoactive potency; a few drops may be applied to a
cigarette or a joint, to the mixture in the pipe, or the oil may be
heated and the vapours inhaled. Whatever method is used, smokers
inhale deeply and hold their breath for several seconds in order to
ensure maximum absorption of THC by the lungs.
Hashish may also be cooked or baked in foods and eaten. When ingested
orally the onset of the psychoactive effects is delayed by about an
hour. The "high" may be of lesser intensity but the duration of
intoxication is longer by several hours. It is easier to titrate the
dose and achieve the desired level of intoxication by smoking than by
ingestion, since the effects from smoking are more immediate. Crude
aqueous extracts of cannabis have been very rarely injected
intravenously, but this route is unpopular since THC is insoluble in
water, and hence, little or no drug is actually present in these
extracts. Moreover, the injection of tiny undissolved particles may
cause severe pain and inflammation at the site of injection, and a
variety of toxic systemic effects.
Dosage
A typical joint contains between 0.5g and 1.0g of cannabis plant
matter, which may vary in THC content between 5mg and 150mg (i.e.
typically between 1 per cent and 15 per cent). The actual amount of
THC delivered in the smoke has been estimated at 20-70 per cent, the
rest being lost through combustion or sidestream smoke. The
bioavailability of THC (the fraction of THC in the cigarette which
reaches the bloodstream) from marijuana cigarettes in human subjects
has been reported to range from 5-24 per cent. Given all of these
variables, the actual dose of THC absorbed when cannabis is smoked is
not easily quantified.
In general, only a small amount of cannabis (e.g. 2-3mg of available
THC) is required to produce a brief pleasurable high for the
occasional user, and a single joint may be sufficient for two or three
individuals. A heavy smoker may consume five or more joints per day,
while heavy users in Jamaica, for example, may consume up to 420mg THC
per day. In clinical trials designed to assess the therapeutic
potential of THC, single doses have ranged up to 20mg in capsule form.
In human experimental research, THC doses of 10mg, 20mg and 25mg have
been administered as low, medium and high doses.
Patterns of use
Cannabis is the most widely used illicit drug in Australia, having
been tried by a third of the adult population, and by the majority of
young adults between the ages of 18 and 25. The most common route of
administration is by smoking, and the most widely used form of the
drug is marijuana. In the majority of cases cannabis use is
"experimental", that is, most users use the drug on a small number of
occasions, and either discontinue their use, or use intermittently and
episodically after first trying it. Even among those who continue to
use the drug over longer periods, the majority discontinue their use
in their mid to late 20s.
Only a small proportion of those who ever use cannabis use it on a
daily basis over an extended period such as several years. Because of
uncertainties about the dose received, there is no good information on
the amount of THC ingested by such regular users. "Heavy" use is
consequently defined approximately in terms of frequency of use rather
than the estimated average dose of THC received. The daily or near
daily use pattern over a period of years is the pattern that probably
places cannabis users at greatest risk of experiencing long-term
health and psychological consequences of use. Daily cannabis users are
more likely to be male and less well educated; they are also more
likely to regularly use alcohol and to have experimented with a
variety of other illicit drugs, such as, amphetamines, hallucinogens,
psychostimulants, sedatives and opioids.
Metabolism of cannabinoids
Different methods of ingesting cannabis give rise to differing
pharmacokinetics, i.e. patterns of absorption, metabolism and
excretion of the active agent. Upon inhalation, THC is absorbed from
the lungs into the bloodstream within minutes. After oral
administration absorption is much slower, taking one to three hours
for THC to enter the bloodstream, and delaying the onset of
psychoactive effects. When cannabis is smoked, the initial metabolism
of THC takes place in the lungs, followed by more extensive metabolism
by liver enzymes, with the transformation of THC to a number of
metabolites. The most rapidly produced metabolite is 9-carboxy-THC,
which is detectable in blood within minutes of smoking. Another major
metabolite produced is 11-hydroxy-THC, which is approximately 20 per
cent more potent than THC, and penetrates the blood-brain barrier more
rapidly. It is present at very low concentrations in the blood after
smoking, but at high concentrations after the oral route. THC and its
hydroxylated metabolites account for most of the observed effects of
the cannabinoids.
Peak blood levels of THC are usually reached within 10 minutes of
smoking, and decline rapidly thereafter to about 5-10 per cent of
their initial level within the first hour. This initial rapid decline
reflects both rapid conversion to its metabolites, as well as the
distribution of unchanged THC to lipid-rich tissues, including perhaps
the brain.
THC and its metabolites are highly fat soluble and may remain for long
periods in the fatty tissues of the body, from which they are slowly
released back into the bloodstream. The terminal half-life of THC (the
time required to clear half of the administered dose from the body) is
significantly shorter for experienced or daily users (19-27 hours)
than for inexperienced users (50-57 hours). Since tissue distribution
is similar for both users and non-users, it is the immediate and
subsequent metabolism that occurs more rapidly in experienced users.
Given the slow clearance of THC, repeated administration results in
the accumulation of THC and its metabolites in the body. Because of
its slow release from fatty tissues back into the bloodstream, THC and
its metabolites may be detectable in blood for several days, and
traces may persist for several weeks. Several studies have examined
measures of cannabinoids in fat, confirming that THC may be stored for
at least 28 days.
Detection of cannabinoids in body fluids
Cannabinoid levels in the body depend on both the dose given and the
smoking history of the individual, but are subject to a vast degree of
individual variability. Plasma levels of THC in man may range between
0-500ng/ml, depending on the potency of the cannabis ingested and the
time since smoking. The detection of THC in blood above 10-15ng/ml
provides evidence of recent consumption of the drug, although how
recent is not possible to determine. A more precise estimate of time
of consumption may be obtained from the ratio of THC to 9-carboxy-THC:
similar concentrations of both in blood indicate very recent use (in
the vicinity of 20-40 minutes) and a high probability of intoxication.
When the levels of 9-carboxy-THC are substantially higher than those
of THC itself, ingestion could be estimated to have occurred more than
half an hour ago. It is very difficult to determine the time of
administration from blood concentrations even if the smoking habits of
the individual and the exact dose consumed were known. Therefore, the
results of blood analyses are not easily interpreted and, at best,
only confirm the "recent" use of cannabis.
Intoxication and levels of cannabinoids
Since there is evidence that cannabis intoxication adversely affects
skills required to drive a motor vehicle (see below), it would be
desirable to have a reliable measure of impairment due to cannabis
intoxication that was comparable to the breath test of alcohol
intoxication. However, there is no clear relationship between blood
levels of THC or its metabolites and degree of either impairment or
subjective intoxication. A general consensus of forensic toxicologists
is that blood concentrations associated with impairment after smoking
cannabis have not been sufficiently established to provide a basis for
legal testimony in cases concerning driving a motor vehicle while
under the influence of cannabis.
Acute psychological and health effects
The major reason for the widespread recreational use of cannabis is
that it produces a "high", an altered state of consciousness which is
characterised by mild euphoria, relaxation, and perceptual
alterations, including time distortion and the intensification of
ordinary sensory experiences, such as eating, watching films, and
listening to music. When used in a social setting the high is often
accompanied by infectious laughter, and talkativeness. Cognitive
effects are also marked. They include impaired short-term memory, and
a loosening of associations, which make it possible for the user to
become lost in pleasant reverie and fantasy. Motor skills and reaction
time are also impaired, so skilled activity of various kinds is
frequently disrupted.
Not all the acute psychological effects of cannabis are welcomed by
users. The most common unpleasant psychological effects are anxiety,
sometimes producing frank panic reactions, or a fear of going mad, and
dysphoric or unpleasant depressive feelings. Psychotic symptoms such
as delusions and hallucinations may be more rarely experienced at very
high doses. These effects are most often reported by naive users who
are unfamiliar with the drug's effects, and by patients who have been
given oral THC for therapeutic purposes. More experienced users may
occasionally report these effects after oral ingestion of cannabis,
when the effects may be more pronounced and of longer duration than
those usually experienced after smoking cannabis. These effects can
usually be prevented by adequately informing users about the type of
effects they may experience, and once developed can be readily managed
by reassurance and support.
The inhalation of marijuana smoke, or the ingestion of THC has a
number of bodily effects. Among these the most dependable is an
increase in heart rate of 20-50 per cent over baseline, which occurs
within a few minutes to a quarter of an hour, and lasts for up to
three hours. Changes in blood pressure also occur, which depend upon
posture: blood pressure is increased while the person is sitting, and
decreases while standing. In healthy young users these cardiovascular
effects are unlikely to be of any clinical significance because
tolerance develops to the effects of THC, and young, healthy hearts
will only be mildly stressed.
The acute toxicity of cannabis, and cannabinoids more generally, is
very low. There are no confirmed cases of human deaths from cannabis
poisoning in the world medical literature. This is unlikely to be due
to a failure to detect such deaths, because animal studies indicate
that the dose of THC required to produce 50 per cent mortality in
rodents is extremely high by comparison with other commonly used
pharmaceutical and recreational drugs. The lethal dose also increases
as one moves up the phylogenetic tree, suggesting by extrapolation
that the lethal dose in humans could not be achieved by either smoking
or ingesting the drug.
Psychomotor effects and driving
The major potential health risk from the acute use of cannabis arises
from its effects on psychomotor performance. Intoxication produces
dose-related impairments in a wide range of cognitive and behavioural
functions that are involved in skilled performances like driving an
automobile or operating machinery. The negative effects of cannabis on
the performance of psychomotor tasks is almost always related to dose.
The effects are generally larger, more consistent and of increased
persistence in difficult tasks which involve sustained attention. The
acute effects of doses of cannabis which are subjectively equivalent
to or higher than usual recreational doses on driving performance in
laboratory simulators and over standardised driving courses, are
similar to those of doses of alcohol that achieve blood alchol
concentrations between 0.07 per cent and 0.10 per cent.
While cannabis impairs performance in laboratory and simulated driving
settings, it is difficult to relate the magnitude of these impairments
to the risk of being involved in motor vehicle accidents. Studies of
the effects of cannabis on on-road driving performance have found at
most modest impairments. Cannabis intoxicated persons drive more
slowly, and generally take fewer risks, than alcohol intoxicated
drinkers, probably because they are more aware of their level of
psychomotor impairment.
There is no controlled epidemiological evidence that cannabis users
are at increased risk of being involved in motor vehicle or other
accidents. This is in contrast to the case of alcohol use and
accidents, where case-control studies have shown that persons with
blood alcohol levels indicative of intoxication are over-represented
among accident victims. All that is available are studies of the
prevalence of cannabinoids in the blood of motor vehicle and other
accident victims, which have found that between 4 per cent and 37 per
cent of such blood samples have contained cannabinoids, typically in
association with blood alcohol levels indicative of intoxication.
These studies are difficult to evaluate for a number of reasons.
First, in the absence of information on the prevalence of cannabinoids
in the blood of non-accident victims, we do not know whether persons
with cannabinoids are over-represented among accident victims. Second,
the presence of cannabinoids in blood indicates only recent use, not
necessarily intoxication at the time of the accident. Third, there are
also serious problems of causal attribution, since more than 75 per
cent of drivers with cannabinoids in their blood also have blood
levels indicative of alcohol intoxication.
Attempts have been made to circumvent the first difficulty by using
NIDA Household survey data (from the United States) to estimate what
proportion of drivers might be expected to have cannabinoids in their
blood and urine. These suggest that cannabis users are two to four
times more likely to be represented among accident victims than
non-cannabis users; cannabis users who also use alcohol, rather than
cannabis only users, are even more likely to be over-represented among
accident victims. Other indirect support for an increased risk of
accidental death associated with cannabis use comes from surveys of
self-reported accidents among adolescent drug users, and from
epidemiological studies of the relationships between cannabis use and
mortality, and health service utilisation.
The known effects of interactions between cannabis and other drugs on
psychomotor performance are what would be predicted from their
separate effects. The drug most often used in combination with
cannabis is alcohol. The separate effects of alcohol and cannabis on
psychomotor impairment and driving performance are approximately
additive.
The effects of chronic cannabis use
Cellular effects and the immune system
There is reasonably consistent evidence that some cannabinoids, most
especially THC, can produce a variety of cellular changes, such as
alterations to cell metabolism, and DNA synthesis, in vitro (i.e. in
the test tube). There is stronger and more consistent evidence that
cannabis smoke is mutagenic in vitro, and in vivo (i.e. in live
animals), and hence, that it is potentially carcinogenic. If cannabis
smoke is carcinogenic then it is probably for the same reasons that
cigarette smoke is, rather than because it contains cannabinoids.
Hence, if chronic cannabis smoking causes cancer, it is most likely to
develop after long-term exposure at those sites which receive maximum
exposure, namely, the lung and upper aerodigestive tract (see below).
There is reasonably consistent evidence that cannabinoids impair both
the cell-mediated and humoral immune systems in rodents. Humoral
immune suppression is seen in decreased antibody formation responses
to antigens, and decreased lymphocyte response to B-cell mitogens.
Cell-mediated immune suppression is revealed by a reduction in
lymphocyte response to T-cell mitogens. These changes have produced
decreased resistance to infection by a bacteria and a virus. There is
also evidence that the non-cannabinoid components of cannabis smoke
impair the functioning of alveolar macrophages, the first line of the
body's defence system in the lungs. The clinical relevance of these
findings is uncertain, however. The doses required to produce these
effects have generally been very high, and the problem of
extrapolating to the effects of doses used by humans is complicated by
the possibility that tolerance may also develop to such effects.
The limited experimental and clinical evidence in humans is mixed,
with a small number of studies suggesting adverse effects that have
not been replicated by others. At present, there is no conclusive
evidence that consumption of cannabinoids predisposes man to immune
dysfunction, as measured by reduced numbers or impaired functioning of
T-lymphocytes, B-lymphocytes or macrophages, or reduced immunoglobulin
levels. There is suggestive evidence that THC impairs T-lymphocyte
responses to mitogens and allogenic lymphocytes.
The clinical and biological significance of these possible
immunological impairments in chronic cannabis users is uncertain. To
date there has been no epidemiological, or even anecdotal, evidence of
increased rates of disease among chronic heavy cannabis users, such as
was seen among young homosexual men in the early 1980s when the
Acquired Immune Deficiency Syndrome was first recognised. There is one
large prospective study of HIV-positive homosexual men which indicates
that continued cannabis use did not increase the risk of progression
to AIDS. Given the duration of large-scale cannabis use by young
adults in Western societies, the absence of any epidemics of
infectious disease makes it unlikely that cannabis smoking produces
major impairments in the immune system.
It is more difficult to exclude the possibility that chronic heavy
cannabis use produces a minor impairment in immunity. Such an effect
would be manifest in small increases in the rate of occurrence of
common bacterial and viral illnesses among chronic users which could
have escaped detection in the few studies that have attempted to
address the issue. Such an increase could nonetheless be of public
health significance because of the increased expenditure on health
services, and the loss of productivity that it would cause among the
young adults who are the heaviest users of cannabis.
The possibility that cannabinoids may produce minor impairments in the
immune system would also raise doubts about the therapeutic usefulness
of cannabinoids in immunologically compromised patients, such as those
undergoing cancer chemotherapy, or those with AIDS. AIDS patients may
provide one of the best populations in which to detect any such
effects. If it was ethical to conduct clinical trials of cannabinoids
to improve appetite and well-being in AIDS patients, then studies of
the impact of cannabis use on their compromised immune systems would
provide one way of evaluating the seriousness of this concern.
The cardiovascular system
There is insufficient new evidence to change the conclusions reached
by the Institute of Medicine in 1982, namely, that although the
smoking of marijuana "causes changes to the heart and circulation that
are characteristic of stress ... there is no evidence ... that it
exerts a permanently deleterious effect on the normal cardiovascular
system..." (p72). The situation may be less benign for patients with
hypertension, cerebrovascular disease and coronary atherosclerosis, in
which case there is evidence that marijuana poses a threat because it
increases the work of the heart. The "magnitude and incidence" of the
threat remains to be determined as the cohort of chronic cannabis
users of the late 1960s enters the age of maximum risk for
complications of atherosclerosis in the heart, brain and peripheral
blood vessels. In the interim, because any such effects could be life
threatening in patients with significant occlusion of the coronary
arteries or other cerebrovascular disease, patients with
cardiovascular disease should be advised not to consume cannabis, and
perhaps not to use THC therapeutically.
The respiratory system
Chronic heavy cannabis smoking impairs the functioning of the large
airways, and probably causes symptoms of chronic bronchitis such as
coughing, sputum production, and wheezing. Given the adverse effects
of tobacco smoke, which is qualitatively very similar in composition
to cannabis smoke, it is likely that chronic cannabis use predisposes
individuals to develop chronic bronchitis and respiratory cancer.
There is reasonable evidence for an increased risk of chronic
bronchitis, and evidence that chronic cannabis smoking may produce
histopathological changes in lung tissues of the kind that precede the
development of lung cancer.
More recently, concern about the possibility of cancers being induced
by chronic cannabis smoking has been heightened by case reports of
cancers of the aerodigestive tract in young adults with a history of
heavy cannabis use. Although these reports fall short of providing
convincing evidence because many of the cases concurrently used
alcohol and tobacco, they are clearly a major cause for concern, since
such cancers are usually rare in adults under the age of 60, even
among those who smoke tobacco and drink alcohol. The conduct of
case-control studies of these cancers should be a high priority for
research which aims to identify the possible adverse health effects of
chronic cannabis use.
Reproductive effects
Chronic cannabis use probably disrupts the male and female
reproductive systems in animals, reducing testosterone secretion, and
sperm production, motility, and viability in males, and disrupting the
ovulatory cycle in females. It is uncertain whether it is likely to
have these effects in humans, given the inconsistency in the limited
literature on human males, and the lack of research in the case of
human females. There is also uncertainty about the clinical
significance of these effects in normal healthy young adults. They may
be of greater concern among young adolescents, and among males with
fertility impaired for other reasons.
Cannabis use during pregnancy probably impairs foetal development,
leading to smaller birthweight, perhaps as a consequence of shorter
gestation, and probably by the same mechanism as cigarette smoking,
namely, foetal hypoxia. There is uncertainty about whether cannabis
use during pregnancy produces a small increase in the risk of birth
defects as a result of exposure of the foetus in utero. Prudence
demands that until this issue is resolved, women should be advised not
to use cannabis during pregnancy, or when attempting to conceive.
There is not a great deal of evidence that cannabis use can produce
chromosomal or genetic abnormalities in either parent which could be
transmitted to offspring. Such animal and in vitro evidence as exists
suggests that the mutagenic capacities of cannabis smoke are greater
than those of THC, and are probably of greater relevance to the risk
of users developing cancer than to the transmission of genetic defects
to children.
There is suggestive evidence that infants exposed in utero to cannabis
may experience transient behavioural and developmental effects during
the first few months after birth. There is a single study which
suggests an increased risk of childhood leukemia occurring among the
children born to women who used cannabis during their pregnancies. Its
replication is of some urgency.
Psychological effects of chronic cannabis use
Adolescent development
There is strong continuity of development from adolescence into early
adult life in which many indicators of adverse development which have
been attributed to cannabis use precede its use, and increase the
likelihood of using cannabis. These include minor delinquency, poor
educational performance, nonconformity, and poor adjustment. A
predictable sequence of initiation into the use of illicit drugs was
identified among American adolescents in the 1970s, in which the use
of licit drugs preceded experimentation with cannabis, which preceded
the use of hallucinogens and "pills", which in turn preceded the use
of heroin and cocaine. Generally, the earlier the age of initiation
into drug use, and the greater the involvement with any drug in the
sequence, the greater the likelihood of progression to the next drug
in the sequence.
The causal significance of these findings, and especially the role of
cannabis in the sequence of illicit drug use, remains controversial.
The hypothesis that the sequence of use represents a direct
pharmacological effect of cannabis use upon the use of later drugs in
the sequence is the least compelling. A more plausible and better
supported explanation is that it reflects a combination of two
processes: the selective recruitment into cannabis use of
nonconforming and deviant adolescents who have a propensity to use
illicit drugs; and the socialisation of cannabis users within an
illicit drug using subculture which increases the exposure,
opportunity, and encouragement to use other illicit drugs.
Although strong conclusions cannot be drawn, on the evidence from
cross-sectional and longitudinal studies of cohorts of American
adolescents in the 1970s and 1980s, there are suggestions that chronic
heavy cannabis use can adversely affect adolescent development in a
number of ways.
There has been suggestive support for the hypothesis that heavy
adolescent use of cannabis impairs educational performance. In
cross-sectional surveys, cannabis use is related to an increased risk
of failing to complete a high school education, and of job instability
in young adulthood. These relationships in cross-sectional studies are
exaggerated because those who are most likely to use cannabis have
lower pre-existing academic aspirations and high school performance
than those who do not use it. When pre-existing academic aptitude and
interest are taken into account, the relationship between cannabis use
and educational and occupational performance is much more modest. Even
though modest, the suggestive adverse effects of cannabis and other
drug use upon educational performance are important because they may
cascade throughout young adult life, affecting choice of occupation,
level of income, choice of mate, and quality of life of the user and
his or her children.
There is weaker but suggestive evidence that heavy cannabis use has
adverse effects upon family formation, mental health, and involvement
in drug-related (but not other types of) crime. In the case of each of
these outcomes, the apparently strong associations revealed in
cross-sectional data are much more modest in longitudinal studies,
after statistically controlling for associations between cannabis use
and other variables which predict these adverse outcomes.
On balance, there are sufficient indications that cannabis use in
adolescence probably adversely affects adolescent development to
conclude that it is desirable to discourage adolescent cannabis use,
and especially regular cannabis use.
Adult adjustment
The evidence that chronic heavy cannabis use produces an amotivational
syndrome among adults is equivocal. The positive evidence largely
consists of case histories, and observational reports. The small
number of controlled field and laboratory studies have not found
compelling evidence for such a syndrome, although their evidential
value is limited by the small sample sizes and limited
sociodemographic characteristics of the field studies, and by the
short periods of drug use, and the youthful good health and minimal
demands made of the volunteers observed in the laboratory studies. If
there is such a syndrome, it is a relatively rare occurrence, even
among heavy, chronic cannabis users.
A dependence syndrome
A cannabis dependence syndrome like that defined in DSM-III-R probably
occurs in heavy, chronic users of cannabis. There is good experimental
evidence that chronic heavy cannabis users can develop tolerance to
its subjective and cardiovascular effects, and there is suggestive
evidence that some users may experience a withdrawal syndrome on the
abrupt cessation of cannabis use. There is clinical and
epidemiological evidence that some heavy cannabis users experience
problems in controlling their cannabis use, and continue to use the
drug despite experiencing adverse personal consequences of use. There
is limited evidence in favour of a cannabis dependence syndrome
analogous to the alcohol dependence syndrome. If the estimates of the
community prevalence of drug dependence provided by the Epidemiologic
Catchment Area study are correct, then cannabis dependence is the most
common form of dependence on illicit drugs.
Recognition of the cannabis dependence syndrome has been delayed by a
number of factors. First, heavy daily cannabis use has been relatively
uncommon, and there have been few individuals who have requested
assistance in stopping their cannabis use. Second, an overemphasis on
evidence of tolerance and a withdrawal syndrome has hindered the
recognition of the syndrome among individuals who have presented for
treatment. Third, the occurrence of cannabis dependence has probably
been overshadowed because it is most common among persons who are
dependent on alcohol and opioids, forms of drug dependence which have
understandably been given higher treatment priority.
Given the widespread use of cannabis, and its continued reputation as
a drug free of the risk of dependence, the clinical features of
cannabis dependence deserve to be better defined. This would enable
the prevalence of a dependence syndrome to be better estimated and
individuals who are dependent on cannabis to be better recognised and
treated. Treatment should probably be on the same principles as other
forms of dependence, although this issue is also in need of research.
Although cannabis dependence is likely to be a larger problem than
previously thought, we should be wary of over-estimating its social
and public health importance. Estimates of the risk of users becoming
dependent suggest that it may be similar to that of alcohol, that it
will be highest among the minority of daily cannabis users, and that
even in this group the prevalence of drug-related problems may be
relatively low by comparison with those of alcohol dependence. There
is likely to be a high rate of remission of cannabis dependence
without formal treatment. While acknowledging the existence of the
syndrome, we should avoid exaggerating its prevalence and the severity
of its adverse effects on individuals. Better research on the
experiences of long-term cannabis users should provide more precise
estimates of the risk.
Cognitive effects
The weight of the available evidence suggests that the long-term heavy
use of cannabis does not produce any severe impairment of cognitive
function. There is reasonable clinical and experimental evidence,
however, that the long-term use of cannabis may produce more subtle
cognitive impairment in the higher cognitive functions of memory,
attention and organisation and integration of complex information.
While subtle, these impairments may affect everyday functioning,
particularly in adolescents with marginal educational aptitude, and
among adults in occupations that require high levels of cognitive
capacity. The evidence suggests that the longer the period that
cannabis has been used, the more pronounced is the cognitive
impairment. It remains to be seen whether the impairment can be
reversed by an extended period of abstinence from cannabis.
There is a need for research to identify the specific cognitive
functions affected by long-term cannabis use, to identify the precise
mechanisms that produce impairment and to relate them to biological
mechanisms, including the cannabinoid receptors and the endogenous
cannabinoid, anandamide. Such research also needs to investigate
individual differences in susceptibility to such effects, and the
impact of long-term cannabis use on adolescents and young adults.
Appropriate treatment programs for long-term dependent cannabis users
will also need to address the subtle cognitive impairments likely to
be found in this population.
Brain damage
A suspicion that chronic heavy cannabis use may cause gross structural
brain damage was provoked by a single poorly controlled study using an
outmoded method of investigation, which reported that cannabis users
had enlarged cerebral ventricles. This finding was widely and
uncritically publicised. Since then a number of better controlled
studies using more sophisticated methods of investigation have
consistently failed to demonstrate evidence of structural change in
the brains of heavy, long-term cannabis users. These negative results
are consistent with the evidence that any cognitive effects of chronic
cannabis use are subtle, and hence unlikely to be manifest as gross
structural changes in the brain. They do not exclude the possibility
that chronic, heavy cannabis use may cause ultrastructural changes at
the receptor level.
Psychotic disorders
There is suggestive evidence that heavy cannabis use can produce an
acute toxic psychosis in which confusion, amnesia, delusions,
hallucinations, anxiety, agitation and hypomanic symptoms predominate.
The evidence for an acute toxic cannabis psychosis comes from
laboratory studies of the effects of THC on normal volunteers and
clinical observations of psychotic symptoms in heavy cannabis users
which seem to resemble those of other toxic psychoses, and which remit
rapidly following abstinence.
There is less support for the hypothesis that cannabis use can cause
either an acute or a chronic functional psychosis which persists
beyond the period of intoxication. Such a possibility is difficult to
study because of the rarity of such psychoses, and the near
impossibility of distinguishing them from schizophrenia and manic
depressive psychoses occurring in individuals who also abuse cannabis.
There is strongly suggestive evidence that chronic cannabis use may
precipitate a latent psychosis in vulnerable individuals. This is only
strongly suggestive because in the best study conducted to date, the
use of cannabis was not documented at the time of diagnosis, there was
a possibility that cannabis use was confounded by amphetamine use, and
there are doubts about whether the study could reliably distinguish
between schizophrenia and acute cannabis-induced, or other
drug-induced, psychoses. Even if this relationship is causal, its
public health significance should not be overstated: the estimated
attributable risk of cannabis use is small (less than 10 per cent),
and even this seems an overestimate, since the incidence of
schizophrenia declined over the period when cannabis use increased
among young adults.
Therapeutic effects of cannabinoids
There is reasonable evidence that THC is an effective anti-emetic
agent for patients undergoing cancer chemotherapy, especially those
whose nausea has proven resistant to the anti-emetic drugs that were
widely used in the late 1970s and early 1980s, when most of the
research was conducted. It is uncertain whether THC is as effective as
newer anti-emetic drugs. Uncertainty also exists about the most
optimal method of dosing and the advantages and disadvantages of
different routes of administration. Nonetheless, there is probably
sufficient evidence to justify THC being made available in synthetic
form to cancer patients whose nausea has proven resistant to
conventional treatment.
There is also reasonable evidence for the potential efficacy of THC
and marijuana in the treatment of glaucoma, especially in cases which
have proved resistant to existing anti-glaucoma agents. Further
research is required to establish the effectiveness and safety of
long-term use, but this should not prevent its use under medical
supervision in individuals with poorly controlled glaucoma.
There is sufficient suggestive evidence of the potential usefulness of
various cannabinoids as anti-spasmodic, and anti-convulsant agents to
warrant further clinical research into their effectiveness. There are
other potential therapeutic uses which require more basic
pharmacological and experimental investigation, e.g. cannabinoids as
possible analgesic and anti-asthma agents.
There is a need for further research into the effectiveness of
cannabis and its derivatives in assisting patients with
HIV/AIDS-related conditions, and in particular, their value in
counteracting weight loss associated with these conditions, improving
mood and easing pain. Case reports have suggested that synthetic THC
may be effective in reducing nausea and stimulating appetite in
symptomatic AIDS patients. While there is a potential concern that
possible effects of cannabinoids on the immune system may have more
serious consequences for HIV positive individuals and AIDS patients, a
recent study has failed to find a relationship between the use of
cannabis, or any other psychoactive drugs, and the rate at which HIV
positive people progress to clinical AIDS.
Despite the basic and clinical research work which was undertaken in
late 1970s and early 1980s, the cannabinoids have not been widely used
therapeutically, nor has further investigation been conducted along
the lines suggested by the Institute of Medicine in 1982. This seems
attributable to the fact that, in the United States, where most
cannabis research has been conducted, clinical research on
cannabinoids has been discouraged by regulation and a lack of funding.
The discouragement of clinical cannabis research, in turn, derives
from the fact that THC, the most therapeutically effective
cannabinoid, is the one that produces the psychoactive effects sought
by recreational users. An unreasonable fear that the therapeutic use
of THC would send "mixed messages" to youth has motivated the
discouragement of research into the therapeutic effects of
cannabinoids.
The recent discovery of a specific cannabinoid receptor and the
endogenous cannabinoid-like substance anandamide may change this
situation by encouraging more basic research on the biology of
cannabinoids which may have therapeutic consequences. It may prove
possible to separate the psychoactive and therapeutic effects of
cannabis, fulfilling the ancient promise of "marijuana as medicine".
Overall appraisal of the health and psychological risks of cannabis
use
The following is a summary of the major adverse health and
psychological effects of acute and chronic cannabis use, classified by
the degree of confidence about the relationship between cannabis use
and the adverse effect.
Acute effects
The major acute adverse psychological and health effects of cannabis
intoxication are:
• anxiety, dysphoria, panic and paranoia, especially in naive
users;
• cognitive impairment, especially of attention and memory;
• psychomotor impairment, and possibly an increased risk of
accident if an intoxicated person attempts to drive a motor vehicle;
• an increased risk of experiencing psychotic symptoms among those
who are vulnerable because of personal or family history of psychosis;
and
• an increased risk of low birth weight babies if cannabis is used
during pregnancy.
Chronic effects
The major health and psychological effects of chronic heavy cannabis
use, especially daily use, over many years, remain uncertain. On the
available evidence, the major probable adverse effects appear to be:
• respiratory diseases associated with smoking as the method of
administration, such as chronic bronchitis, and the occurrence of
histopathological changes that may be precursors to the development of
malignancy;
• development of a cannabis dependence syndrome, characterised by
an inability to abstain from or to control cannabis use; and
• subtle forms of cognitive impairment, most particularly of
attention and memory, which persist while the user remains chronically
intoxicated, and may or may not be reversible after prolonged
abstinence from cannabis.
The following are the major possible adverse effects of chronic, heavy
cannabis use which remain to be confirmed by further research:
• an increased risk of developing cancers of the aerodigestive
tract, i.e. oral cavity, pharynx, and oesophagus;
• an increased risk of leukemia among offspring exposed in utero;
• a decline in occupational performance marked by underachievement
in adults in occupations requiring high level cognitive skills, and
impaired educational attainment in adolescents; and
• birth defects occurring among children of women who used cannabis
during their pregnancies.
High risk groups
A number of groups can be identified as being at increased risk of
experiencing some of these adverse effects.
Adolescents
• Adolescents with a history of poor school performance may have
their educational achievement further limited by the cognitive
impairments produced by chronic intoxication with cannabis.
• Adolescents who initiate cannabis use in the early teens are at
higher risk of progressing to heavy cannabis use and other illicit
drug use, and to the development of dependence on cannabis.
Women of childbearing age
• Pregnant women who continue to smoke cannabis are probably at
increased risk of giving birth to low birth weight babies, and perhaps
of shortening their period of gestation.
• Women of childbearing age who smoke cannabis at the time of
conception or while pregnant possibly increase the risk of their
children being born with birth defects.
Persons with pre-existing diseases
Persons with a number of pre-existing diseases who smoke cannabis are
probably at an increased risk of precipitating or exacerbating
symptoms of their diseases. These include:
• individuals with cardiovascular diseases, such as coronary artery
disease, cerebrovascular disease and hypertension;
• individuals with respiratory diseases, such as asthma, bronchitis
and emphysema;
• individuals with schizophrenia who are at increased risk of
precipitating or of exacerbating schizophrenic symptoms; and
• individuals who are dependent on alcohol and other drugs, who are
probably at an increased risk of developing dependence on cannabis.
Two special concerns
Storage of THC
There is good evidence that with repeated dosing of cannabis at
frequent intervals, THC can accumulate in fatty tissues in the human
body where it may remain for considerable periods of time. The health
significance of this fact is unclear. The storage of cannabinoids
would be serious cause for concern if THC were a highly toxic
substance which remained physiologically active while stored in body
fat. The evidence that THC is a highly toxic substance is weak and its
degree of activity while stored has not been investigated. One
potential health implication of THC storage is that stored
cannabinoids could be released into blood, producing a "flashback",
although this is likely to be a very rare event, if it occurs at all.
Whatever the uncertainties about health implications of THC storage,
all potential users of cannabis should be aware that it occurs.
Increases in the potency of cannabis?
It has been claimed that the existing medical literature on the health
effects of cannabis underestimates its adverse effects, because it was
based upon research conducted on less potent forms of marijuana than
became available in the USA in the past decade. This claim has been
repeated and interpreted in an alarmist fashion in the popular media
on the assumption that an increase in the THC potency of cannabis
necessarily means a substantial increase in the health risks of
cannabis use.
It is far from established that the average THC potency of cannabis
products has substantially increased over recent decades. If potency
has increased, it is even less certain that the average health risks
of cannabis use have materially changed as a consequence, since users
may titrate their dose to achieve the desired effects. Even if the
users are inefficient in titrating their dose of THC, it is not clear
that the probability of all adverse health effects will be thereby
increased. Given the existence of these concerns about THC potency, it
would be preferable to conduct some research on the issue rather than
to rely upon inferences about the likely effects of increased cannabis
potency. Studies of the ability of experienced users to titrate their
dose of THC would contribute to an evaluation of this issue.
A comparative appraisal of health risks: alcohol, tobacco and cannabis
use
The probable and possible adverse health and psychological effects of
cannabis need to be placed in comparative perspective to be fully
appreciated. A useful standard for such a comparison is what is known
about the health effects of 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 its
intoxicating and euphoriant effects. Although allowance has to be made
for the very different prevalence of use of the two drugs, and for the
fact that we know a great deal more about the adverse effects of
alcohol and tobacco use, the comparison serves the useful purpose of
reminding us of the risks we currently tolerate with our favourite
psychoactive drugs.
Acute effects
Alcohol. The major risks of acute cannabis use are similar to the
acute risks of alcohol intoxication in a number of respects. First,
both drugs produce psychomotor and cognitive impairment, especially of
memory and planning. The impairment produced by alcohol increases
risks of various kinds of accident, and the likelihood of engaging in
risky behaviour, such as dangerous driving, and unsafe sexual
practices. It remains to be determined whether cannabis intoxication
produces similar increases in accidental injury and death, although on
the balance of probability it does.
Second, there is good evidence that substantial doses of alcohol taken
during the first trimester of pregnancy can produce a foetal alcohol
syndrome. There is suggestive but far from conclusive evidence that
cannabis used during pregnancy may have similar adverse effects.
Third, there is a major health risk of acute alcohol use that is not
shared with cannabis. In large doses alcohol can cause death by
asphyxiation, alcohol poisoning, cardiomyopathy and cardiac infarct,
whereas there are no recorded cases of fatalities attributable to
cannabis.
Tobacco. The major acute health risks that cannabis share with tobacco
are the irritant effects of smoke upon the respiratory system, and the
stimulating effects of both THC and nicotine on the cardiovascular
system, both of which can be detrimental to persons with
cardiovascular disease.
Chronic effects
Alcohol. There are a number of risks of heavy chronic alcohol use,
some of which may be shared by chronic cannabis use. First, heavy use
of either drug increases the risk of developing a dependence syndrome
in which users experience difficulty in stopping or controlling their
use. There is strong evidence for such a syndrome in the case of
alcohol and reasonable evidence in the case of cannabis. A major
difference between the two is that it is uncertain whether a
withdrawal syndrome reliably occurs after dependent cannabis users
abruptly stop their cannabis use, whereas the abrupt cessation of
alcohol use in severely dependent drinkers produces a well defined
withdrawal syndrome which can be potentially fatal.
Second, there is reasonable clinical evidence that the chronic heavy
use of alcohol can produce psychotic symptoms and psychoses in some
individuals. There is suggestive evidence that chronic heavy cannabis
use may produce a toxic psychosis, precipitate psychotic illnesses in
predisposed individuals, and exacerbate psychotic symptoms in
individuals with schizophrenia.
Third, there is good evidence that chronic heavy alcohol use can
indirectly cause brain injury - the Wernicke-Korsakov syndrome - with
symptoms of severe memory defect and an impaired ability to plan and
organise. With continued heavy drinking, and in the absence of vitamin
supplementation, this injury may produce severe irreversible cognitive
impairment. There is good reason for concluding that chronic cannabis
use does not produce cognitive impairment of comparable severity.
There is suggestive evidence that chronic cannabis use may produce
subtle defects in cognitive functioning, that may or may not be
reversible after abstinence.
Fourth, there is reasonable evidence that chronic heavy alcohol use
produces impaired occupational performance in adults, and lowered
educational achievements in adolescents. There is at most suggestive
evidence that chronic heavy cannabis use produces similar, albeit more
subtle impairments in occupational and educational performance of
adults.
Fifth, there is good evidence that chronic, heavy alcohol use
increases the risk of premature mortality from accidents, suicide and
violence. There is no comparable evidence for chronic cannabis use,
although it is likely that dependent cannabis users who frequently
drive while intoxicated with cannabis increase their risk of
accidental injury or death.
Sixth, alcohol use has been accepted as a contributory cause of cancer
of the oropharangeal organs in men and women. There is suggestive
evidence that chronic cannabis smoking may also be a contributory
cause of cancers of the aerodigestive tract (i.e. the mouth, tongue,
throat, oesophagus, lungs).
Tobacco. The major adverse health effects shared by chronic cannabis
and tobacco smokers are chronic respiratory diseases, such as chronic
bronchitis, and probably, cancers of the aerodigestive tract. The
increased risk of cancer in the respiratory tract is a consequence of
the shared route of administration by smoking. It is possible that
chronic cannabis smoking also shares the cardiotoxic properties of
tobacco smoking, although this possibility remains to be investigated.
Implications for harm reduction
Anyone who wishes to avoid the probable acute and chronic adverse
health effects of cannabis should abstain from using the drug. This
advice is especially pertinent for persons with any of the diseases
(e.g. cardiovascular) or conditions (e.g. pregnancy) which would make
them more vulnerable to the adverse effects of cannabis.
Current cannabis users should be aware of the following risks of using
the drug. First, the risk of being involved in a motor vehicle
accident is likely to be increased when cannabis users drive while
intoxicated by cannabis. The combination of alcohol and cannabis
intoxication will substantially increase this risk. Second, the
chronic smoking of cannabis poses significant risks to the respiratory
system, apart from any specific effects of THC. Third, the respiratory
risks of cannabis smoking are amplified if deep inhalation and
breath-holding are used to maximise the absorption of THC in the
lungs. This technique greatly increases the delive
1. Summary of repo
particulate matter and tar. Fourth, daily or near daily use of
cannabis is to be avoided, as it has a high risk of producing
dependence.