Dr G.B. Chesher
Department of Pharmacology University of Sydney and National Drug and
Alcohol Research Centre University of New South Wales.
|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
|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
|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: