|
Dr G.B. Chesher
Department
of Pharmacology University of Sydney and National Drug and
Alcohol Research Centre University of New South Wales.
Dr Chesher
provides an extensive coverage of the latest Australian and
overseas research on the impairing effects on driving of cannabis,
particularly relative to those of alcohol.
Contents:
1.
Executive summary
2.
Introduction
-
2.1 Pharmacology
and pharmacokinetics
-
2.2 Behavioural
pharmacology and psychology
3.
Studies using the techniques of epidemiology
-
3.1 Pharmacology
and pharmacokinetics
-
3.2 Pharmacokinetics
4.
A comparison of the effects of alcohol and cannabis on skill
performance and driving skills
-
4.1 Laboratory
tests
-
4.2 Duration
of cannabis-induced impairment in laboratory tests
-
4.3 The
effect on laboratory tasks of alcohol and cannabis in combination
-
4.4 Driving
simulators
-
4.5 On-road
driving
5.
Epidemiology
-
5.1 Questionnaire
based surveys
-
5.2 Incidence
of drug detection in crash involved drivers
-
5.3 Attempts
to assess whether or not the driver who has detectable drugs
in the blood stream was culpable in the accident
6.
The use of 'Responsibility Analysis' or estimation of 'culpability'
to determine the role of drugs in crashes
7.
Alcohol and cannabis in epidemiological studies
8.
Summary (of the evidence presented above)
1. EXECUTIVE SUMMARY
There is no
doubt that cannabis, smoked or taken by mouth produces a dose-related
deficit in tests of performance skills as conducted in a laboratory.
Using driving
simulators and on-road real vehicles, cannabis has been shown
to affect driving performance. However, the effects are less
severe than would be anticipated from the evidence obtained
from the laboratory studies of individual tests of skills
performance.
A description
is given of epidemiological studies to determine the role
of cannabis in road crashes. The pharmacological problems
associated with these studies are described. The results of
studies within the last 10 years have failed to present clear
evidence for a role of cannabis in road crashes. The role
of alcohol in all studies has proved to be dominant.
The evidence
indicates that there is a clear difference in the mode of
action of cannabis and alcohol, both pharmacological and behavioural
and this is presented and the implications described.
The most recent
of studies of cannabis and driving (Robbe & O'Hanlon,
1993), which was sponsored by the U.S. National Highway Safety
Traffic Administration included a review of the literature.
The authors' comments in summary of their literature review
and of their own results include the following:
The foremost impression one gains from reviewing the literature
is that no clear relationship has ever been demonstrated between
marijuana smoking and either seriously impaired driving performance
or the risk of accident involvement. The epidemiological evidence,
as limited as it is, shows that the combination of THC and
alcohol is over-represented in injured and dead drivers and
more so in those who actually caused the accidents to occur.
Yet there is little if any evidence to indicate that drivers
who have used marijuana alone are any more likely to cause
serious accidents than drug free drivers.
Of
the many psychotropic drugs, licit and illicit, that are available
and used by people who subsequently drive, marijuana may well
be among the least harmful. Campaigns to discourage the use
of marijuana by drivers are certainly warranted. But concentrating
a campaign on marijuana alone may not be in proportion to
the safety problem it causes.
2. INTRODUCTION
In this paper
I will examine briefly the studies which have sought an understanding
of the effect of cannabis and of alcohol on driving skills
and their role in road crashes. This information has been
based upon scientific data which have been collected from
several scientific disciplines. I have outlined these in earlier
papers and will only mention them briefly here.
The major
purpose of this paper is to compare the two drugs, alcohol
and cannabis and the status of the evidence as to their role
in road crashes.
The determination
of the legal limit for alcohol has been achieved in a scientific
manner. There are pharmacological reasons why it has not been
possible to follow these same techniques with drugs other
than alcohol, including cannabis. This paper will draw attention
to these problems.
First, we
might briefly outline the nature of the evidence which has
been generated to examine the effects of cannabis on driving
skills and as a causative factor in road crashes. This information
has been derived from the employment of three scientific disciplines:
2.1 Pharmacology
and pharmacokinetics
Pharmacology
is the study of the way a drug exerts its action in the body.
This involves an understanding of the sites and the body systems
where the drug acts and the consequences of this drug-system
interaction. Information obtained from these studies can help
to formulate an hypothesis as to how the drug may influence
driving behaviour.
The pharmacological
discipline known as pharmacokinetics studies the fate of the
drug after it has been taken. It provides information as to
the rate of absorption from the site of administration; the
manner of its distribution in the body up to the delivery
to its site of action (eg. the brain). Pharmacokinetics also
studies the way the body eliminates the drug from the body
and includes the understanding of the metabolism and excretion
of the drug.
2..2 Behavioural
pharmacology and psychology
These involve
studies of the effects of the drug on human behaviour. The
behaviour of relevance to this discussion concerns those skills
which are (or are related to) those necessary for the safe
control of a motor vehicle or other items of machinery. Psychological
studies also involve the effects of the drug on mood and cognition.
The three
classifications of these studies are:
(i) Those
performed on specific tests of behaviour or psychological
functioning (for example, tests of reaction times of various
degrees of complexity; tracking; divided attention or vigilance);
(ii) Those
performed in a driving simulator; and
(iii) Those
performed in a real car, either in a closed course or in real
traffic.
3. STUDIES USING THE TECHNIQUES
OF EPIDEMIOLOGY
These studies
aim to determine whether or not a causal relationship between
drug use and a motor vehicle crash exists.
I shall look
at each of the above factors and will compare the two drugs
alcohol and cannabis in the light of current evidence. In
interests of time and space I have in this summary referred
to reviews of the literature and have made only a brief description
of the studies themselves. A fuller description of these can
of course be sourced from the original literature of the cited
reviews.
3.1 Pharmacology
First, the
drugs themselves. With the increase in pharmacological knowledge
it is known that most drugs act upon specific receptors. A
receptor is a specific site in tissues, frequently on the
cell membrane, which has a specific structural affinity (shape)
for a naturally occurring molecule. The interaction between
receptor and the endogenous molecule is part of the body's
normal, physiological functioning. Most drugs exert their
activity by acting upon these receptors. Examples of such
drug-receptor interactions are the opioids (morphine etc)
and the opioid receptors; the antihistamines and the histamine
receptors and the benzodiazepines which act on the benzodiazepine
receptors. The endogenous substances that physiologically
act on these receptors are, respectively, the endorphins and
enkephalins on the opioid receptors; histamine on the histamine
receptors; however the identification of the physiological
substance for the benzodiazepine receptor has yet to be identified.
Research within
the last five years has revealed that the cannabinoids, such
as delta-9-tetrahydrocannabinol (THC) from the cannabis plant
exert their effects on specific receptors known as the cannabinoid
receptors. To date two cannabinoid receptors have been described
and an endogenous (physiological) substance has been identified.
This has been given the name 'anandamide'. It is very likely
that in the near future more cannabinoid receptors will be
described and more endogenous substances that act on these
receptors will be identified. An historical overview of these
findings has recently been published.
In contrast,
the evidence strongly indicates that the drug alcohol does
not act on a specific receptor, but acts more widely in a
non-specific manner on the cell membranes themselves. This
understanding is supported by the evidence that alcohol exerts
effects on most of the tissues of the body and in excess is
toxic to most tissues. The reader is referred to a recent
review on this subject by Dufor and Caces.
Drugs which
act upon a specific receptor produce their effects in doses
measured usually as nanograms or micrograms per kilogram of
body weight. Alcohol doses are measured in grams per kilogram
- many hundreds of thousands times greater than those of most
other drugs. Alcohol is a very non-specific drug.
Another important
factor is that receptor-specific drugs exert their activity
only on those cells which bear the specific receptor. In the
case of the cannabinoids these receptors are found only in
the brain in the basal ganglia, the cerebellum, the brain
stem, thalamic nuclei, hypothalamus and corpus callosum. On
the other hand alcohol affects all nerve cells to which it
is delivered by the circulating blood.
Consequently
it is not surprising that differences in the action of alcohol
and the cannabinoids have been described in their effects
on mood and behaviour. These will be discussed below.
3.2 Pharmacokinetics
The pharmacokinetics
of alcohol and the cannabinoids could hardly be more different.
The apparent
volume of distribution of alcohol (the volume of fluid in
which the drug seems to be dissolved throughout the body)
is quite low, consisting of the 41 litres of body water, providing
a value of about 0.59 litres/kg. Cannabinoids, on the
other hand, are very fat soluble and have a high volume of
distribution which has been estimated to be about 10 litres/kg.
The meaning
of these values is that the concentration of alcohol in the
blood provides a reliable estimate of the concentration of
the drug in the brain. This in turn provides a reliable estimate
of the degree of impairment of the drinker. In addition to
this, alcohol is excreted via the lungs to the breath and
the blood : breath ratio is such that the determination
of the alcohol in breath provides a reliable estimate of the
blood alcohol concentration. It is because of these pharmacokinetic
properties of alcohol that it has been possible to accumulate
the epidemiological data upon which our drink-driving laws
have been based.
Cannabinoids,
on the other hand are lipophilic (fat loving) and are distributed
in the fatty tissues of the body. When smoked, which is the
most common route of administration, the cannabinoids are
rapidly absorbed from the lungs into the bloodstream. Being
so fat soluble the cannabinoids readily cross membranes, leave
the circulation and are rapidly 'dumped' into various tissues
of the body, including the brain. In this way the concentration
of cannabinoid in the blood declines very rapidly as indicated
in Fig 1.
As indicated
in the Figure, we can describe the concentration of cannabinoid
across time in the blood in the three phases: absorption,
re-distribution and elimination. The steep upward curve of
THC represents the inhaled THC being absorbed into the blood
through the lungs; the equally sudden drop in the concentration
of THC represents the drug being 'dumped' from the bloodstream
into fatty tissues. This redistribution phase 'flattens' out
as the 'dumped' THC re-enters the blood and is then metabolised
in the liver-the
elimination phase. It is important to note that the sudden
decline in the concentration of THC (the psychologically active
cannabinoid) in the blood does not represent drug metabolism
but rather the rapid re-distribution of the drug from the
blood into other tissues. The metabolism of the cannabinoids
takes place when these 'dumped' cannabinoids are released
back into the bloodstream whence they pass through the liver
and are very rapidly metabolised and subsequently excreted.
Figure
1. The
blood concentration of THC (squares) and its inactive metabolite,
carboxy THC (THC Acid; diamonds) after the smoking of a marijuana
cigarette. Each point is the mean of results from six volunteers,
all of whom were free from cannabinoids before smoking the
drug. [The 925±7mg refers to the average weight of
the cigarettes and the 1.32% refers to the dry weight concentration
of THC]
Figure 1 also
shows the blood picture of the inactive metabolite, carboxy
THC (or THC acid). It is important to note several points
about the pharmacokinetics of this substance. First, in the
study indicated here (Fig 1) all of the volunteers had no
cannabinoids in their blood before they began smoking. Second,
the THC acid is formed in the liver from the metabolism of
THC, therefore its appearance in blood follows that of the
parent, THC. Third, the THC acid concentration then increases
and surpasses that of the parent molecule in the blood. At
a time when the parent THC is in the blood at only a very
low concentration, that of the metabolite is higher and exists
in the blood for a longer time. Therefore, should the smoker
smoke again before the parent molecule and its metabolite
have been eliminated, the ratio of the concentrations of THC
and of the THC acid will be different from that shown in Figure
1. This is because there will exist a higher concentration
of the metabolite than of the THC in blood at the time when
the next dose of cannabis is smoked.
For this reason,
analytical data that provides a value only for the
metabolite can only be validly interpreted as indicating recent
consumption of cannabis; however the time of this consumption
could be a matter of hours or days. For this reason the quantitative
determination of only the metabolite is of no value to determine
possible impairment.
To assess
possible impairment the analyst must provide data for the
active molecule, THC. And when this occurs, the only interpretation
possible on present knowledge is to infer the recent consumption
of the drug by smoking. To date no meaningful correlation
between blood concentration of THC and impairment in laboratory
tasks has been established. This point will be clarified when
the results of the recent epidemiological studies are discussed
below.
Yet another
problem arises in the interpretation of blood concentrations
of cannabinoids. The pharmacokinetics of the cannabinoids
are quite different when the drug is taken by mouth. Space
in this discussion precludes further discussion of the pharmacokinetics
after oral administration, but suffice to say the absorption
of cannabinoids taken orally is slow and erratic. The absorbed
THC passes through the liver and is rapidly metabolised. This
results in a different proportion of THC to the metabolite,
THC acid than encountered after smoking. There is a greater
amount of entero-hepatic 'recycling' as some of the cannabinoids
are stored in the bile in the gall bladder. These cannabinoids
can later be 'recycled' and reabsorbed into the bloodstream
when the gall bladder empties. In this country, most who use
cannabis, smoke it.
It is also
important to note that the detection of cannabinoids in a
urine sample provide evidence only that the donor of that
urine has been exposed to cannabis at some time in the past.
It gives no indication at all of impairment or of intoxication.
A frequent, heavy cannabis user may be excreting cannabinoids
in urine for some weeks or in some cases, for more than a
month. Those who take the drug by mouth also will be excreting
the drug for a longer period.
4. A COMPARISON OF THE EFFECTS OF
ALCOHOL AND CANNABIS ON SKILLS PERFORMANCE AND DRIVING SKILLS
4.1 Laboratory
tests
Laboratory
tests isolate specific psychological functions and determine
the skill of the test subject on that function. Most studies
test each volunteer on each test before and after taking the
drug. For testing alcohol and cannabis, the choice of these
tests rests upon an assessment of their relationship to the
task of driving a motor vehicle. However, the fact is that
no battery of separate tests comprehensively defines the actual
task of driving. In fact, Joscelyn and others (Joscelyn et
al., 1980) examined the plethora of methods employed in
these studies and commented:
... many tests routinely employed have limited validity or
no demonstrable relation to real-world driving. Measuring
the 'same' behaviors often differ, raising questions about
the comparability of experimental findings.
Laboratory
tests, nevertheless do provide a 'screening' of the potential
for drugs to impair specific behaviours. However, results
from such laboratory testing should not form the sole basis
for any judgement of the potential of a drug to impair actual
driving skills or to increase the probability of an accident.
For this reason, evidence for the traffic hazard associated
with any drug should be confirmed by studies of actual driving
(either using driving simulators or a real car) and by studies
using epidemiological methods.
The data from
laboratory testing of alcohol has been reviewed by Moskowitz
and Austin and of the effects of cannabis by Klonoff, Moskowitz,
and by Chesher. It is clear that both alcohol and cannabis
cause dose-dependent deficits in the performance of specific
laboratory tasks.
It is to be
noted that the doses of cannabinoids in these tests are lower
than those in use by many smokers of cannabis today. However,
they may have been appropriate to the cannabis experience
of the volunteers when these studies were conducted. In many
of these studies, the volunteers were asked to rate the effect
of the dose given with that of their general experience with
the drug. In many (but not all) cases the doses given produced
subjective effects which were as great as those generally
experienced by the volunteers in their social use of the drug.
Looking at
the Australian studies across time, from the 1970s to the
1990s these observations are in accord with the results expressed
in a recent publication concerning the patterns of cannabis
use in Australia. The earlier studies produced deficits in
testing which were greater than those in the later studies.
The data presented by Donnelly and Hall (1994) indicate that:
The prevalence of cannabis use seems to have been very low
by contemporary standards in the early 1970s. It increased
substantially throughout the 1970s and 1980s, levelled off
in the late 1980s, and has probably shown a small increase
in the early 1990s.
The phenomenon
of tolerance to cannabis is well established and this in turn
is a serious confounding variable in the studies with this
drug. Tolerance develops with the regular and frequent use.
This in turn depends upon the pattern of use of those in the
study sample. The correlation of performance : dose : and
tolerance requires further study. There is very little information
available as to the change in doses used across the years
since the 1970s as most data refer only to frequency of use.
Studies involving high doses of cannabis should be undertaken,
but with due consideration given to the degree of tolerance
of the volunteers to be studied.
The Australian
data presented by Donnelly and Hall indicate that:
Most cannabis use is infrequent and intermittent, with about
three-quarters of adult women and two-thirds of adult men
having discontinued their use, or continued to use less often
than weekly. The proportion of users who are weekly users
is highest in the younger age groups. Rates of weekly and
lifetime use are highest among those aged 20 to 24 years,
and decline markedly with increasing age.
4.2 Duration
of cannabis-induced impairment in laboratory tests.
Most studies
have reported a duration of cannabis-induced impairment of
the order of 4 hours. On the other hand there have been three
studies which have reported a longer duration of cannabis
effects of between 10 to 24 hours. However, these reports
have been questioned for methodological or reasons of interpretation.
That of Yesavage et al. did not include a control group.
Subsequently the study was repeated by Leirer et al. in
an attempt to replicate this effect using a control group
but was only able to show an effect up to four hours after
smoking (ie. that described in the many other studies of this
effect). A third study, also with a control group, did demonstrate
an effect at 24 hours after smoking. The statistical significance
of the effect required a statistical procedure (one tail 't'
test) which is of questionable validity when there was no
previous statistical proof that the effect was expected. This
means that the effect was at best, only marginally significant.
The study by Moskowitz et al, as described in Moskowitz's
1985 review (Moskowitz, 1985) was of a:
.... compensatory tracking task performed while simultaneously
executing a visual search task as well as a critical tracking
task. Performance was significantly impaired on the compensatory
tracking task for more than 2 hours and upon the critical
tracking task for up to 10 hours, albeit, intermittently during the period from 4 hours on.
[emphasis added]
At present
I think it is fair to conclude that the evidence for the long
duration of cannabis induced impairment requires more study
to confirm its validity. Furthermore, both tasks in which
it was described are very difficult tasks. It has been argued
that the use of cannabis by pilots in the 24 hours preceding
flying may be more an indicator of poor judgement rather than
a cause for concern about the residual psychomotor effects
of cannabis.
4.3 The
effect on laboratory tasks of alcohol and cannabis in combination
The effect
of this drug combination has been reviewed and only an outline
will be given here.
There is very
clear evidence from numerous studies of the effect of alcohol
and of cannabis on the performance of specific tasks in the
laboratory. Both drugs produce a dose related impairment on
these tasks and the effect of the drugs when given in combination
is essentially additive. Although of more academic than practical
interest is the evidence as to the nature of this additivity.
Several studies have observed a trend that the effect of cannabis
plus alcohol is less than additive, meaning that 1 + 1 is
less than 2. In the most recent study, Dauncey et al.
reported this effect, found to be statistically significant,
and termed it to be a 'de-intensification'. In the light of
the present knowledge of the quite different mode of action
of cannabis and alcohol such an interaction is not necessarily
surprising.
What is quite
surprising and important however, is the result of a study
by Perez-Reyes. For pharmacological reasons the researchers
studying the alcohol-cannabis interaction administered the
drugs such that the peak of blood concentration of both drugs
occurred as near as possible at the same time. Such is the
thinking of the pharmacologist! Indeed Perez-Reyes and his
colleagues had reported such a study showing an additive decremental
effect of the drug combination. Interestingly, in their later
study they had the volunteers smoke marijuana (placebo; 1.7%
and 3.58% THC) before they commenced drinking alcohol (0.85g/kg)
over a period of 30 mins. This would have produced a BAC of
the order of 0.1g%. Their results showed a dose-dependent
effect for cannabis and the characteristic effects expected
for the one dose of alcohol. However, no significant interaction
between the two drugs was recorded. The authors concluded:
The lack of interactive effects, particularly on psychomotor
performance, highlights the influence that the order of administration
of the companion drug has on its interaction with the reference
drug.
4.4 Driving
simulators
A driving
simulator is also a laboratory based apparatus. It is important
to realise that it is only a simulation of real life driving
and driving simulators vary greatly in the degree to which
they can simulate the real event. It is fair to say that all
but the most sophisticated and extremely expensive simulators
are to the test subject, still a laboratory piece of equipment.
They lack realism both in the dynamics of car driving and
in the visual presentation of the road and other traffic.
Nevertheless they are able to present simulated dangerous
presentations to which the driver must respond. The effects
of cannabis on performance in a driving simulator have been
reviewed and a summary only is given here.
The early
driving simulator studies, for the driver, were not interactive
with the 'driving scenery' which was generally a film of the
road to be covered and the driver had little or no control
over the presented imagery.ÊÊ These studies showed no significant
effects of marijuana on car control. However marijuana did
produce the following effects, namely:
(a) An
increase in decision latency before starting, stopping or
overtaking;
(b) Impaired
monitoring of a speedometer; and
(c) Reduced
risk-taking behaviour in tasks requiring a decision to overtake
a vehicle in the presence of an oncoming car.
Later simulator
studies with apparatus with a more realistic driving dynamics
and an interaction between 'scenery' and the driving manoeuvres
did show marijuana effects on car control. The study by Smiley
et al. found that cannabis increased lateral position
variability, headway variability, and caused the 'driver'
to miss more signs that indicated the need to follow another
route. On the other hand, cannabis caused the subjects to
drive in a more conservative manner inasmuch as they maintained
a longer headway when car following, refused more opportunities
to overtake a vehicle in front and when they accepted this
opportunity, they began to do so at a greater distance from
the approaching vehicle. The effects of alcohol (at about
0.08g% BAC) in this study were surprisingly small.
Another and
very similar study by Stein et al. showed alcohol effects
were as one would expect and significantly affected practically
every performance parameter. Alcohol (at about 0.1g% BAC)
was associated with significantly increased 'accidents' (hitting
obstacles or exceeding road edges by a full car width) and
'traffic tickets' (exceeding speed limit by 32 'radar checks').
Alcohol was also associated with increased lane deviations,
speed variability, response times to signs, and errors in
sign recognition. In contrast, cannabis was associated with
few changes. The mean speed travelled was lower and two measures
of steering control changed significantly. Alcohol and cannabis
in combination were associated with more adverse reactions
than alcohol alone. Alcohol was consumed first and the performance
testing was begun 15 minutes after the end of cannabis smoking.
4.5 On-road
driving
Driving studies
with a real car, conducted in an open field, of course present
a more realistic experience of a motor vehicle than do simulators.
However they usually require the driver to undertake manoeuvres
that are not necessarily part of normal driving - such as weaving
between cones. Those studies undertaken in on-road traffic
naturally require great care on the part of the experimenter
to avoid dangerous driving. Therefore these studies are restricted
in the measures that can be realistically taken. They are
somewhat akin, for both the experimenter and the test driver,
to a driver undertaking a test for a driving licence. Indeed,
experimental studies of the effects of drugs using in-car
performance have been described by Smiley as being really
a simulation of real driving.
On-road driving
studies vary considerably in their experimental design and
in the tests of driving employed. In this paper, only the
broadest outline of the results is given in the interests
of brevity. Reviews of these studies have been presented and
published. The reader is referred to the original studies
or to the cited reviews for more information.
There have
been to date, seven on-road studies to examine the effects
of cannabis on driving performance. Each of these is outlined
below:
1. Klonoff
studied volunteers in a closed course as well as in-traffic
on a city road. The closed course study comprised eight tests
and the response scores rested essentially on the number of
cones struck. Testing was conducted in 4 blocks, each of 5
trials. The first three were taken as practice and the fourth,
after drug treatment, were the test trials. The anticipated
scores in the fourth block were determined by regression analysis
on the assumption that the rate of learning or performance
would continue at the same rate. Using this technique the
author concluded that there was an impairment under cannabis.
While the mean of the impairment was not large, the trend
was clear.
The
city traffic study was conducted rather in the manner of a
driving test by a driving examiner. The subjects drove for
about 45 minutes on a course of 16.8 miles after being given
their dose of cannabis. A strong trend towards impaired performance
was indicated by the lower scores given by the examiner on
judgement and concentration after the higher dose of cannabis.
2. Hansteen
et al. conducted a closed course study in which
subjects were required to drive six times around a 1.1 mile
course set out on an airfield. The course was set out with
cones and poles and the number of these hit were counted.
The course involved curves and straight sections and drivers
were required to undertake various manoeuvres. The mean number
of struck objects per lap increased from a mean of 13.2 in
the placebo condition, 13.4 in the low cannabis dose, 16.8
for the high cannabis and 17.4 for the alcohol dose (BAC 0.07g%).
The effects for the high cannabis dose and the alcohol dose
achieved significance.
3. Casswell
conducted a closed course study in which the behaviours sampled
were more typical of those for real driving, than for the
studies outlined above. Driving behaviours recorded included
overtaking, responding to road signs, making a hairpin turn
and driving through a narrow gap. A subsidiary reaction time
task was also included to monitor attention. Driving behaviour
under cannabis, alcohol and the combination was tested. After
alcohol, and alcohol plus cannabis, the subjects showed poorer
tracking performance and drove at increased speed over various
segments of the course, including the hairpin bend, and the
straight section. Under alcohol alone, the speed through the
narrow gap was also increased.
On the
other hand, marijuana alone was not accompanied by steering
or tracking errors. The mean speed dropped significantly after
cannabis, both on the hairpin bend and on the straight section
of the course.
Casswell
suggested that drivers under the influence of cannabis appeared
to compensate for what they perceived as being an adverse
effect on driving. Compensation was exhibited by driving more
slowly. This contrasted with the effects of alcohol. The increased
reaction times to the subsidiary task under cannabis suggests
an effect on attention. The extent of this effect was of the
same order as that measured by the author in another study
after 8 hours of continuous driving.
4. Attwood
conducted a study on a closed course constructed on an airfield
and, like Casswell, used measures appropriate to real driving
including acceleration, following a lead car which varied
its speed and responding to 'traffic signals'. The drug effects
(alcohol, and two doses of cannabis alone and together with
alcohol) recorded were not particularly robust, even with
a complicated multivariate analysis which did distinguish
the treatment conditions from each other.
5. The
study by Peck and colleagues (Peck et al., 1986) from
the California Department of Motor Vehicles, is best summarised
by the authors' own summary.
Approximately 80 volunteer male marijuana and alcohol users
received one of four experimental treatments: (1) marijuana,
(2) alcohol, (3) marijuana and alcohol, or (4) double placebo.
After consumption, each subject drove a vehicle over a test
course which simulated a number of real-world driving conditions.
Four post-drug runs were involved, separated by one hour intervals.
The subject's performance was rated by an in-car examiner,
outside observers, and computerised vehicle measurements.
Blood and urine specimens were extracted after each run to
establish levels of tetrahydrocannabinol (THC), serum carboxy,
and alcohol. A variety of multivariate statistical techniques
were applied in evaluating treatment effects.
Both marijuana and alcohol had significant effects on driving
performance, and the effects were particularly detrimental
under the both-drugs treatment. The effects of marijuana were
more rapid than those of alcohol and somewhat less severe
for most tasks.
In this
study cannabis was smoked after the consumption of the alcohol
dose. In discussing their results and comparing them with
other studies, they had this to say:
There is a vast amount of empirical evidence documenting the
effects of marijuana on a wide array of human performance
measures-cognitive, psychomotor and affective. Although the
literature has clearly established that marijuana affects
all three domains and results in detriments in the ability
to perform many psychomotor and cognitive tasks, the evidence
is somewhat more equivocal on the question of actual driving
skill and even more equivocal on the question of those aspects
of driving skill that are related to safety and accident
avoidance.
[Emphasis that of Peck et al.]
6. Smiley
et al. tested the effects of cannabis (placebo and
two doses) and alcohol (placebo and BAC of 0.05 g%) in combination
and the effect of alcohol alone (BAC 0.08g%) on driving in
a closed course study using an instrumented car.
The
high dose of cannabis significantly increased headway
and headway variability (ie distance from a car in front).
Alcohol alone at the BAC 0.05g% produced an increase in speed,
both in the straight sections of the road and in curves. In
her review of her own study, and those of others, Smiley (Smiley,
1986) concluded:
In
conclusion, marijuana does appear to impair driving behaviour.
However, this impairment is mediated in that subjects under
marijuana treatment appear to perceive that they are indeed
impaired. When they can compensate, they do, for example,
by not overtaking, by slowing down and by focussing their
attention when they know a response will be required. Unfortunately,
such compensation is not possible where events are unexpected
or where continuous attention is required. Effects on driving
behaviour are present shortly after smoking but do not continue for extended periods.
[emphasis added]
7. The most
recent and most comprehensive study of the effect of cannabis
on driving on city roads and a public highway is that conducted
in The Netherlands and was sponsored by the U.S. National
Highway Safety Traffic Administration. An intelligent departure
in methodology in this study from the others reviewed here
is that the dose of cannabis used was determined in a pilot
study using the volunteers who were to take part in the main
study. The aim was to estimate the dose these volunteers generally
use on a social occasion. Accordingly socially appropriate
doses (for these subjects) were chosen for the driving study.
Three driving studies were then performed. The first was conducted
on a closed section of a public highway with no traffic; the
second on a highway with traffic and the third in city traffic.
The measure they have found to be of significance is the standard
deviation of lateral position on the roadway (SDLP). It is
a measure of the 'automatic' function of information processing
in the driving task. Cannabis, in all tests produced a dose-related
increase in the SDLP. Mean speed was somewhat reduced under
cannabis as was the headway distance from the lead vehicle
in the test in highway traffic.
The test under
city driving conditions was conducted under one dose of cannabis
and as a comparison, subjects were also tested under alcohol
at a BAC of 0.04g%. Results in this test showed that this
modest dose of alcohol, but not cannabis, produced a significant
impairment of driving performance relative to placebo. Alcohol
impaired driving performance but subjects did not perceive
it. Cannabis did not impair driving performance yet the subjects
thought it had. After alcohol, there was a tendency towards
faster driving and after cannabis, slower.
This research
group has conducted many studies with the same methodology
and has accumulated much data on the effects of other drugs.
They therefore were able to indicate the extent of the impairment
on the measure of SDLP. The greatest effects of cannabis in
this study were 3.7 and 2.9cm. In other studies drugs, for
example diazepam (Valium), or lorazepam (Ativan), produced
increases of 7 and 10cm respectively. The authors commented:
In
so far as its effects on SDLP are concerned THC was just another
moderately impairing drug.
The authors
go on to say that the effects of cannabis differ qualitatively
from those of other depressant drugs, especially alcohol:
Very importantly our city driving study showed that drivers
who drank alcohol overestimated their performance quality
whereas those who smoked marijuana underestimated it. Perhaps
as a consequence, the former invested no special effort for
accomplishing the task whereas the latter did, and successfully.
This evidence strongly suggests that alcohol encourages risky
driving whereas THC encourages greater caution, at least in
experiments.
Finally, Robbe
contrasted the effects of cannabis when measured with laboratory
based, individual tests in the laboratory, with those conducted
in an on-road vehicle:
The results of these studies corroborate those of previous
driving simulator and closed-course tests by indicating that
THC in single inhaled doses up to 300 µg/kg has significant,
yet not dramatic, dose-related impairing effects on driving
performance. They contrast with results from many laboratory
tests, reviewed by Moskowitz (1985), which show that even
low doses of THC impair skills deemed to be important for
driving, such as perception, coordination, tracking and vigilance.
The present studies also demonstrated that marijuana can have
greater effects in laboratory than driving tests. The last
study, for example showed a highly significant effect of THC
on hand unsteadiness but not on driving in urban traffic.
5. EPIDEMIOLOGY
The studies
outlined above indicate that cannabis does cause dose-dependent
effects on laboratory based tests of human skills. Furthermore,
studies utilising driving simulators and on-road driving also
indicate a degree of cannabis induced impairment of driving
skills. However in these cases the extent of the impairment
indicated from laboratory studies is not replicated in the
simulator or in-car studies.
The effects
of alcohol on the other hand can be demonstrated both in laboratory
studies and in simulated or on-road driving at very much the
same dose levels. Explanations for these differences between
alcohol and cannabis have been suggested and rest essentially
upon the difference in the awareness by the drug taker of
the presence of drug impairment. This in turn may be explained
by the present understanding of the quite different ways alcohol
and cannabis are known to act on the brain.
Also mentioned
above and in other publications our present laws on alcohol
and driving have been based upon the scientific principles
outlined here and in particular on the results of epidemiological
studies. It is pertinent therefore to discuss briefly the
nature of the epidemiological studies undertaken to date with
cannabis and road crashes.
Epidemiological
studies with alcohol are greatly facilitated by the pharmacokinetics
of that drug. Alcohol is excreted in the breath and the ratio
of the concentration on the breath and in the blood is relatively
constant. Therefore the determination of the concentration
of alcohol in the breath (by a 'breathalyser') provides a
reasonably and acceptably accurate indication of the blood
concentration. It is unfortunate therefore that cannabinoids
are not excreted on the breath and the concentration of cannabinoids
that can be detected on breath represent only that contained
in the 'dead-space air' in the upper respiratory tract. The
cannabinoids so detected do not correlate in any way with
the blood concentration. In addition to this the blood concentration
of cannabinoids do not show any useful relationship to the
degree of impairment or the degree of subjective effects of
the drug. The blood concentration of alcohol on the other
hand does exhibit a reasonable correlation with the degree
of impairment.
These properties
of cannabis mean that the determination of the role of cannabis
in road crashes by the same techniques of the case-control
study as used for alcohol, is not an easy task. The pharmacokinetics
of cannabis make this an exceedingly difficult task. The difficulty
is not only related to the poor correlation between blood
concentration and impairment, but also because it requires
the collection of a blood sample-from both the crash case
and the controls. The collection of the latter sample is likely
to involve a high refusal rate, and this alone would almost
certainly invalidate the study. One does not know the reason
for the refusal!
The studies
that have been undertaken to date can be described within
three groups and these are:
(i) Questionnaire
based surveys;
(ii) Incidence
of drug detection in accident involved drivers; and
(iii) Attempts
to assess whether or not the driver who has detectable drug
in bloodstream was culpable in the accident.
Studies along
the lines outlined above have been reviewed by Simpson.
5.1 Questionnaire
based surveys
Questionnaire
based surveys by definition depend upon self report data and
their reliability is questionable. Furthermore, the incidence
of cannabis use and the likelihood of a driver admitting to
such use is likely to change across time.
5.2 Incidence
of drug detection in crash involved drivers
This technique
involves the analysis of blood or urine samples taken from
crash involved drivers. The detection of cannabinoids in urine
provides information only that the drug has been consumed
within the last day or even month. It provides no indication
at all of impairment. Therefore only the analysis of a blood
sample is likely to be helpful. However, the detection of
cannabis in a blood sample does not itself prove impairment
or crash culpability. This fact has been well expressed by
Compton as follows:
Knowing only the frequency with which crash-involved drivers
use drugs does not allow one to know the danger posed by the
drugs. It may simply reflect the general drug usage pattern
in the driving public at large. For example, finding that
30% of crash-involved drivers have nicotine in their blood
does not imply that nicotine was involved in the occurrence
of their crashes. It may be that 30% of the general driving
population smokes cigarettes and the smoking of cigarettes
is unrelated to crash occurrence. Finding that a drug was
overrepresented in crash-involved drivers (as compared to
non-crash involved drivers) would strongly suggest it played
a role in increasing crash risk. However, this approach requires
knowing the drug usage rate of the general driving public,
something we do not know and can not easily determine.
Furthermore,
any comparisons of the incidence of cannabis detections in
crash-involved drivers with those of non-crash involved drivers
should be collected from a comparable population and at the
same time. The patterns of cannabis use vary not only across
time but also across populations.
Therefore
studies reporting the incidence of drugs in the blood of crash-involved
drivers is essentially meaningless without some control of
the incidence of drug use in non-crash involved drivers. Nevertheless,
such studies have been reported and are reviewed by Simpson
who summarised that:
-
Marijuana
users are certainly among drivers who are injured in road
crashes (suggested by the presence of cannabinoids in urine);
-
More importantly,
recent use, as indexed by the presence of THC in blood,
is evident in perhaps less than 10% of injured drivers;
and
-
When cannabis
is detected, there is an 80% chance that alcohol will also
be found.
5.3 Attempts
to assess whether or not the driver who has detectable drugs
in the bloodstream was culpable in the accident
Of the first
attempts to assess culpability has been an ongoing series
of data collected by McBay of fatal, single vehicle crashes.
Culpability in single vehicle crashes is assumed to be that
of the driver (assuming no mechanical fault can be found)
and the choice of fatal crashes assumes that death occurred
shortly after the accident; meaning that drug metabolism ceased
at death and therefore the blood sample from the dead body
will represent the blood picture at the time of the crash.
Cannabis was detected in 7.8% of 600 such cases, but 88% of
these also contained alcohol in concentrations which of themselves
could have accounted for the crash.
6. THE USE OF 'RESPONSIBILITY ANALYSIS' OR ESTIMATION
OF 'CULPABILITY' TO DETERMINE THE ROLE OF DRUGS IN) CRASHES
In the absence
of a separate control group (as used in the assessment of
crash probability with alcohol as described above) an alternative
of a 'culpability index' is currently being employed in drug
studies. The basic construct is first to formulate a means
of determining the responsibility or culpability of a driver
involved in a crash. There have been several means of constructing
this 'culpability index' and this must be done with each of
the accident cases by observers who have no information as
to the drug status of each driver. The responsibility (or
culpability) ratio is then determined as the proportion of
drug-bearing drivers who were determined to be culpable, to
the non-drug bearing drivers who were deemed to be culpable.
The null hypothesis predicts a culpability ratio of 1.00 (ie,
the drug has had no causal relationship with crashes).
To date there
have been six studies employing this technique (two of which
have involved the re-analysis of earlier generated data).
These are briefly outlined below:
1. Warren
and others re-analysed the data of Cimbura and found a culpability
index for cannabis of 1.7, the same as that found for alcohol.
However, the original data comprised a total of 484 drivers
and pedestrians, 3.7% of whom were positive for cannabis.
However, 88% of these people were also positive for alcohol.
This left a very small number from which to assess a culpability
ratio for cannabis alone.
2. Terhune
also has previously collected data independently re-analysed
to estimate a culpability ratio. All BACs over 0.10% were
judged significantly more culpable than the drug-free group.
The cannabis group also had a higher culpability ratio than
the drug-free group, but this was only marginally significant
(58.8% vs 34.4%). This estimation was also compromised by
the small sample size for cannabis only (n=17). The cannabis
plus alcohol group was analysed separately.
3. Donelson
began a very ambitious project but was unfortunately thwarted
by funding problems which precluded the complete analysis
of the collected data. However, a random sample of 415 cases
was analysed. The results cautiously suggested a finding consistent
with those of Warren et al. and Terhune above.
4. Williams
et al. in a study involving 440 cases, demonstrated
as in the above studies that alcohol had a higher culpability
ratio compared with culpable drug-free drivers (92% vs 71%).
However, those drivers in whom only cannabis was detected
were less likely to be responsible for the crashes (53% vs
71%).
5. Terhune
et al. reported a very comprehensive study involving
1 882 cases. They found that alcohol was the dominant
drug in fatal crashes, although the basic focus of their research
was to describe the effect of drugs other than alcohol. They
reported that fully 40% of the drivers had only alcohol in
their systems and another 11% had alcohol combined with drugs.
Among the drivers with BACs at or above 0.10% (n=625) their
responsibility rate:
... was an extraordinary 94%, well above that found for any
other single substance.
Of cannabis,
the authors stated that while cannabinoids were detected in
7% of the drivers, the psychoactive agent THC was found in
only 4%. Of the drivers with only one substance in their system,
only 1.1% had cannabis alone, either as the THC the psychoactive
compound or had the inactive metabolite carboxy THC. The presence
of the inactive metabolite and the absence of detectable THC
infers less recent ingestion of cannabisÑassuming an efficient
analysis.
The
THC only drivers had a responsibility rate below that of the
drug-free driversÑie. as with the study by Williams et
al. (1985) they were considered to be less likely to have
been a cause of the crash than the drug-free drivers.
The
report also indicated the range of THC concentrations found
in the blood. There were 109 cases of THC alone; of these,
22.9% contained what the authors called a 'trace' ie. 1 to
2 nanograms THC per millilitre of blood (ng/ml); 69.7% contained
'low' concentrations between 3 to 19 ng/ml; and 7.3% contained
a 'high' concentration of equal to or greater than 20 ng/ml.
6. Drummer
reported a study of 1 045 fatalities in New South Wales,
Victoria and Western Australia and used the technique of responsibility
analysis (culpability index).
As with
other studies, the dominant drug was alcohol, being found
overall in 36% of all driver fatalities, 33% of which were
over the legal limit of 0.05g%. Cannabis was found in 11%
of cases of which 56% (n= 63) also contained alcohol (mean
BAC 0.16 g% ± 0.08g%). There was no significant difference
in the BAC of the alcohol only drivers and those with alcohol
plus cannabis.
Assessment
of the culpability ratio by Drummer provided the same result
as those of Williams et al. and Terhune et al;
there was a trend to a decrease in relative risk when either
THC or the metabolite carboxy THC was measured in blood or
urine. The relative risk was 0.6 relative to drug-free drivers,
although this was not significant statistically.
7. ALCOHOL AND CANNABIS IN EPIDEMIOLOGICAL STUDIES
The relative
risk for drivers with alcohol plus cannabis was also greater
than that for the control group, but this culpability ratio
was no different from the alcohol only group. Also in this
study (as indicated above), there was no significant difference
in the BAC of the alcohol-only drivers and those with alcohol
plus cannabis.
The same finding
was reported by Terhune who also suggested that the high levels
of alcohol are primarily responsible for the increased crash
risk.
Therefore
the effects of alcohol in road crashes are really profound.
The studies reviewed here using the method of 'responsibility
analysis' have confirmed the information already established
by the case-control methods-that alcohol is the dominant drug
associated with risky and dangerous driving and road crashes.
There have
been suggestions throughout the studies reviewed here that
the crash responsibility rates associated with the low BAC
plus other drug, might be higher than in the low alcohol-only
groups. The interaction of other drugs and alcohol (including
cannabis) require further study using epidemiological techniques.
One must remember the description by Perez-Reyes of the effect
of the order of administration of alcohol and cannabis in
these interaction studies.
8. SUMMARY (OF THE EVIDENCE PRESENTED ABOVE)
The most recent
of the reports of studies of the effects of cannabis on actual
driving performance included a summary of the published literature
on marijuana and driving. They concluded this review with
the following paragraph:
The foremost impression one gains from reviewing the literature
is that no clear relationship has ever been demonstrated between
marijuana smoking and either seriously impaired driving performance
or the risk of accident involvement. The epidemiological evidence,
as limited as it is, shows that the combination of THC and
alcohol is over-represented in injured and dead drivers and
more so in those who actually caused the accidents to occur.
Yet there is little if any evidence to indicate that drivers
who have used marijuana alone are any more likely to cause
serious accidents than drug free drivers. To a large extent,
the results from driving simulator and closed-course tests
corroborate the epidemiological findings by indicating that
THC in single inhaled doses up to 250 µg/kg has relatively
minor effects on driving performance, certainly less than
BACs in the range of 0.08Ê-Ê0.10g%.
Apart from
the above, a very important finding in the reviewed studies
is the difference in the drug users' awareness of the effect
of the drugs alcohol and cannabis. Alcohol use is accompanied
by increased confidence, an impairment of judgement to the
extent that driving behaviour becomes more risky, with faster
speeds and a greater willingness to take risks. Cannabis use
on the other hand, is accompanied by compensatory driving
behaviour, including a reduced willingness to take risks and
slower driving speeds. Indeed the compensation was described
by Robbe and O'Hanlon in the following manner:
Very importantly our city driving study showed that drivers
who drank alcohol overestimated their performance quality
whereas those who smoked marijuana underestimated it. Perhaps
as a consequence, the former invested no special effort for
accomplishing the task whereas the latter did, and successfully.
This evidence strongly suggests that alcohol encourages risky
driving whereas THC encourages greater caution, at least in
experiments.
The task of
driving has been described as a 'self-paced' task. That is,
drivers choose their own levels of task difficulty. There
is a difference therefore between a driver's skills performance,
as measured in individual laboratory tasks and driver behaviour.
Driver performance, or skills performance is what a driver
can do. Driver behaviour is what a driver
actually does. Driving skills (or driver skills
performance) differ very widely within a community. Some of
us may be extremely cautious and others much less so. The
correlation between driver skills and crash probability is
not as great as many may imagine. For example, it is held
by many that superior driver skills lead to reduced crashes
and this led to the concept of 'advanced driver training'.
Indeed, an editor of a road magazine claimed: 'I have for
many years claimed that the licensed racer is far safer than
ordinary chaps, on the grounds of practised skills, mental
ability, cognisance of hazards in driving, keen interest in
driving as well, and so on.'
In order to
examine the possibility that unusually skilled drivers really
did have different on-the-road driving records from the average
driver, a comparison was made of the on-the-road driving records
of a group of licensed racing drivers with those of other
drivers matched for such characteristics as sex and age, etc.
What they found was that in all measures of traffic violations
including crashes, speeding violations, other moving violations
as well as non-moving violations, the rates for the racing
drivers exceed those of the comparison drivers, in most cases
by a considerable margin.
In the light
of the above, Terhune et al. asked the following questions:
A
nagging question which qualifies conclusions from epidemiological
studies of drugs in crashes is: If certain drugs are linked
to elevated crash risks, how much of the elevation is due
to characteristics of the people who use these drugs?
For example,
Terhune in a literature review remarked that research revealed
a striking similarity between the personal correlates of marijuana
use and the correlates of crash involvement. Rebellious, deviant,
youthful males were prominent among marijuana users and among
those in crashes. Jessor et al. also addresses these
issues.
A general
conclusion made by Robbe and O'Hanlon when discussing the
results of their study and of their review of the literature
is worth citing here as a general conclusion to this review:
In
summary, this program of research has shown that marijuana,
when taken alone, produces a moderate degree of driving impairment
which is related to the consumed THC dose.
The impairment manifests itself mainly in the ability to maintain
a steady lateral position on the road, but its magnitude is
not exceptional in comparison with changes produced by many
medicinal drugs and alcohol.
Drivers under the influence of marijuana retain insight in
their performance and will compensate where they can, for
example, by slowing down or increasing effort. As a consequence
THC's adverse effects on driving performance appear relatively
small. Still we can easily imagine situations where the influence
of marijuana smoking might have an exceedingly dangerous effect
ie, emergency situations which put high demands on the driverÕs
information processing capacity, prolonged monotonous driving,
and after THC has been taken with other drugs especially alcohol.
We
therefore agree with Moskowitz's conclusion that 'any situation
in which safety both for self and others depends on alertness
and capability of control of man-machine interaction precludes
the use of marijuana'.
However, the magnitude of marijuana's relative to many other
drugs' effects also justify Geringer's (1988) conclusion that
'marijuana impairment presents a real, but secondary, safety
risk; and that alcohol is the leading drug-related risk factor'.
Of the many psychotropic drugs, licit and illicit, that are
available and used by people who subsequently drive, marijuana
may well be among the least harmful.
Campaigns to discourage the use of marijuana by drivers are
certainly warranted. But concentrating a campaign on marijuana
alone may not be in proportion to the safety problem it caused.
|
