WHO Project on Health Implications of Cannabis Use:
A Comparative Appraisal of the Health and Psychological
Consequences of Alcohol, Cannabis, Nicotine and Opiate Use
August 28, 1995
By Wayne Hall,
National Drug and Alcohol Research Centre,
University of New South Wales
and
Robin Room and Susan Bondy,
Addiction Research Foundation,
Toronto
Contents
I. OUR APPROACH
II. THE PROBABLE HEALTH EFFECTS OF CANNABIS USE
• Acute Psychological and Health Consequences
• The Health Effects of Chronic Cannabis Use
• Psychological Effects of Chronic Cannabis Use
III. A QUALITATIVE COMPARISON OF THE HEALTH RISKS OF ALCOHOL,
CANNABIS, NICOTINE AND OPIATE USE
• Acute Effects
• Chronic Effects
IV. COMPARING THE MAGNITUDE OF RISKS
• Quantifying the Relative Risks of Adverse Health Effects of Cannabis Use
• Public Health Significance
• Some Direct Comparative Evidence on Consequences: What Users Report
V. CONCLUSIONS & REFERENCES
TABLE 1: SUMMARY OF RATINGS OF OVERALL EFFECT OF DRUG USE BY
CURRENT USERS (PERCENT)
TABLE 2:TYPES OF PROBLEMS REPORTED IN THE PAST 12MONTHS BY
CURRENT USERS AGE 18 TO 34 (ONTARIO 1992)
WHO Project on Health Implications of Cannabis Use:
A Comparative Appraisal of the Health and Psychological
Consequences of Alcohol, Cannabis, Nicotine and Opiate Use
I. OUR APPROACH
On the face of it there is a reasonable cause for concern about the public health significance
of cannabis use in many developed societies. First there is a high prevalence of cannabis use
in such societies, especially among adolescents and young adults. Second, cannabis is an
intoxicant like alcohol that is usually smoked like tobacco so there is a reasonable
presumption that it shares at least some of the adverse health effects of these two drugs, both
of which have a substantial public health impact.
There are a number of obstacles to providing a confident appraisal of the personal and public
health significance of cannabis use. The first set of issues concerns difficulties in making
causal inferences about the connections between cannabis use and the adverse health and
psychological consequences, which have been attributed to it. The second set of issues
concerns the quantification of the seriousness of the risks of cannabis use for users and for the
broader community.
A third set of issues concerns the difficulties in making comparative appraisals of risk. Since
no human activity is ever risk free, the appraisal of the health risks of cannabis presupposes a
comparison of its risks with those of other relevant activities. The most obvious comparison is
with the risks of using the other major recreational drugs in Western societies namely,
alcohol, and tobacco. We have also included some comparisons with opiates, which, serves
the useful purpose of calibrating the health risks of cannabis against those of a drug that is
widely regarded as a major public concern even though it is not widely used.
Our purpose in making these comparisons is not to promote one drug over another but rather
to minimise the double standards that have operated in appraising the health effects of
cannabis by persons on both sides of the debate about its legal status. On the one hand, there
has been a disproportionately greater concern about the use of cannabis than alcohol on the
part of many older persons who are opposed to cannabis use. On the other hand, younger
cannabis users have denied the existence any adverse health effects of cannabis despite the
fact that it intoxicates like alcohol and is smoked like tobacco. A further reason for the
comparison is that many of our inferences about the probable adverse health effects of
cannabis use depend upon analogies between the health effects of alcohol, cannabis and
tobacco.
A factor which complicates the comparative assessment is the way in which the drug is taken.
In present-day developed societies, the main route of administration of cannabis and of
tobacco is by smoking, that is, inhaling the smoke of a smouldering preparation containing the
drug. In pharmaceutical use, opiates are administered orally or by injection, while nonmedical
use is primarily by injection, snorting, or smoking. Alcoholis consumed orally, although in
combination with a wide variety of other substances. The route of administration of a drug
can change over time in a given society: for instance, in North America tobacco was primarily
chewed or sniffed in the late 19th century, and there is evidence there of some shifting at
present from injecting to smoking heroin. In this analysis, we have focused on predominant
routes of administration in developed societies, but it should be recognised that a shift in route
of administration can substantially change the size and profile of adverse effects. In particular,
the most serious adverse health problems of cannabis and tobacco are associated with
smoking as the mode of administration.
The approach we have adopted in addressing each of these issues is as follows. First, we have
identified the most probable causal relationships between cannabis use and specific health
effects. In doing so we have used standard criteria for assessing the strength of evidence for a
causal relationships, although we have had to relax the degree of confidence required so that
some provisional conclusions could be drawn.
Second, in so far as it is possible we have attempted to quantify the severity of personal and
public health risk for each adverse health effect that can be reasonably attributed to cannabis.
We have attempted to estimate the probable relative risk, and the prevalence of the relevant
pattern of use.
Third, we have compared these estimates with the best estimates of the mortality and
morbidity burden of alcohol, opiates and tobacco. This has been done initially in a qualitative
way by indicating whether or not particular adverse health effects that may reasonably be
attributed to cannabis have also been attributed to alcohol, nicotine, and opiates. This is
followed by a discussion of the probable quantitative risks of cannabis by comparison with
those of alcohol and nicotine, and some direct comparative evidence on consequences
reported by users of the three drugs.
In making these comparisons we have relied on epidemiological evidence on the health and
psychological consequences of cannabis use which is largely based on studies conducted in
the English-speaking countries, and most particularly the United States. Unfortunately,
countries with a long tradition of heavy cannabis use are not well represented in there search
literature. The preponderance of American research on the health effects of cannabis use
reflects societal concern about the emergence over the past several decades of widespread
cannabis use among adolescents and young adults in the USA; concern that has been
translated into funding for epidemiological studies of the health and psychological
consequences of cannabis use. The conduct of research on cannabis use in developing
countries should be a priority, especially in the countries that have a long history of traditional
use, including very heavy use among some subpopulations. These subpopulations are the ones
most likely to show any adverse health and psychological effects of chronic heavy use.
Our comparisons of health effects are also largely confined to the effects on the health of
users. We have said little about the effects of cannabis use on the health and well being of
other persons who do not use cannabis. Such indirect health effects have not been well studied
for most drugs, with the limited exceptions of motor vehicle accidents, and violence for
alcohol, and passive smoking for tobacco. They perhaps deserve more attention that they have
hitherto received but in the absence of the necessary research we are unable to address them
in this review.
Next chapter
WHO Project on Health Implications of Cannabis Use:
A Comparative Appraisal of the Health and Psychological
Consequences of Alcohol, Cannabis, Nicotine and Opiate Use
II. THE PROBABLE HEALTH EFFECTS OF CANNABIS
USE
Acute Psychological and Health Consequences
The acute toxicity of cannabis is very low. There are no confirmed cases of human deaths
from cannabis poisoning in the world medical literature. Animal studies indicate that the dose
of THC required to produce 50% 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 increases as
one moves up the phylogenetic tree, suggesting by extrapolation that the lethal dose in
humans could not be very easily achieved by smoking or ingesting the drug (Grinspoon and
Bakalar, 1993; Rosencrantz, 1983).
Dysphoric effects
The most common unpleasant acute psychological effects of cannabis use are anxiety,
sometimes producing unpleasant depressive feelings (Tart, 1970; Weil, 1970). 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 receiving a much larger than intended dose of
THC. These effects can usually be prevented by adequate preparation of users about the type
of effects they may experience, or they can be managed by reassurance and support
(Weil,1970).
Motor vehicle accidents
The major potential health risks from the acute use of cannabis arise from its effect son
cognitive and psychomotor performance. Intoxication produces dose-related impairments in a
wide range of cognitive and behavioural functions that are relevant to a skilled performance
like driving an automobile or operating machinery. These include: slowed reaction time and
information processing, impaired perceptual-motor coordination and motor performance,
impaired short term memory, signal detection, tracking behaviour and slowed time
perception. (Chait and Pierri, 1992).
The negative effects of cannabis on the performance of psychomotor tasks is almost always
related to dose (Chait and Pierri, 1992). The effects are generally larger, more consistent and
persistent in different tasks which involve sustained attention. The acute effects of
"recreational" doses of cannabis on driving performance in laboratory simulators and over
standardised driving courses are similar to those of doses of alcohol that achieve BACs
between 0.07% and 0.10% (Hansteen, Miller, Lonero, Reid and Jones, 1976;Peck et al, 1986;
Smiley, 1986).
While cannabis impairs performance in laboratory and simulated driving settings, it is
difficult to relate the magnitude of these impairments to an increased risk of being involved in
motor vehicle accidents. Students of the effects of cannabis on on-road driving performance
have found at most modest impairments (e.g. Sutton, 1983). Cannabis intoxicated persons
drive more slowly perhaps because they are more aware of their level of psychomotor
impairment than alcohol intoxicated drinkers who generally drive at faster speeds (Smiley,
1986).
No controlled epidemiological studies have established that cannabis users are at increased
risk of motor vehicle accidents. A prospective Swedish study of mortality over15 years
among military conscripts found an increased risk of premature mortality among men who
had smoked cannabis 50 or more times by age 18. Violent deaths were the major contributor
to this excess, of which 26% were motor vehicle and 7% other accidents (e.g. drownings and
falls). The increased risk disappeared, however, after multivariate statistical adjustment for
confounding variables such as alcohol and other drug use (Andreasson and Allebeck, 1990).
Uncertainty about the role of cannabis in motor vehicle accidents is likely to remain since
case-control studies are difficult to conduct and interpret (see chapter by Smiley this volume).
Blood levels of cannabinoids do not indicate whether a driver or pedestrian was intoxicated
with cannabis at the time of an accident, and many drivers with cannabinoids in their blood
were also intoxicated with alcohol at the time of the accident(Smiley, 1986). Factors other
than psychomotor performance also contribute to the danger of drug use when driving.
Foremost among these is the user's preparedness to take risks when intoxicated, which the
available evidence suggests is reduced by cannabis intoxication by contrast with alcohol
intoxication which consistently increases risk-taking (Smiley, 1986)
The Health Effects of Chronic Cannabis Use
The Immune System
There is reasonably consistent evidence that THC can produce cellular changes such as
alterations in cell metabolism, and DNA synthesis, in vitro (Bloch, 1983). There is even
stronger evidence that cannabis smoke is mutagenic in vitro, and in vitro, and hence, that it is
potentially carcinogenic for the same reasons as tobacco smoke (Leuchtenberger, 1983).
There is reasonably consistent evidence that cannabinoids impair both the cell-mediated and
humoral immune systems in rodents (Munson and Fehr, 1983). These changes have decreased
resistance to infection by bacteria and viruses. 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 (Munson and Fehr,1983). The relevance of these
findings to human health is uncertain: the doses required to produce these effects are often
very high, and the problem of extrapolating from the effects of these doses to those used by
humans is complicated by the possibility that tolerance develops to the effects on the immune
system (Hollister, 1992).
Moreover, the limited experimental and clinical evidence on immune effects in humans is
mixed, with a small number of early studies that have suggested adverse effects not being
replicated by later ones (Munson and Fehr, 1983; Hollister, 1992). At present, there is no
conclusive evidence that consumption of cannabinoids predisposes humans to immune
dysfunction, as measured by reduced numbers or impaired functioning of T-lymphocytes, B-
lymphocytes or macrophages, or reduced immunoglobulin levels.
The clinical and biological significance of these possible immunological impairments in
chronic cannabis uses is uncertain. To date there has been no epidemiological evidence of
increased rates of disease among chronic heavy cannabis users. 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 (Kaslow et al, 1989). 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 minor
impairments in immunity. Such effects would produce small increases in the rate of
occurrence of common bacterial and viral illnesses among chronic users which would be of
public health significance because of the increased expenditure on health services, and the
increased loss of productivity that this would entail among the young adults who are the
heaviest users of cannabis. A recent epidemiological study by Polen at al (1993)which
compared health service utilisation by non smokers and daily cannabis only smokers has
provided the first suggestive evidence of an increased rate of presentation for respiratory
conditions among cannabis smokers. This remains suggestive, however, because infectious
and non infectious respiratory conditions were not distinguished.
The Cardiovascular System
The conclusion reached by the Institute of medicine in 1982 still stands: the smoking of
marijuana "causes changes to the heart and circulation that are characteristics of stress ...[but]
there is no evidence ... that it exerts a permanently deleterious effect on the normal
cardiovascular system ..." (p 72). The cardiovascular effects of cannabis may be less benign in
patients with hypertension, cerebrovascular disease and coronary atherosclerosis for whom
marijuana poses a threat by increasing the work of the heart (Aronow and Cassidy, 1974,
1975).
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, and wheezing(Bloom et al,
1987; Huber et al, 1988; Tashkin et al, 1988a, 1990). Given the documented adverse effects
of tobacco smoke, which is qualitatively very similar in composition to cannabis, smoke
(Tashkin, 1993; Wu et al, 1988). There is as yet little direct evidence that the latter occurs
(Huber et al, 1988) although there is evidence that chronic cannabis smoking may produce
histopathological changes in lung tissues of the kind that precede the development of lung
cancer (Fligiel et al, 1988).
More recently, concern about respiratory cancers has been heightened by a series of case
reports of cancers of the aerodigestive tract in young adults with a history of heavy cannabis
use (e.g. Caplan and Brigham, 1989; Donald, 1991; Taylor, 1988). Although these reports fall
short of providing convincing evidence because they were uncontrolled and many of the cases
concurrently used alcohol and tobacco, they are clearly cause for concern since such cancers
are rare in adults under the age of 60, even among those who smoke tobacco and drink
alcohol (Tashkin, 1993). Smoking cannabis may also pose an acute risk to individuals with
respiratory diseases such as asthma. Evidence linking tobacco smoke to asthma and asthmatic
symptoms is increasing.
The potential adverse effects of cannabis on the respiratory system are specific to smoking as
the route of administration, and could not result from oral ingestion.
Reproductive Effects
Chronic cannabis use probably disrupts the male and female reproductive systems in animals,
reducing the secretion of testosterone, and sperm production, motility, and viability in males,
and disrupting the ovulatory cycle in females (Bloch, 1983; Institute of Medicine, 1982). It is
uncertain whether it is these effects in humans, given the inconsistency in the limited
literature on human males (Mendelson and Mello, 1984), and the lack of research in the case
of human females (Hollister, 1986). 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 whose fertility has been impaired for other reasons.
Cannabis smoking during pregnancy probably impairs foetal development Gibson et al,1983;
Hatch and Bracken, 1986; Tennes et al, 1985; Zuckerman et al, 1989, leading to a reduction in
birthweight (Abel, 1985). This may be a consequence of a shorter gestation period, and
probably occurs 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. There is some animal
evidence of such effects although these studies have usually involved very high doses by the
oral route (Abel, 1985). The limited studies in humans have generally but not consistently
produced null results (Gibson et al, 1983; Hatch and Bracken, 1986; Hingson et al, 1982;
Zuckerman et al, 1989).
There is not a great deal of evidence that cannabis use can produce chromosomal orgenetic
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 ther isk of users developing
cancer than to the transmission of genetic defects to children(Bloch, 1983; Hollister, 1986).
There is suggestive evidence that infants exposed in utero to cannabis may experience
transient behavioural and developmental effects during the first few month safter birth (e.g.
Fried 1985, 1989). There are several case-control studies which suggest that there is an
increased risk of certain childhood cancers (namely, astrocytomas and leukemia) among
children born to women who reported that they had used cannabis during their pregnancies
(Kuitjen et al, 1990; Robison et al, 1989).
Possible Health Effects of Contaminants in Cannabis
Because cannabis is an illegal drug its cultivation, harvesting and distribution are not subject
to quality control mechanisms to ensure the reliability and safety of the product used by
consumers. It is well recognised in developing countries, such as Kenya, that illicit alcohol
production can result in the contamination with toxic by-products or adulterants that can kill
or seriously affect the health of users. The same may be true of illicit drugs such as opiates,
cocaine and amphetamine in developed societies. There is no evidence of comparable health
effects for cannabis although there were concerns expressed about the possible health effects
of the use of cannabis contaminated by herbicides (such as paraquat) that were used to control
illicit cannabis cultivation in the US in the1970s. These concerns proved unfounded
(Hollister, 1986). There have also been concerns about the microbial contamination of
cannabis leaf but there has been little evidence(other than a small number of case histories)
that this has adversely affected the health of cannabis users (Hollister, 1986).
Psychological Effects of Chronic Cannabis Use
Adult Motivation
One of the major concerns about the psychological effects of chronic heavy cannabis use has
been that it impairs adult motivation. The evidence for an "amotivational syndrome" among
adults consists largely of case histories and observational reports(e.g. Kolansky and Moore,
1971; Millman and Sbriglio, 1986). The small number of controlled field and laboratory
studies have not found compelling evidence for such a syndrome (Dornbush, 1974; Negrete,
1983; Hollister, 1986). The evidential value of the field studies is limited by their small
sample sizes, and the limited sociodemographic characteristics of their samples, while the
evidential value of the laboratory studies is limited by the short periods of drug use, the
youthful good health of the volunteers, and minimal demands made on volunteers in the
laboratory (Cohen, 1982). Some regular cannabis users report a loss of ambition and impaired
school and occupational performance as adverse effects of their use (e.g. Hendin et al, 1987)
and that some ex-cannabis users give impaired occupational performance as a reason for
stopping (Jones, 1984). Nonetheless, it is doubtful that cannabis use produces a well defined
amotivational syndrome. It may be more parsimonious to regard the symptoms of impaired
motivation as symptoms of chronic cannabis intoxication rather than inventing a new
psychiatric syndrome.
Adolescent Development
In the United States in the 1970s and 1980s, cannabis use appears to have increased the risk of
discontinuing a high school education, and of experiencing job instability in young adulthood
(Newcombe and Bentler, 1988). The apparent strength of these relationships in cross-
sectional studies (e.g. Kandel, 1984) has been exaggerated because those adolescents who are
most likely to use cannabis have lower academic aspirations and poorer high school
performance prior to using cannabis than their peers who do not (Newcombe and Bentler,
1988). It remains possible that factors other than the marijuana use account for apparent
causal relations. To the extent they may exist, these adverse effects of cannabis and other drug
use upon development over and above the effect of pre-existing nonconformity may cascade
throughout young adult life, affecting choice of occupation, level of income, choice of mate,
and the quality of life of the user and his or her children.
A major finding of research into the adult consequences of adolescent cannabis use has been
the strong evidence of a regular sequence of initiation into the use of illicit drugs among
American adolescents in the 1970s in which cannabis use preceded involvement with "harder"
drugs such as stimulants and opioids (Kandel et al, 1984; Donovan and Jessor, 1983;
Yamaguchi and Kandel, 1984 a, b). The causal significance of this sequence of initiation into
drug use remains controversial. The hypothesis that it represents a direct effect of cannabis
use upon the use of the later drugs in the sequence is the least compelling. There is better
support for two other hypotheses which are not mutually exclusive: that there is a selective
recruitment into cannabis use of nonconforming adolescents who have a propensity to use
other illicit drugs; and that once recruited to cannabis use, the social interaction with other
drug using peers, and exposure to other drugs when purchasing cannabis on the black-market,
increases the opportunity to use other illicit drugs (Baumrind, 1983; Goode, 1974; Kandel,
1988).
A Dependence Syndrome
A cannabis dependence syndrome as defined in DSM-IV (American Psychiatric
Association,1994) can occur 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. There is also suggestive evidence that some users may experience a
withdrawal syndrome on the abrupt cessation of cannabis use, although one that is much
milder and less marked than that experienced when withdrawing from alcohol or opiates
(Compton, Dewey and Martin, 1990; Jones and Benowitz, 1976). DSM-IV notes that
"symptoms of possible cannabis withdrawal (e.g. irritable or anxious mood accompanied by
physical changes such tremor, perspiration, nausea and sleep disturbances) have been
described in association with the use of very high doses, but their clinical significance is
uncertain." (American Psychiatric Association, 1994:215).
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 (Jones, 1984; Roffman et al,1988; Weller et al, 1984).
There is limited clinical evidence for a cannabis dependence syndrome analogous to the
alcohol dependence (Kosten et al, 1987). Epidemiological surveys of the prevalence of drug
dependence in the general population (e.g. Anthony and Helzer,1991) show that cannabis
dependence, as defined in the diagnostic manuals, is among the most common forms of drug
dependence in Western societies by virtue of its high prevalence of use. On the other hand,
relatively few users seek treatment for cannabis dependence (American Psychiatric
Association, 1994: 220-221).
Cognitive Effects
The weight of the available evidence suggests that even the long-term heavy use of cannabis
does not produce any severe or grossly debilitating impairment of cognitive function (Carter
et al, 1980; Fehr and Kalant, 1983b, Rubin and Comitas, 1975; Wert and Raulin, 1986). If it
did research to date should have detected it. There is some 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 the integration of
complex information (Page et al, 1988; Solowij et al,1991, 1992, 1993 and see chapter by
Solowij in this volume). While subtle, these impairments may affect everyday functioning,
particularly among individuals 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 (Solowij et al, 1992, 1993). It remains to be seen
whether the impairment can be reversed by an extended period of abstinence from cannabis.
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 (Campbell et al,1971).
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
(e.g. Co et al, 1977; Kuehnle et al, 1977). 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.
Serious Psychiatric Disorder
There is suggestive evidence that large doses of THC can produce an acute psychosis in
which confusion, amnesia, delusions, hallucinations, anxiety, agitation and hypomanic
symptoms predominate. The evidence comes from laboratory studies of the effects of THC on
normal volunteers and clinical observations of psychotic symptoms in heavy cannabis users
which remit rapidly following abstinence (Bernardson and Gunne, 1972; Chopra and
Smith,1974; Edwards, 1976).
There is less support for the hypothesis that cannabis use can cause either an acute or a
chronic functional psychosis (Thornicroft, 1990). Such possibilities are 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 use
cannabis (Ghodse, 1986).
There is strongly suggestive evidence from a prospective study that heavy cannabis use may
precipitate schizophrenia in vulnerable individuals (Andreasson et al, 1987; Schneier and
Siris, 1987; Thornicroft, 1990). This relationship is still only strongly suggestive because in
the only prospective study conducted to date (Andreasson et al, 1987) 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, or other drug-induced, psychoses
(Negrete, 1989; Thornicroft, 1990).
There is better evidence that cannabis use can adversely affect the course of schizophrenia in
affected individuals who continue to use it (Cleghorn et al, 1991; Jablensky et al, 1991;
Martinez-Arevalo et al, 1994).
Next chapter
WHO Project onHealth Implications of Cannabis Use:
A Comparative Appraisal of the Health and Psychological
Consequences of Alcohol, Cannabis, Nicotine and Opiate Use
III. A QUALITATIVE COMPARISON OF THE HEALTH RISKS OF
ALCOHOL, CANNABIS, NICOTINE AND OPIATE USE
A useful way of assessing the health risk posed by cannabis use is a comparative qualitative
appraisal of its risks with those of other widely used recreational of its risks with those of
other widely used recreational drugs such as alcohol and tobacco (ARF/WHO, 1981). The
motive for such comparisons is to use a common standard when making societal decisions
about the control and regulation of cannabis use. Like tobacco, cannabis is most commonly
smoked, and like alcohol, cannabis is commonly used for its intoxicating and euphoriant
effects in developed societies(although it may be used for more utilitarian reasons, such as,
making heavy physical work tolerable, in some developing countries). The opiates provide a
useful illicit drug class against which to calibrate the adverse effects of cannabis since this
class of drugs has a fearsome although not always deserved reputation as a major risk to the
health of young adults. Nonmedical use of opiates is initially primarily for euphoria or for
relief of pain.
In undertaking this qualitative comparison we have avoided the necessity to comprehensively
review the vast literatures on the health effects of alcohol and tobacco by using the following
authorities as the warrant for our assertions about their health risks: Anderson et al (1993);
Holman et al's (1988) compendium of the health effects of alcohol and tobacco; the Institute
of Medicine (1987); the International Agency for Research into Cancer (1990); Roselle et al
(1993); and the Royal College of Physicians(1987).
In the absence of an authoritative current review of the health effects of the opioids as a class
of drugs, it was necessary to look to several sources to identify the health effects of opioids.
General pharmacological texts, and other reviews, were used to describe the pharmacological
effects of the opioids (e.g., Belkin and Gold, 1991; Jacobs and Fehr, 1987; Duggan and North,
1983). In addition, information on the chronic health effects and social consequences of illicit
opiates (injectable and non-injectable) and of methadone was taken from reports of several
longitudinal studies of opioid users (e.g.Vaillant, 1973; O'Donnell, 1969; Maddux and
Desmond, 1981; Simpson, Joe, Lehman and Sells,1986; Joe and Simpson, 1987; 1990). These
cohort studies typically involve populations in contact with drug treatment services rather
than representative samples of users.
Acute Effects
Alcohol
The major risks of acute cannabis use show some parallels with the acute risks of alcohol
intoxication. 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. It may also increase the likelihood of engaging in risky behaviour such as
dangerous driving, and unsafe sexual practices. While cannabis intoxication increases the
risks of casualties in hazardous situations, it remains to be determined to what extent it
increases the likelihood of engaging in risky behaviour.
Alcohol and cannabis intoxication appear to differ in their relation to intentional rather than
accidental casualties. Alcohol intoxication is strongly associated with aggressive and violent
behaviour. The relationship is complex, and the nature and extent of drinking's causal effect
remains controversial at the level of the individual drinker (Pernanen, 1991; Martin, 1993;
Pohorecky, Brick and Milgram, 1993). But there is good causal evidence that changes in the
level of alcohol consumption affect the incidence of violent crime, at least in some
populations (Room, 1983; Lenke, 1990; Cook and Moore,1993). There is also increasing
evidence to indicate that alcohol may play a role in suicide (Edwards et al., forthcoming).
There is little to suggest that causal relationship of cannabis use to aggression or violence, at
least in present-day developed societies.
Second, there is good evidence that substantial doses of alcohol taken during pregnancy can
produce a foetal alcohol syndrome. There is suggestive but far from conclusive evidence that
cannabis can also adversely affect the development of the foetus when used during pregnancy.
A clear equivalent for cannabis of the foetal alcohol syndrome has not been established.
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. There are no recorded cases of overdose fatalities attributed to cannabis, and
the estimated lethal dose for humans extrapolated from animal studies is so high that it cannot
be achieved by recreational users.
Tobacco
The major acute health risks that cannabis shares 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 and
respiratory diseases. For both drugs, the respiratory effects do not apply to ingestion that is
not by inhalation.
Opioids
Some of the opioids share with alcohol and cannabis an acute intoxicating effect, although the
sedative effect is more pronounced. Acute administration of heroin causes euphoria in many
users, although other opioids such as methadone do not have this effect in tolerant individuals.
The extent of euphoria is also affected by route of administration. As is found with cannabis,
some naive users report unpleasant feelings with opiate use, specifically nausea and
dysphoria. All opioids are CNS depressants and as such can reduce level of consciousness and
cause sleep.
The literature on the effects of opiates on driving and other exacting skills is not well
developed. A maintenance dose in a tolerant user may produce little psychomotor or cognitive
impairment. A heroin user who has reached a stage of "nodding" is in no condition to drive a
car, but will probably have little inclination to do so. As with cannabis, there is little direct
epidemiological evidence of opiate-induced casualties. One study showed that the driving-
related skills of persons maintained on stable doses o fmethadone were not impaired when
assessed on a laboratory task that is sensitive to the effects of alcohol (Chesher, Lemon,
Gomal and Murphy, 1989).
While there is no risk of overdose associated with cannabis, use of illicit opioids carries a real
risk of overdose. High doses of most opioids can lead to suppression of breathing rate and
blood pressure and cause respiratory arrest. The risk of overdose is worsened by use in
combination with alcohol or other drugs, and is thought to be worsened by variations in the
potency of opiates obtained illegally.
Opioids, like cannabis, cause some suppression of hormone levels. These decreased hormonal
levels, however, do not necessarily result in infertility in men or women using opioids\do for
extended periods (Belkin and Gold, 1991; Duggan and North, 1983; Martin and Martin,
1980). Like alcohol, tobacco and cannabis, the opiates have been associated with miscarriage,
foetal death and low birth-weight. There is no clear relationship with an identifiable syndrome
of foetal defects from opioids that parallels foetal alcohol syndrome. Although poor nutrition
and pre-natal care clearly contribute to the risk of adverse outcomes in pregnant women
addicted to street drugs, even methadone maintenance has been found to result in higher rates
of pregnancy problems. Methadone and other orally administered opioids have been shown to
cause foetal death and low birthweight in laboratory animals (Martin and Martin, 1980;
Caviston, 1987; Woody and O'Brien, 1991).
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 of such a syndrome in the case of alcohol and reasonable
evidence in the case of cannabis. A major difference between the two is that withdrawal
symptoms are either absent or mild 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, either during acute
intoxication or during the process of withdrawal in dependent drinkers. There is some clinical
evidence that chronic heavy cannabis use may produce a toxic psychosis. One prospective
epidemiological study suggests that heavy cannabis use may precipitate schizophrenia in
predisposed individuals,. that is, those with a personal or a family history of psychiatric
disorder. There is better evidence that continued cannabis use may worsen the course of
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 in the absence of countervailing cultural beliefs
chronic heavy alcohol use generally impairs occupational performance in adults and
educational achievements in adolescents. There is 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 would 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 clinical evidence that chronic cannabis
smoking may also be a contributory cause of cancers of the aerodigestive tract. There is also
some epidemiological evidence that alcohol use moderately increases the risk of cancer of the
breast in women and of the colon in both sexes.
Seventh, alcohol use is a major cause of liver cirrhosis, accounting for upward of 80%of cases
in non-tropical countries with substantial alcohol consumption levels. Heavy drinking is also
implicated in gastritis, high blood pressure, stroke, cardiac arrhythmias, cardiomyopathy,
pancreatitis, and polyneuropathy. On the other hand, regular drinking of small amounts of
alcohol appears to reduce the risk of coronary heart disease, particularly in older individuals
with positive risk factors such as tobacco smoking or a fatty diet. No equivalent protective
effects have been found for cannabis although there is some evidence for the therapeutic
usefulness of some cannabinoids (Hall et al, 1994).
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 (i.e. the mouth, tongue, throat, oesophagus, lungs). The increased risk of cancer in the
aerodigestive 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. These respiratory risks could be
avoided by a change to the oral route of administration which would also reduce but not
eliminate the cardiovascular risk since THC affects the cardiovascular system when taken
orally.
Tobacco smoking is associated with a wide variety of other chronic health conditions for
which cannabis smoking has not so far been implicated. These include cancer of the cervix,
stomach, bladder and kidney, coronary heart disease, peripheral vascular disease, and stroke,
as well as cataracts and osteoporosis.
Opioids
The specific health effects of opioid use largely depend on the route of administration. The
use of injectable opiates carries risks not common to alcohol, tobacco or cannabis, especially
when associated with illegally obtained injectables and shared needles. Injecting heroin or
morphine can lead to trauma, inflammation and infection at the site of administration. Liver
damage in opiate addicts may be caused by viral hepatitis contracted through needle sharing
or from chronic alcohol abuse. Serious infection such as endocarditis is also possible. Local
tissue and organ damage may also result from the adulterants in injection drugs obtained on
the street (Belkin and Gold,1991). Intravenous drug use is a major concern for the
transmission of communicable diseases such as viral hepatitis and AIDS.
Chronic use of non-injected opioids appears to carry little risk of adverse health effects other
than a modest effect on endocrine activity, some suppression of the immune system which has
similar implications to the immune suppression associated with cannabis use, and chronic
constipation.
While it is unclear that a withdrawal syndrome exists for cannabis, physical dependence on
opiates has been recognised for centuries. Opiate withdrawal is associated wit hconsiderable
discomfort but is rarely life-threatening. The withdrawal syndrome is generally less dangerous
than rapid withdrawal from sedatives-hypnotics or from alcohol, although it may be life-
threatening in neonates. Despite the low risk, avoidance of withdrawal appears to be a
powerful motive for continued use of opiates among very heavy users.
Chronic opioid users may experience instability of mood, anorexia, lethargy and depression
which are related to acute drug effects. Opioids have not been linked to chronic psychiatric
disorders, but street addicts have a shortened life expectancy and more frequently experience
social and emotional problems. This is in part due to their exposure to infection, violence and
poor living conditions rather than their drug use.
WHO Project on Health Implications of Cannabis Use:
A Comparative Appraisal of the Health and Psychological
Consequences of Alcohol, Cannabis, Nicotine and Opiate Use
IV. COMPARING THE MAGNITUDE OF RISKS
The standard ways of measuring the magnitude of health risks are relative risk and population
attributable risk. The relative risk of cannabis use, for example, is the increase in the odds of
experiencing an adverse health outcome among those who use cannabis compared to those
who do not. The population attributable risk represents the proportion of cases with an
adverse outcome, which is attributable to cannabis use. Relative risk is of most relevance to
individuals attempting to estimate the increase in their risk of experiencing an adverse
outcome if they use a drug. Attributable risk is of most relevance to a societal appraisal of the
harms of drug use.
The personal and public health importance of the two measures of risk magnitude depends
upon the prevalence of drug use and the base rate of the adverse outcome. An exposure with a
low relative risk may have a low personal significance but a large public health impact if a
large proportion of the population is exposed (e.g. cigarette smoking and heart disease).
Conversely, an exposure with a high relative risk may have little public health importance
because very few people are exposed to it but major personal health implications for those
who are exposed. Consequently, an appraisal of the personal and public health importance of
cannabis and other illicit drug use must take account not only of the relative risk of harm but
also the prevalence of use and the base rate of the adverse effect.
The Relative Risks of Adverse Health Effects of Cannabis Use
Many of the quantitative risks of cannabis use can only be guessed at in the absence of studies
of the dose-response relationship between cannabis use and the various adverse health effects.
The following are guesstimates of the risks of cannabis use for the most probable adverse
health effects. When in doubt we have adopted the strategy of assuming as a worst case that
the relative risks of cannabis use are comparable to the relevant risks of alcohol or tobacco.
Motor Vehicle Accidents
If we assume that driving while intoxicated with cannabis produces a comparable increase in
the risk of accidents to that produced by driving while intoxicated with alcohol (say with a
blood alcohol level of 0.05% to 0.10%), then a RR in the range of 2 to 4 would be reasonable.
The fact that alcohol and cannabis are often used in combination complicates the task of
estimating the relative risk of cannabis use alone to motor vehicle accidents.
Respiratory Diseases
If we assume that a daily cannabis user who smokes 5 or more joints per day faces a
comparable risk of respiratory disease to that of a 20 a day tobacco smoker, then the RR of
developing chronic bronchitis would be 5 or greater for those who had ever smoked cannabis,
and substantially higher among those who also used tobacco and those had been daily
smokers over many years (Holman et al, 1988). The increased risk of respiratory disease is, of
course, specific to use of cannabis by smoking.
Respiratory Tract Cancers
If we make the same worst case assumptions about daily cannabis smoking then the relative
risks of various cancers of the respiratory tract would be of the order of: 4 for oral cancer, 6
for pharyngeal cancers, 4 for oesophageal cancer, and 7 for lung cancer(Holman et al, 1988).
Again these risks could be substantial higher among cannabis smokers who also smoke
tobacco, but would be minimal for non-smoking cannabis use.
Low Birth weight Babies
Making a worst-case assumption in the absence of good data, a woman who smokes cannabis
during pregnancy approximately doubles her chance of giving birth to a low birthweight baby
(Holman et al, 1988).
Schizophrenia
This is one of the few health consequences for which there is quantitative estimate of relative
risk. If we use the estimated RR from the study by Andreasson et al (1987) after adjustment
for confounding variables, then an adolescent who had smoked cannabis 50 or more times by
age 18 would have approximately a 2 to 3 times higher risk of developing schizophrenia than
an adolescent who had not been a cannabis smoker.
Dependence
Since cannabis use is a necessary condition of developing dependence, it is not appropriate to
estimate a relative risk. The best way of quantifying the risk of dependence is to estimate the
proportion of those who have ever used cannabis, or who have had a history of daily use, who
become dependent on the drug. The best estimates of these percentages are based primarily
upon US data from the late 1970s and early 1980s. These are that 10% to 20% of those who
have ever used, and 33% to 50% of those who have had a history of daily use, will become
dependent on cannabis (see Hall et al, 1994). Comparable percentages for tobacco and opiates
would be higher than these.
Summary
From the perspective of the individual cannabis user, the major health risks of cannabis use
are, with one exception, most likely to be experienced by those who smoke the drug daily
over a period of years. These are in order of decreasing risk: developing a cannabis
dependence syndrome, developing chronic bronchitis, and being involved in a motor vehicle
accident if driving while intoxicated. In all these cases, the risk will be increased if cannabis is
combined with either alcohol or tobacco or both. The risk most likely to be experienced by
the occasional user is an increased risk of a motor vehicle accident if used when driving a car,
especially if cannabis is combined with alcohol.
Public Health Significance
Motor Vehicle Accidents
An assessment of the public health significance of motor vehicle accidents caused by
cannabis is made difficult by the strong association between cannabis and alcohol use. The
epidemiological studies indicate that in its own right, cannabis makes at most a very small
contribution to motor vehicle accidents, and so on the whole it may seem be a minor road
safety problem by comparison with alcohol. Its major public health significance for road
safety may be in amplifying the adverse effects of alcohol in those of drivers who combine
alcohol and cannabis intoxication.
Respiratory Diseases
The public health significance of respiratory diseases caused by cannabis smoking is probably
greater than that for respiratory cancers. This is so for two reasons. First, respiratory cancers
require a greater length of exposure to cigarette smoke (15 to 20years) than is required to
develop chronic bronchitis. Second, there are very few cannabis users who use the drug for
more than 5 years. The exposure period for chronic bronchitis may be shorter still among
those cannabis smokers who also smoke tobacco since there is good evidence that concurrent
tobacco and cannabis smoking have additive adverse effects on the respiratory system. The
contribution of cannabis to respiratory diseases is more a matter of morbidity than mortality.
Respiratory Tract Cancers
Even if we make the worst-case assumption that the risks of cancer are comparable among
daily tobacco and cannabis smokers then cannabis smoking will make at most a small
contribution to the occurrence of these cancers, at least on the basis of current patterns of use
in developed societies. This is because only a minority of those who ever use cannabis
become daily users, and a much smaller proportion of these daily users persist in smoking
cannabis beyond their middle twenties by comparison with the proportions of tobacco
smokers who do so. Among this minority concurrent cannabis and tobacco use may amplify
the adverse respiratory effects.
Low Birth weight Babies
Again making a worst-case assumption, cannabis smoking during pregnancy may double the
risks of a woman giving birth to a low birthweight baby. The public health significance is
likely to be much lower than that of tobacco smoking during pregnancy because the
prevalence of cannabis use is likely to be much lower. Although foetal exposure to cannabis
smoke may be relatively low, the risks of a low birthweight baby will be even higher among
those women who also smoke tobacco, as do most of those smoking cannabis during
pregnancy.
Schizophrenia
As argued in detail elsewhere (Hall et al, 1994), there is uncertainty about whether the
association observed between cannabis use and schizophrenia is a token of a causal
relationship. But even if it is, its public health significance should not be overstated.
Schizophrenia affects approximately 1% of the adult population, and on the data of
Andreasson et al, cannabis use would account for less than 10% of cases of schizophrenia.
Even this low figure seems unlikely, however, since the incidence of schizophrenia has
probably declined during the period when cannabis use among adolescents and young adults
has increased (Der et al, 1991).
Dependence
Cannabis dependence is potentially a larger public health problem than any of the other
potentially adverse health effects of cannabis. On the ECA estimates, approximately 4% of
the adult US population met diagnostic criteria for cannabis abuse or dependence, as against
14% who met diagnostic criteria for alcohol abuse and dependence. This is a nontrivial
proportion of the population, although its consequences are somewhat ameliorated because
there is probably a high rate of remission of symptoms in the absence of treatment.
Summary
Overall, most of these risks are small to moderate in size. In aggregate they are unlikely to
produce public health problems comparable in scale to those currently produced by alcohol
and tobacco. This is largely because on current patterns of use in developed societies the
proportion of the population that uses cannabis heavily over a period of years is much smaller
than the proportions that use alcohol or tobacco in a comparable way (Hall, 1995).
We should beware of becoming too complacent about this situation. The comparison based
upon existing patterns of use cannot be used to predict what would happen if there was a
major change in the prevalence of cannabis use, as some may argue would happen if existing
criminal penalties were removed or replaced with civil penalties. But even if there were more
users, it is unlikely that the proportion of cannabis users who become very heavy users would
ever be as high in industrial societies as it often for stimulants such as tobacco or cocaine,
since heavy use of a stimulant fits more easily into the rhythms of daily life in such societies.
In principle, it would seem a simple matter to estimate what the health risks of cannabis use
would be if its prevalence was the same as that of alcohol and tobacco. Although conceptually
a simple matter, a number of assumptions have to be made. The most questionable
assumption is that the public health consequences of an increased prevalence of cannabis use
would simply be the product of the current patterns of use multiplied by the ratio of the new
to old users. Such a calculation assumes that the risks are the same regardless of the
characteristics of the user, or the legal regime under which the drug is used.
The first assumption may be unreasonable. It may be, for example, that cannabis is used by a
different population when its prevalence of use is low than when it was high. This
phenomenon has been reported with alcohol, for example, with different patterns of alcohol
consumption and problems in "dry" and "wet" cultures. If adult use were legalised, it might
also be easier to reduce some of these health risks. For example, with greater availability it
may be possible to reduce the major respiratory risks of cannabis smoking, either by
encouraging cannabis users to ingest rather than to smoke the drug, or by increasing the THC
content and reducing the tar content of marijuana, for those who continue to smoke. It would
also be easier if cannabis use were legal to give users advice on other ways of reducing their
risks of using the drug. Estimating the net effects of such harm reduction efforts is difficult,
however, because it would also be likely that decriminalising cannabis for adult use would
lead to an increased use by adolescents, and the health effects of this would be difficult to
predict.
For these reasons we have not attempted to provide estimates of the health risks of cannabis if
its prevalence of use were to approach those of alcohol and tobacco. All that can be said with
any confidence is that if the prevalence of cannabis use increased to the levels of cigarette
smoking and alcohol use, its public health impact would increase. It is impossible to say by
how much with any precision. However, on even the most worst-case scenario, it is unlikely
that the public health effect of cannabis use would approach those of alcohol or tobacco use.
Unlike alcohol, cannabis does not produce cirrhosis for example. Moreover, in developed
societies cannabis appears to play little role in injuries caused by violence, as does alcohol,
although recently concern has been expressed in some developing countries that cannabis may
be used to fortify criminal offenders. Unlike tobacco, all the evidence suggests that the
proportion of cannabis smokers who become daily smokers is substantially less than the
proportion of tobacco smokers who do so.
Some Direct Comparative Evidence on Consequences:
What Users Report
To a limited extent, epidemiological data are available on the consequences of drug use that
users attribute to their drug use. Since this data has not been collated and reviewed, we
summarise some of it here. As we shall discuss, the data should be interpreted with caution.
And it should be recognised that the range of consequences considered here reaches far
beyond the bounds of the clinically significant physical and mental illnesses which are our
focus elsewhere in this review.
In a large sample of U.S. men aged 20 - 30, interviewed in 1974 (Table 1), a higher
proportion of tobacco smokers rated the effects of their use as bad, and more drinkers of
alcohol gave a bad than a good rating. Good ratings outweighed bad for marijuana users. In a
survey of Ontario adults in 1994 (Table 1), current users aged 18 to 34 gave a similarly
negative weighting to tobacco, but gave alcohol a relatively more favourable weighting.
Again, marijuana users were the most likely to give a favourable rating.
In another Ontario survey in 1992, current users were asked whether their use of a drug had a
harmful effect on different aspects of their life in the past 12 months. Table 2 shows the
results for users of alcohol, tobacco and marijuana, and also for heavier or more frequent
users of each drug: drinkers who drank five or more drinks on an occasion at least once a
month, marijuana users who smoked at least once a month, and tobacco smokers who smoked
at least 11 cigarettes a day. Tobacco smokers were more likely than marijuana or alcohol
users to report harm to their physical health, to their finances, and to their friendships or social
life, among both lighter and heavier users. The small number of regular marijuana users
seemed more likely than heavier drinkers to report harm to their home life or marriage and to
their finances. On other comparisons, the proportions reporting harm for each drug were fairly
similar.
In the 1991 U.S. National Household Survey on Drug Abuse, large samples of current
tobacco, alcohol and marijuana users were asked comparable questions about 11
consequences of use. Marijuana users were a little more likely to report consequences (15.5%
reporting any of the 11 consequences) than alcohol users (11.4%) or cigarette smokers
(11.2%). If these rates are extrapolated to the whole population, including nonusers, then
1.9% of the population reported consequences of marijuana use, 7.2% reported consequences
of drinking, and 3.4% reported consequences of cigarette smoking. Marijuana users reported
noticeably higher rates on four items: "became depressed or lost interest in things", "found it
difficult to think clearly", "got less work done than usual at school or on the job", and "felt
suspicious and mistrustful of people". Responses to the last two items may be particularly
influenced by marijuana's illegal status. Drinkers reported higher rates of "arguments and
fights with family or friends" and "found it difficult to think clearly". Cigarette smokers
reported higher rates of "felt very nervous and anxious" and "had health problems"
(USDHHS, 1993, Table 9.2).
Great caution must be used in interpreting the results of such comparisons. In the first place,
the base of users is different for each drug. Those using a widely-used drug are likely to differ
on salient characteristics from those using a more rarely used drug. Second, the reported
consequence may not be seen by the respondents themselves as adverse. For instance, if the
purpose of use in intoxication, it may not be seen as a problems that the respondent "found it
difficult to think clearly". Third, responses are likely to be influenced by cultural beliefs about
causal connections. The high proportion of young adult smokers reported smoking has
harmed their health may reflect acceptance of conventional wisdom as much s personal
experience. Fourth and most important, the connection between drug use and adverse
consequences will be influenced by a variety of factors applying differentially to different
drugs. In particular, a drug's illegal status can itself create adverse consequences for the user,
not only directly, through arrest, but also indirectly, for instance in the form of "harm to home
life" from the adverse reactions by others to the drug use that involves a risk of arrest.
Keeping these caveats in mind, it is clear that a minority of marijuana users do report harm
from their smoking, and some would be likely to do so even if cannabis were legalised. In an
era where the health consequences of tobacco smoking are well recognised, tobacco smokers
seem to be more likely than users of either cannabis or alcohol to regard their use as doing
more harm than good in their lives, and the good is seen as outweighing the bad more often
by cannabis smokers than by drinkers or tobacco smokers. In the present circumstances of
North America, cannabis smokers are least as likely as alcohol drinkers to report adverse
consequences of their use. But the higher rate for alcohol of" arguments and fights with
family or friends" reminds us of the special potential alcohol consumption has to have
harmful effects on others. Given current patterns of use, when rates of consequences are
restated on the basis of the whole population, consequences of alcohol and tobacco use are
clearly of greater public health significance than consequences of marijuana use.
Next chapter
WHO Project on Health Implications of Cannabis Use:
A Comparative Appraisal of the Health and Psychological
Consequences of Alcohol, Cannabis, Nicotine and Opiate Use
V. CONCLUSIONS
There are health risks of cannabis use, most particularly when it is used daily over a period of
years or decades. Considerable uncertainty remains about whether these effects are
attributable to cannabis use alone, and about what the quantitative relationship is between
frequency, quantity and duration of cannabis use and the risk of experiencing these effects.
Using analogies with the known effects of alcohol and tobacco, the most probable of the
health risks of chronic heavy cannabis use over a period of years are; the development of a
dependence syndrome; an increased risk of being involved in motor vehicle accidents; an
increased risk of developing chronic bronchitis; an increased risk of respiratory cancers; an
increased risk of giving birth to low birthweight babies when used during pregnancy; and
perhaps, an increased risk of developing schizophrenia among those who are vulnerable.
Many of these risks are shared with alcohol and tobacco, which is not surprising given that
cannabis is an intoxicant like alcohol, which is typically smoked like tobacco.
On existing patterns of use, cannabis poses a much less serious public health problem than is
currently posed by alcohol and tobacco in Western societies. This is no cause for
complacency, however, as the public health significance of alcohol and tobacco are major,
and the public health significance of cannabis could increase if the prevalence of its heavy
daily use were to approach that of heavy alcohol use among young adults, or the prevalence
of daily cigarette smoking among adults.
REFERENCES
Addiction Research Foundation/World Health Organization (1981) Report of an ARF/WHO
Scientific Meeting on the Adverse Health and Behavioral Consequences of Cannabis
Use. Addiction Research Foundation, Toronto.
Allebeck, P. (1991) Cannabis and schizophrenia: is there a causal association? In G.G. Nahas
and C. Latour (Eds) Physiopathology of Illicit Drugs: Cannabis, Cocaine,
OpiatesPergamon Press, Oxford.
Allebeck, P., Adamsson, C., Engstrom, A. and Rydberg, U. (1993) Cannabis and
schizophrenia: a longitudinal study of cases treated in Stockholm county. Acta Psychiatrica
Scandinavica, 88, 21-24.
American Psychiatric Association. (1987) Diagnostic and Statistical Manual of Mental
Disorders (DSM-II-R). (3rd Edition, Revised) Washington: American
PsychiatricAssociation.
Andreasson, S., Allebeck, P. and Rydberg, U. (1989) Schizophrenia in users and nonusers of
cannabis. Acta Psychiatrica Scandinavica, 79, 505-510.
Andreasson, S., Allebeck, P., Engstrom, A. and Rydberg, U. (1987) Cannabis and
schizophrenia: A longitudinal study of Swedish conscripts. Lancet, 2, 1483-1486.
Andreasson, S. and Allebeck, P. (1990) Cannabis and mortality among young men:
Alongitudinal study of Swedish conscripts. Scandinavian Journal of Social Medicine,18, 9-
15.
Angrist, B. (1983) Psychoses induced by central nervous system stimulants and related drugs.
In I. Creese (ed) Stimulants: Neurochemical, Behavioral and Clinical Perspectives. Raven
Press, New York.
Anthony, J.C. and Helzer, J.E. (1991) Syndromes of drug abuse and dependence. In
L.N.Robins and D.A. Regier (eds) Psychiatric Disorders in America. Free Press,
MacMillan, New York.
Arndt, S., Tyrrell, G., Flaum, M. and Andreasen, N.C. (1992) Comorbidity of substance abuse
and schizophrenia: the role of premorbid adjustment. Psychological Medicine,22, 379-388.
Baumrind, D. (1983) Specious causal attribution in the social sciences: there formulated
stepping stone hypothesis as exemplar. Journal of Personality and Social Psychology, 45,
1289-1298.
Baumrind, D. and Moselle, K.A. (1985) A developmental perspective on adolescent drug
abuse. Advances in Alcohol and Substance Abuse, 5, 41-67.
Belkin, B.M. and Gold, M.S. (1991) Opioids. pp. 537-547 in N.S. Miller (Ed.),
Comprehensive Handbook of Drug and Alcohol Addiction, New York: Marcel Dekker.
Bell, D. (1973) The experimental reproduction of amphetamine psychosis. Archives of
General Psychiatry, 29, 35-40.
Bland, R.C., Newman, S.C. and Orn, H. (1987) Schizophrenia: lifetime co-morbidity in a
community sample. Acta Psychiatrica Scandinavica, 75, 383-391.
Bloch, E. (1983) Effects of marijuana and cannabinoids on reproduction, endocrine function,
development and chromosomes. In K.O. Fear and H. Kalant (eds) Cannabis and Health
Hazards. Addiction Research Foundation, Toronto.
Block, R.I., Farnham, S., Braverman, K., Noyes, R., Jr. and Ghoneim, M.M. (1990).Long-
term marijuana use and subsequent effects on learning and cognitive functions related to
school achievement: preliminary study. In J.W. Spencer and J.J. Boren (Ed.), Residual
Effects of Abused Drugs on Behavior, National Institute on Drug Abuse Research
Monograph 101 Rockville, MD: U.S. Department of Health and Human Services.
Bloom, J.W., Kaltenborn, W.T., Paoletti, P., Camilli, A. and Lebowitz, M.D. (1987)
Respiratory effects of non-tobacco cigarettes. British Medical Journal, 295,1516-1518.
Bondy, S. (1994) Self-reported harm from alcohol, tobacco and marijuana use:
Ontario1992/94. Working paper. Toronto: Addiction Research Foundation.
Breakey, W.R., Goodell, H., Lorenz, P.C. and McHugh, P.R. (1974) Halucinogenic drugs as
precipitants of schizophrenia. Psychological Medicine, 4, 255-261.
Brill, N.Q. and Christie, R.L. (1974). Marihuana use and psychosocial adaptation: Follow-up
study of a collegiate population. Archives of General Psychiatry, 31713-719.
Brook, J.S., Cohen, P., Whiteman, M. and Gordon, A.S. (1992). Psychosocial risk factor sin
the transition from moderate to heavy use or abuse of drugs. In M. Glantz and R.Pickens (eds)
Vulnerability to Drug Abuse. American Psychological Association, Washington.
Bruun, K. Edwards, G., Lumio, M., Makela, K., Pan, L., Popham, R.E., Room, R.,
Schmidt,W., Skog, O.J., Sulkunen, P. & Osterberg, E. (1975) Alcohol Control Policies in
Public Health Perspective, Volume 25, Helsinki: Finnish Foundation for AlcoholStudies.
Caplan, G.A. and Brigham, B.A. (1989) Marijuana smoking and carcinoma of the tongue. Is
there an association? Cancer, 66, 1005-1006.
Carter, W.E., Coggins, W. and Doughty, P.L. (1980) Cannabis in Costa Rica: A study of
chronic marihuana use. Institute for the Study of Human Issues, Philadelphia.
Caviston, P. (1987) Pregnancy and Opiate Addiction. British Medical Journal,295, 285-286.
Chait, L.D. & Pierri, J. (1992) Effects of smoked marijuana on human performance: Acritical
review. In A. Murphy & J. Bartke (Eds) Marijuana/Cannabinoids: Neurobiology and
Neurophysiology, CRC, Boca Raton.
Chesher, G., Lemon, J., Gomel, M. and Murphy, G. The effects of methadone, as used in a
methadone maintenance program, on driving-related skills. National Drug and
AlcoholResearch Centre Technical Report Number 3. National Drug and Alcohol
Research Centre, Sydney, 1989.
Chopra, G.S. and Smith, J.W. (1974) Psychotic reactions following cannabis use in East
Indians. Archives of General Psychiatry, 30, 24-27.
Cimbura, G., Lucas, D.M., Bennet, R.C., Warren, R.A. and Simpson, H.M. (1982) Incidence
and toxicological aspects of drugs detected in 484 fatally injured drivers and pedestrians in
Ontario. Journal of Forensic Science, 27, 855-867.
Cleghorn, J.M., Kaplan, R.D., Szechtman, B., Szechtman, H., Brown, G.M. and Franco,
S.(1991) Substance abuse and schizophrenia: effect on symptoms but not on neurocognitive
function. Journal of Clinical Psychiatry, 52, 26-30.
Cohen, S. (1982) Cannabis effects upon adolescent motivation. In National Institute on Drug
Abuse. Marijuana and Youth: Clinical Observations on Motivation and Learning.
National Institute on Drug Abuse. Rockville, Maryland.
Compton, D.R., Dewey, W.L. and Martin, B.R. (1990) Cannabis dependence and
toleranceproduction. Advances in Alcohol and Substance Abuse, 9, 128-147.
Connell, P.H. (1959) Amphetamine Psychosis. Maudsley Monograph Number 5,Institute of
Psychiatry, Oxford University Press, London.
Consensus Report, C.D.P. Research Technology Branch, National Institute on Drug
Abuse.(1985) Drug concentrations and driving impairment. Journal of the American
Medical Association, 254(18), 2618-2621.
Cook, P.J. and Moore, M.J. (1993) Economic perspectives on reducing alcohol-related
violence. Pp. 193-212 in S.E. Martin (ed) Alcohol and interpersonal Violence: Fostering
Multidisciplinary Perspectives. NIAAA Research Monograph 24, NIH Publication No.93-
3496, Department of Health and Human Services.
Day, N.L., Wagener, D.K. and Taylor, P.M. (1985) Measurement of substance use during
pregnancy: methodologic issues. In T.M. Pinkert (ed) Current Research on the
Consequences of Maternal Drug Abuse. NIDA Research Monograph No 59, Department of
Health and Human Services.
Day, N.L., Richardson, G.A., Goldschmidt, L., Robles, N., Taylor, P.M., Stoffer, D.S.,
Cornelius, M.D. and Geva, D.D. (in press) The effect of prenatal marijuana exposure in the
cognitive development of offspring at age three. Neonatology and Teratology.
Der, G., Gupta, S. and Murray, R.M. (1990) Is schizophrenia disappearing? Lancet, 1,513-
516.
Dixon, L., Haas, G., Wedien, P.J., Sweeney, J. and Frances, A.J. (1990) Acute effects of drug
abuse in schizophrenic patients: clinical observations and patients' self-reports.
Schizophrenia Bulletin, 16, 69-79.
Dixon, L., Haas, G., Wedien, P.J., Sweeney, J. and Frances, A.J. (1991) Drug abuse in
schizophrenic patients: clinical correlates and reasons for use. American Journal of
Psychiatry, 148, 224-230.
Doll, R. and Peto, R. (1980) The Causes of Cancer. Oxford University Press,1981.
Donald, P.J. (1991a) Marijuana and upper aerodigestive tract malignancy in young patients.
In G. Nahas and C. Latour (eds) Physiopathology of Illicit Drugs: Cannabis, Cocaine,
Opiates. Oxford, Pergamon Press.
Donald, P.J. (1991b) Advanced malignancy in the young marijuana smoker. In H.
Freidman,S. Specter, and T.W. Klein (eds) Drugs of Abuse, Immunity, and
Immunodeficiency. London, Plenum Press.
Donnelly, N. and Hall, W. (1994). Patterns of Cannabis Use in Australia. Review prepared
for the Australian National Task Force on Cannabis.
Donovan, J.E., and Jessor, R. (1983) Problem drinking and the dimension of involvement
with drugs: A Guttman Scalogram analysis of adolescent drug use. American Journal of
Public Health, 73, 543-552.
Duggan, A.W. and North, R.A. (1983) Electrophysiology of opioids. Pharmacologic
Reviews, 35, 219-282.
Duncan, D.F. (1987) Lifetime prevalence of "amotivational syndrome" among users and non-
users of hashish. Psychology of Addictive Behaviors 1, 114-119.
Edwards, G. (1982) Cannabis and the question of dependence. Advisory Council on the
Misuse of Drugs. Report of the Expert Group on the Effects of Cannabis Use.
HomeOffice, London.
Edwards, G., Arif, A. & Hodgson, R. (1981) Nomenclature and classification of drug and
alcohol related problems: A WHO memorandum. Bulletin of the World Health
Organization, 59(2), 225-242
Edwards, G., Anderson, P., Babor, T.F., Casswell, S., Ferrence, R., Giesbrecht, N.,Godfrey,
C., Holder, H.D., Lemmens, P., Makela, K., Midanik, L.T., Norstrom, Osterberg, E,Romelsjo,
Room, R., Simpura, J. and Skog, O-J. (1994) Alcohol Policy and the Public Good Oxford:
Oxford University Press.
Fehr, K. O. and Kalant, H. (1983) (eds.) Cannabis and Health Hazards. Addiction Research
Foundation, Toronto.
Fligiel, S.E.G., Beals, T. F., Venkat, H. , Stuth, S., Gong, H. and Tashkin, D. P.(1988)
Pulmonary pathology in marijuana smokers. In G. Chesher, P. Consroe, and R. Musty(eds)
Marijuana: An International Research Report. National Campaign Against Drug Abuse
Monograph Number 7, Australian Government Publishing Service, Canberra.
Fried, P.A. (1980) Marijuana use by pregnant women: Neurobehavioural effects in neonates.
Drug and Alcohol Dependence, 6, 415-424.
Fried, P.A. (1982) Marijuana use by pregnant women and effects on offspring: an update.
Neurobehavioral Toxicology and Teratology, 4, 451-454.
Fried, P.A. (1985) Postnatal consequences of maternal marijuana use. In T. M. Pinkert(ed.)
Current Research on the Consequences of Maternal Drug Abuse. NIDA Research
Monograph No. 59, Department of health and Human Services.
Fried, P.A. (1986) Marijuana and human pregnancy. In I. Chasnof (Ed.) Drug Use in
Pregnancy: Mother and Child. MAP Press, Lancaster.
Fried, P.A. (1989) Postnatal consequences of maternal marijuana use in humans. Annals of
the New York Academy of Sciences, 562, 123-132.
Fried, P.A. (1993) Prenatal exposure to tobacco and marijuana: Effects during pregnancy,
infancy and early childhood. Clinical Obstetrics and Gynecology, 36,319-337.
Fried, P.A. and Watkinson, B. (1990) 36- and 48-month neurobehavioral follow-up of
children prenatally exposed to marijuana, cigarettes and alcohol. Development and
Behavioral Pediatrics, 11, 49-58.
Fried, P.A., Buckingham, M. and Von Kulmiz, P. (1983) Marihuana use during pregnancy
and perinatal risk factors. American Journal of Obstetrics and Gynecology, 146,992-992.
Fried, P.A., O'Connell and Wakinson, B. (1992) 60- and 72-month follow-up of children
prenatally exposed to marijuana, cigarettes, and alcohol: cognitive and languageassessment.
Developmental and Behavioral Pediatrics, 13, 383-391.
Gawin, F. H. and Ellinwood, E.H. (1988) Cocaine and other stimulants: Actions, abuseand
treatment. New England Journal of Medicine, 318, 1173-1182.
Ghodse, A.H. (1986) Cannabis psychosis. British Journal of Addiction, 81,473-478.
Gieringer, D.H. (1988) Marijuana, driving and accident safety. Journal of Psychoactive
Drugs, 20, 93-101.
Gibson, G.T., Baghurst, P. A. and Colley, D.P. (1983) Maternal alcohol, tobacco and cannabis
consumption and the outcome of pregnancy. Australian and New Zealand Journal of
Obstetrics and Gynaecology, 23, 15-19.
Goldberg, L. (1968a) Drug abuse in Sweden. Part I. Bulletin on Narcotics, 20,91), 1-31. (a)
Goldberg, L. (1968b) Drug abuse in Sweden. Part II. Bulletin on Narcotics, 20,(2) 9-36. (b)
Gong, H., Fliegel, S., Tashkin, D.P. and Barbers, R.G. 91987) Tracheobronchial changesin
habitual, heavy smokers of marijuana with and without tobacco. American Review of
Respiratory Disease, 136, 142-149.
Goode, E. (1974) Marijuana use and the progression to dangerous drugs. In L.L. Miller(Ed.)
Marijuana: Effects on Human Behavior. Academic Press, New York.
Greenland, S., Staisch, K.J., Brown, N. and Gross, S.J. (1982a) The effects ofmarijuana use
during pregnancy. I. A preliminary epidemiologic study. American Journalof Obstetrics
and Gynecology, 143, 408-413. (a)
Greenland, S., Staisch, K.J., Brown, N. and Gross, S.J. (1982b) Effects of marijuana onhuman
pregnancy, labor and delivery. Neurobehavioral Toxicology and Teratology, 4,447-450. (b)
Halikas, J.A., Weller, R.A., Morse, C. and Shapiro, T. (1982) Incidence andcharacteristics of
amotivational syndrome, including associated findings, among chronicmarijuana users. In
National Institute on Drug Abuse. Marijuana and Youth: ClinicalObservations on
Motivation and Learning. National Institute on Drug Abuse. Rockville,Maryland.
Hall, W. (1995) The public health implications of cannabis use. Australian Journalof Public
Health, 19, 235-242.
Hall, W., Solowij, N. and Lemon, J. (1994) Health and Psychological Consequences
ofCannabis Use. Report to the National Taskforce on Cannabis.
Hatch, E.E. and Bracken, M.B. (1986) Effect of marijuana use in pregnancy on fetalgrowth.
American Journal of Epidemiology, 124, 986-993.
Hawkins, J.D., Catalano, R.F. and Miller, J.Y. (1992) Risk and protective factors foralcohol
and other drug problems in adolescence and early adulthood: implications forsubstance abuse
prevention. Psychological Bulletin, 112, 64-105.
Helzer, J.E., Burnham, A. and McEvoy, L.T. (1991) Alcohol abuse and dependence. In
L.N.Robins and D.A. Regier (eds.) Psychiatric Disorders in America. Free
Press,MacMillan, New York.
Henderson, R.L., Tennant, F.S., and Guerry, R. (1972) Respiratory manifestations ofhashish
smoking. Archives of Otolaryngology, 95, 248-251.
Hingson, R., Heeren, T., Mangione, T., Morelock, S. and Mucatel, M. (1982) Teenagedriving
after using marijuana or drinking and traffic accident involvement. Journal ofSafety
Research, 13, 33-37.
Hingson, R., Alpert, J., Day, N., Dooling, E., Kayne, H., Morelock, S., Oppenheimer, E.and
Zuckerman, B. (1982) Effects of maternal drinking and marijuana use on fetal growthand
development. Pediatrics, 70, 539-546.
Hollister, L.E. (1986) Health aspects of cannabis. Pharmacological Reviews,38,1-20.
Hollister, L.E. (1992) Marijuana and immunity. Journal of Psychoactive Drugs,24, 159-164.
Holman, C.D., Armstrong, B. et al (1988) The Quantification of Drug-Caused
Morbidityand Mortality in Australia. Commonwealth Department of Community Services
and Health.
Huber, G.L., Griffith, D.L. and Langsjoen, P.M. (1988) The effects of marihuana on
therespiratory and cardiovascular systems. In G. Chesher, P. Consroe, and R. Musty (eds.)
Marijuana:An International Research Report. National Campaign Against Drug Abuse
MonographNumber 7, Australian Government Publishing Service, Canberra.
Institute of Medicine. (1982) Marijuana and Health. National Academy Press,Washington,
DC.
International Agency on Cancer (1990) Cancer: Causes, Occurrence and Control.(Ed.) L.
Tomatis. International Agency on Cancer, Lyon.
Jablensky, A., Sartorius, N., Ernberg, G., Anker, M., Korten, A., Cooper, J.E., Day, R.and
Bertelsen, A. (1991) Schizophrenia: manifestations, incidence and course in differentcultures.
A World Health Organization Ten-Country Study. Psychological MedicineMonograph
Supplement No, 20. 1991.
Jacobs, M.R., and Fehr, L., O'B. (1987) Drugs and drug abuse: A Reference Text,Toronto:
Addiction Research Foundation.
Jessor, R. and Jessor, S.L. (1977) Problem Behavior and Psychosocial Development:
ALongitudinal Study of Youth. New York, Academic Press.
Joe, G.W. and Simpson, D.D. (1987) Mortality rates among opioid addicts in alongitudinal
study. American Journal of Public Heatlh, 77, 347-348.
Joe, G.W. and Simpson, D.D. (1990) Death Rates and Risk Factors, pp. 193-202 in S.B.Sells
and B.S. Brown (Eds.), Opioid Addiction and Treatment: A 12-year Follow-up.Malabar
FL: Robert E. Krieger Pub. Co., 1990.
Johnson, B.A., Smith, B.L. and Taylor, P. (1988) Cannabis and schizophrenia. Lancet,1., 592-
593.
Johnston, L.D., O'Malley, P.M. and Eveland, L.K. (1978) Drugs and delinquency: A searchfor
causal connections. In D.B. Kandel (ed.) Longitudinal Research on Drug Use:Empirical
Findings and Methodological Issues. John Wiley and Sons, New York.
Johnston, L.D., O'Malley, P.M. and Bachman, J.G. (1991) Drug Use Among American
HighSchool Seniors, College Students and Young Adults, 1975-1990. Volumes I and
II.National Institute on Drug Abuse, Rockville MD.
Kandel, D.B. (1984) Marijuana users in young adulthood. Archives of GeneralPsychiatry,
41, 200-209.
Kandel, D. and Faust, R. (1975) Sequence and stages in patterns of adolescent drug
use.Archives of General Psychiatry, 32, 923-932.
Kandel, D.B., Davies, M., Karus, D. and Yamaguchi, K. (1986) The consequences in
youngadulthood of adolescent drug involvement. Archives of General Psychiatry, 1986,
43,746-754.
Kandel, D.B. and Raveis, V.H. (1989) Cessation of illicit drug use in young adulthood.
Archivesof General Psychiatry, 46, 109-116.
Kandel, D.B. and Davies, M. (1992) Progression to regular marijuana
involvement:Phenomenology and risk factors for near daily use. In M. Glantz and R. Pickens
(eds.) Vulnerabilityto Drug Abuse. American Psychological Association, Washington.
Kaslow, R.A., Blackwelder, W.C., Ostrow, D.G.., Yerg, D., Palenick, J., Coulson, A.H.and
Valdiserri, R.O. (1989) No evidence for a role of alcohol or other psychoactive drugsin
accelerating immunodeficiency in HIV-1-positive individuals: A report form theMulticenter
AIDS Cohort Study. Journal of the American Medical Association, 261,4324-3429.
Knudsen, P. and Vilmar, T. (1984) Cannabis and neuoleptic agents in schizophrenia.
ActaPsychiatrica Scandinavica, 69, 162-174.
Kolansky, H. and Moore, W.T. (1971) Effects of marihuana on adolescents and youngadults.
Journal of the American Medical Association, 216, 486-492.
Kuijten, R.R., Bunin, G.R., Nass, C.C. and Meadows, A.T. (1990) Gestational andfamilial
risk factors for childhood astrocytoma: results of a case-control study. CancerResearch, 50,
2608-2612.
Lantner, I.L. (1982) Marijuana abuse by children and teenagers: a pediatrician's view.Cohen,
S. (1982) Cannabis effects upon adolescent motivation. In National Institute onDrug Abuse.
Marijuana and Youth: Clinical Observations on Motivation and Learning.National
Institute on Drug Abuse. Rockville, Maryland.
Lenke, L. (1990) Alcohol and Criminal Violence -- Time Series Analyses in
aComparative Perspective. Almqvist and Wiksell, Stockholm.
Leuchtenberger, C. (1983) Effects of marihuana (cannabis) smoke on cellularbiochemistry of
in vitro test systems. In K.O. Fehr and H. Kalant (Eds.) Cannabisand Health Hazards.
Addiction Research Foundation, Toronto.
Linn, L., Schoenbaum, S., Monson, R., Rosner, R., Stubblefield, P.C. and Ryan, K.J.(1983)
The association of marijuana use with outcome of pregnancy. American Journal ofPublic
Health, 73, 1161-1164.
Maddux, J.F. and Desmond, D.P. (1981) Careers of Opioid Users, New York:Praeger.
McBay, A.J. (1986) Drug concentrations and traffic safety. Alcohol, Drugs andDriving, 2,
51-59.
McGee, R.O. and Feehan, M. (1993) Cannabis use among New Zealand adolescents.
NewZealand Medical Journal, 106, 345.
Martin, C.A. and Martin, W.R. (1980) Opiate dependence in women, pp. 465-486 in O.Kalant
(Ed.) Alcohol and Drug Problems in Women: Research Advances in Alcohol and
DrugProblems, Volume 5, New York: Plenum Press.
Martin, S.E. (Ed.) (1993) Alcohol and Interpersonal Violence: FosteringMultidisciplinary
Perspectives. NIAAA Research Monograph 24, NIH Publication No.93-3496, Department of
Health and Human Services.
Martinez-Arevalo, M.J., Calcedo-Ordonez, A and Varo-Prieto, J.R. (1994)
Cananbisconsumption as a prognostic factor in schizophrenia. British Journal of
Psychiatry,164, 679-681.
Mason, A.P. and McBay, A.J. (1984) Ethanol, marijuana and other drug use in 600
driverskilled in single-vehicle crashes in North Carolina 1978-1981. Journal of
ForensicScience, 29, 987-1026.
Malinger, G.D., Somers, R.H., Davidson, S.T. and Manheimer, D.I. (1976) Theamotivational
syndrome and the college student. Annals of the New York Academy ofSciences, 282, 37-
55.
Moore, M.H. and Gerstein, D.K. (Eds.) (1981) Alcohol and Public Policy: Beyond
theShadow of Prohibition. National Academy Press, Washington.
Munson, A.E. and Fehr, K.O. (1983) Immunological effects of cannabis. In K.O. Fehr andH.
Kalant (Eds.) Cannabis and Health Hazards. Addiction Research Foundation,Toronto.
Nahas, G.G. (1984) Toxicology and pharmacology. In G.G. Nahas Marihuana in
Scienceand Medicine. New York, Raven Press.
Nahas, G. and Latour, C. (1992) The human toxicity of marijuana. Medical Journal
ofAustralia, 156, 495-497.
National Institute on drug Abuse. (1992) National household survey on drug
abuse:population estimates 1991 - Revised November 20, 1992. Rockville, MD:
NationalInstitute on Drug Abuse.
Neglia, J.P., Buckley, J.D. and Robinson, L.L. (1991) Maternal marijuana use andleukemia in
offpsring. In G. Nahas (Eds.) Physiopathology of Illicit Drugs: Cannabis,Cocaine, Opiates.
Oxford, Pergamon Press.
Negrete, J.C. (1989) Cannabis and schizophrenia. British Journal of Addiction,84, 349-351.
Negrete, J.C., Knapp, W.P., Douglas, D. and Smith, W.B. (1986) Cannabis affects theseverity
of schizophrenic symptoms: results of a clinical survey. PsychologicalMedicine, 16, 515-
520.
Newcombe, M.D. (1992) Understanding the multidimensional nature of drug use and
abuse:The role of consumption, risk factors and protective factors. In M. Glantz and R.
Pickens(Eds.) Vulnerability to Drug Abuse. American Psychological Association,
Washington.
Newcombe, M.D. and Bentler, P. (1988) Consequences of Adolescent Drug Use: Impact
onthe Lives of Young Adults. Sage Publications, Newbury Park, California.
Norton, R. and Colliver, J. (1988) Prevalence and patterns of combined alcohol andmarijuana
use. Journal of Studies in Alcohol, 49, 378-380.
O'Donnell, J.A. (1969) Narcotic Addicts in Kentucky, (US Public Health ServiceP. No.
1881). Washington, DC: US Government Printing Office.
O'Donnell, J.A., Voss, H.L., Clayton, R.R., Slatin, G.T. and Room, R.G.W. (1976)
YoungMen and Drugs: A Nationwide Survey. NIDA Research Monograph No. 5, DHEW
PublicationNo. (ADM) 76-311. Rockville, MD: U.S. Department of Health, Education and
Welfare,National Institute on Drug Abuse.
Osgood, D.W., Johnston, L.D., O'Malley, P.M. and Bachman, J.G. (1988) The generality
ofdeviance in late adolescence and early adulthood. American Sociological Review, 53,81-
93.
Pernanen, K. (1991) Alcohol in Human Violence. New York and London: Guilford.
Pohorecky, L.A., Brick, J. and Milgram, G.G. (Eds.) (1993) Alcohol and
Aggression.Journal of Studies on Alcohol, Supplement No. 11, September.
Polen, M.R., Sidney, S., Tekawa, I.S., Sadler, M. and Friedman, G.D. (1993) Health careuse
by frequent marijuana smokers who do not smoke tobacco. Western Journal of
Medicine,158, 596-601.
Robinson, L.I., Buckley, J.D., Daigle, A.E., Wells, R., Benjamin, D., Arthur, D.C.
andHammond, G.D. (1989) Maternal drug use and the risk of childhood nonlymphoblastic
leukemiaamong offpsring: An epidemiologic investigation implicating marijuana. Cancer,
63,1904-1911.
Roffman, R.A., Stephens, R.S., Simpson, E.E. and Whitaker, D.L. (1988) Treatment
ofmarijuana dependence: preliminary results. Journal of Psychoactive Drugs, 20,129-137.
Room, R. (1983) Alcohol and crime: behavioral aspects. Pp. 35-44 in S.H. Kadish (Ed.)
Encyclopaediaof Crime and Justice, Vol. 1. Free Press, New York.
Room, R. (1994) Alcohol and ethnography: A case of problem deflation?
CurrentAnthropology, 25, 169-191.
Rottanburg, D., Robins, A.H., Ben-Arie, O., Teggin, A. and Elk, R. (1982)Cannabis-
associated psychosis with hypomanic features. Lancet, 2, 1364-1366.
Rounsaville, B.J., Bryant, K., Babor, T., Kranzler, H. and Kadden, R. (1993)Cross-system
agreement for substance use disorders. Addiction, 88, 337-348.
Rubin, V. and Comitas, L. 91975) Ganja in Jamaica: A Medical Anthropological Studyof
Chronic Marihuana Use. Mouton, The Hague.
Schneier, F.R. and Siris, S.G. (1987) A review of psychoactive substance use and abusein
schizophrenia: patterns of drug choice. Journal of Nervous and Mental Disorders.175, 641-
652.
Scheier, L.M. and Newcombe, M.D. (1991) Psychosocial predictors of drug use initiationand
escalation: an expansion of the multiple risk factors hypothesis using longitudinaldata.
Contemporary Drug Problems, 18, 31-73.
Shedler, J. and Block, J. (1990) Adolescent drug use and psychological health.
AmericanPsychologist, 45, 612-630.
Simpson, D.D., Joe, G.W., Lehman, W.E.K. and Sells, S.B. Addiction Careers:
etiology,treatment and 12 year follow-up outcomes. The Journal of Drug Issues, 1986,
16(1),107-121.
Simpson, H.M. (1986) Epidemiology of road accidents involving marijuana. Alcohol,Drugs
and Driving, 2, 15-30.
Smart, R.G. (1983) The epidemiology of cannabis use and its health consequences inWestern
countries. In K.O. Fehr and H. Kalant (eds.) Cannabis and Health Hazards.Addiction
Research Foundation, Toronto.
Smart, R.G. and Fejer, D. (1976) Drug use and driving risk among high school students.
AccidentAnalysis and Prevention, 8, 33-38.
Smiley, A. (1986) Marijuana: on-road and driving simulator studies. Alcohol, Drugsand
Driving, 2, 121-134.
Soderstrom, C.A., Triffilis, A.L., Shankar, B.S., Clark, W.E., Cowley, R.A. (1988)Marijuana
and alcohol use among 1023 trauma patients. Archives of Surgery, 123,733-737.
Soueif, M.I. (1971) The use of cannabis in Egypt: A behavioural study. Bulletin onNarcotics,
23(4), 17-28.
Spooner, C. and Flaherty, B. (1992) Comparison of Data Collection Methodologies forthe
Study of Youth Illicit Drug Users. Sydney: Drug and Alcohol Directorate, N.S.W.Health
Department, In House Report Series No. 92-2.
Stefanis, C., Dornbush, R. and Fink, M. (Eds.) (1977) Hashish: Studies on Long-TermUse.
Raven Press, New York.
Tashkin, D.P. (1993) Is frequent marijuana smoking harmful to health? WesternJournal of
Medicine, 158, 635-637.
Tashkin, D.P., Coulson, A.H., Clark, V.A., Simmons, M., Bourque, L.B., Duann, S.,Spivey,
G.H. and Gong, H. (1987) Respiratory symptoms and lung function in habitual heavy
smokers of marijuana alone, smokers of marijuana and tobacco, smokers of tobacco alone,
and nonsmokers. American Review of Respiratory Diseases, 135, 209-216.
Tashkin, D.P., Wu, T.C., Djahed, B. and Rose, J.E. (1988) Smoking topography and delivery
of insoluble particulates and carbon monoxide to the lung during the smoking of tobacco and
marihuana of varying potency in habitual smokers of both substances. In G.Chesher, P.
Consroe, and R. Musty (Eds.) Marijuana: An International Research Report. National
Campaign Against Drug Abuse Monograph Number 7, Australian Government Publishing
Service, Canberra.
Tashkin, D.P., Fligiel, S., Wu, T.C., Gong, H., Barbers, R.G., Coulson, A.H., Simmons, M.S.,
and Beals, T.F. (1990) Effects of habitual use of marijuana and/or cocaine on the lung. In
C.N. Chiang and R.L. Hawks (Eds.) Research Findings on Smoking of AbuseSubstances.
National Institute on Drug Abuse Research Monograph 99, National Instituteon Drug Abuse
Research Monograph 99, National Institute on Drug Abuse, Rockville, Maryland.
Taylor, F.M. (1988) Marijuana as a potential respiratory tract carcinogen: aretrospective
analysis of a community hospital population. Southern Medical Journal,81, 1213-1216.
Tennant, F.S., Preble, M., Prendergast, T.J. and Ventry, P. (1971) Medical manifestations
associated with hashish smokers. In L.S. Harris (Ed.) Problems of Drug Dependence, 1979,
Volume 127. National Institute on Drug Abuse, Rockville Maryland.
Tennes, K., Aritable, N., Blackard, C., Boyles, C., Hassoun, B., Holmes, L. and Kreye,M.
91985) Marihuana: prenatal and postnatal exposure in the human. In T.M. Pinkert (Ed.)
Current Research on the Consequences of Maternal Drug Abuse. NIDA Research
Monograph No. 59,Department of Health and Human Services.
Terhune, K.W. (1986) Problems and methods in studying drug crash effects. Alcohol, Drugs
and Driving, 2, 1-13.
Thomas, H. (1993) Psychiatric symptoms in cannabis users. British Journal ofPsychiatry,
163, 141-149.
Thornicroft, G. (1990) Cannabis and psychosis: Is there epidemiological evidence
forassociation. British Journal of Psychiatry, 157, 25-33.
Turner, W.M. and Tsuang, M.T. (1990) Impact of substance abuse on the course andoutcome
of schizophrenia. Schizophrenia Bulletin, 16, 87-372.
USDHHS (1993) National Household Survey on Drug Abuse: Main Findings, 1991.
DHHS Publication No. (SMA) 93-1980. Rockville, MD: U.S. Department of Health and
HumanServices, Substance Abuse and Mental Health Administration.
Vaillant, G.E. (1973) A 20-year follow-up of New york narcotic addicts. Archives of
General Psychiatry, 29, 237-241.
Weil, A. (1970) Adverse reactions to marihuana. New England Journal of Medicine,282,
997-1000.
Wells, J.E., Bushnell, J.A., Joyce, P.R., Oakley-Browne, M.A. and Hornblow, A.R.
(1992)Problems with alcohol, drugs and gambling in Christchurch, New Zealand. In M.
Abbot and K.Evans (Eds.) Alcohol and Drug Dependence and Disorders of Impulse
Control. AlcoholLiquor Advisory Council, Auckland.
Williams, A.G., Peat, M.A., Crouch, D.J., Wells, J.K. and Finkle, B.S. (1985) Drugs in fatally
injured young male drivers. Public Health Reports, 100, 19-25.
Woody, G.E., Cottler, L.B. and Caciola, J. (1993) Severity of dependence: data from
theDSM-IV field trials. Addiction, 88,1573-1579.
Woody, G.E. and O'Brien, C.P. (1991) Update of Methadone Maintenance, pp. 1113-1125
inN.S. Miller (Ed.), Comparison Handbook of Drug and Alcohol Addiction, New
york:Marcel Dekker.
Wu, T., Tashkin, D.P., Djahed, B. and Rose, J.E. (1988) Pulmonary hazards of
smokingmarijuana with tobacco. New England Journal of Medicine, 318, 347-351.
Yamaguchi, K. and Kandel, D.B. (1984a) Patterns of drug use from adolescence toadulthood.
II Sequences of progression. American Journal of Public Health, 1984,74,668-672.
Yamaguchi, K. and Kandel, D.B. (1984b) Patterns of drug use from adolescence toadulthood.
III Predictors of progression. American Journal of Public Health, 1984,74, 673-681.
Zuckerman, B., Frank, D., Hingson, R., Amaro, H., Levenson, S., Kayne, H., Parker, S.,Vinci,
R., Aboagyen, K., Fried, L., Cabral, H., Timperi, R. and Bauchner, H. (1989)Effects of
maternal marijuana and cocaine use on fetal growth. New England Journal ofMedicine,
320, 762-768.
WHO Project on Health Implications of Cannabis Use:
A Comparative Appraisal of the Health and Psychological
Consequences of Alcohol, Cannabis, Nicotine and Opiate Use
Table 1:
Summary of ratings of overall effects of drug use by current
users (Percent)
United States 1974: Males aged 20 - 30
O'Donnell et al., 1976:79
LIFETIME USERS OF:
RESPONSES
MARIJUANA
ALCOHOL TOBACCO
OR HASHISH
Total N (2434) (2211) (1382)
"Very good" or
"more good than 33 12 45
bad"
No effect 21 22 22
"More bad than
good" or "very 46 66 33
bad"
Ontario 1994: Both sexes aged 18 - 34
Bondy, 1994
CURRENT USERS OF:
RESPONSES
MARIJUANA
ALCOHOL TOBACCO
OR HASHISH
Total (601) (256) (121)
More good than
19 3 29
harm
Harm and good
70 7 59
about equal
More harm than
11 50 12
good
WHO Project onHealth Implications of Cannabis Use:
A Comparative Appraisal of the Health and
PsychologicalConsequences of Alcohol, Cannabis, Nicotine
and Opiate Use
Table 2:
Types of problems reported in the past 12 months by current
users age 18 to34 (Ontario 1992)
ALCOHOL TOBACCO CANNABIS
[IN THE PAST
12 MONTHS] Total Total Total Frequency of
Was there ever a Frequency 5+ Cigs/day
use
time that your use
of ____ had a 12+ 1+
less
harmful effect on times times
0 - 11 0 - 11 11+ than
your ...? in per
monthly
year month
Total N 338 255 77 126 44 82 42 19 24
Friendship or
5 3 11 18 20 17 7 - 12
social life
Physical health 10 4 21 58 60 56 11 1 20
Home life or
4 1 9 10 8 10 11 2 18
marriage
Work, studies or
employment 4 1 8 7 8 6 7 - 12
opportunities
Financial
6 3 12 43 26 52 14 - 24
situation
One or more 17 9 35 69 63 72 28 4 47
Two or more 6 2 18 39 26 47 8 - 14
