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"Prohibition will work great injury to the cause of temperance. It is a species of intemperance within itself, for it goes beyond the bounds of reason in that it attempts to control a man's appetite by legislation, and makes a crime out of things that are not crimes. A Prohibition law strikes a blow at the very principles upon which our government was founded."

Abraham Lincoln - Former U.S. President

Cannabis & Health

Cannabis & Driving

Cannabis & Driving

by Dr Greg Chesher [ This email address is being protected from spambots. You need JavaScript enabled to view it. ]


I want to mention the present understanding about Cannabis and driving. You may already be quite familiar with these studies, but in case you are not, the following might interest you. The law about alcohol which proscribes driving with BAC >0.05 g% blood alcohol has been determined by epidemiological studies employing the case-control method. At 0.05g% the driver is about twice as likely to be involved in a crash as a driver with zero BAC. As the BAC increases, so in a very steep fashion, does the probability of being involved in a crash. The role of alcohol in road crashes has been very clearly demonstrated. The drink-driving laws are based upon sound science!

As for other drugs, including Cannabis, the pharmacokintetics do not permit this technique. There is no correlation between the blood concentration of Cannabinoids and impairment as determined on laboratory tasks. Furthermore, the study would require the taking of blood from the crash involved drivers as well as that of the control drivers--not involved in a crash. There is no equivalent to the alcohol breathalyser. Cannabinoids are not excreted on the breath. (It is the collection of adequate data from a control group that really precludes the case-control method). So to overcome this, the technique of "culpability analysis" has been employed.

In this case, data for crashes are presented to an independent group of observers who are ignorant (blind) as to whether any of the drivers had any drug at all in their blood. By studying the information of the crash (events before and up to the crash) a score apportioning the degree of blame to each driver is given. From this "culpability" is determined.

So far there have been four studies using this technique, two in the USA and two in Australia.

As far as Cannabis is concerned, it is quite remarkable that in all cases the results were so similar as to be the same finding. The culpability ratio for the drivers bearing Cannabinoids in blood revealed that they were no more likely to be considered as a cause of the crash as those who had no drugs at all in their blood. Indeed in each of these four studies the Cannabinoid drivers were less (but not significantly so) likely to have been a cause than those with no drug at all. In all of these studies alcohol-bearing drivers were overwhelmingly culpable.

So at the moment, the present data suggest that cannabis is not involved as a causative factor in road crashes.

Two things must be considered. First, it is early days so far. The total number of cases in all of these studies totals about 9000 or a little less.

Second, the determination of the culpability score is dependent upon the integrity of the initial data describing the accident. In most cases this is from the attending police. This is not always reliable. However, as the numbers increase with more studies, we will have more confidence with the findings.

There is another Australian study currently being analysed and is due to be released shortly.....SOON is the advice I have from the author.


Greg Chesher



Drummer, O. (1994). Drugs and drivers killed in Australian Road traffic accidents. The use of responsibility analysis to investigate the contribution of drugs to fatal accidents: Victorian Institute of Forensic Pathology. Monash University.

Hunter, C., Lokan, R., Longo, M., White, J. & White, M. (1998). The Prevalence and Role of Alcohol, Cannabinoids, Benzodiazepines and stimulants in Non-Fatal Crashes. Adelaide: Forensic Science, Department for Administrative and Information Services, South Australia.

Terhune, K., Ippolito, C., Hendricks, D., Michalovic, J., Bogema, S., Santinga, P., Blomberg, R. & Preusser, D. (1992). The incidence and role of drugs in fatally injured drivers.: US Department of Transportation National Highway Traffic Safety Administration.

Williams, A., Peat, M., Crouch, D., Wells, J. & Finkle, B. (1985). Drugs in fatally injured young male drivers. Public Health Reports, 100, 19-25

Drugs and Accident Risk in Fatally-Injured Drivers

Drugs and Accident Risk in Fatally-Injured Drivers

Olaf H. Drummer, Ph.D.

Victorian Institute of Forensic Pathology, Department of Forensic Medicine, Monash University, 57-83 Kavanagh Street, South Melbourne 3205, Australia


Risk analysis studies to investigate the contribution of drugs to accident causation are limited. We have used a method based on establishing the responsibility of a driver to investigate the involvement of drugs other than alcohol in 1052 fatally injured drivers. The proportion of drivers deemed to be responsible in a drug-free group were compared to drivers with target drugs found in their blood stream.

Drugs (including alcohol) were detected in 49% of the drivers. Alcohol was detected in 36% of the cases, whilst drugs were detected in 22%. 13% had only drugs detected. The remaining 9% of the population involved a combination of drugs and alcohol. The order of prevalence of drugs were marijuana (112 cases), amphetamines and related stimulants (35), benzodiazepines (34) and opiates (34).

Drivers in whom only opiates were detected had an odd's ratio of 2.4, whilst marijuana cases provided a relative risk of 0.6. Drivers in whom stimulants were detected gave an odd's ratio of 1.4 whilst benzodiazepines gave an odd's ratio of 1.0. By contrast the odd's ratio for alcohol was 6.8.

Drivers with higher than therapeutic concentrations detected represented 22 drivers (2.1%). Most of these drivers were found to be culpable. Multiple drug cases also tended to be culpable. The culpability rate in this group was 89% compared to 70% in drug-free drivers.

These data show that only a small proportion of impaired drivers are drug effected, the remainder being impaired by alcohol. The relative risk for psychoactive drugs is also not uniform, with marijuana use providing the least effect on risk, whilst opiate use seems to provide the largest increase in risk compared to the other drug groups studied.


While certain psychoactive drugs other than alcohol can adversely affect driving skills in simulated studies, epidemiological risk analysis data which provides an assessment of the contribution, of specific drugs or drug classes to accident causation is limited. The effect of benzodiazepines and minor tranquillisers on accident risk are uncertain [Skegg et al, 1979; Jick et al, 1981; Lagier et al, 1993], while the effects of THC appears to be slight or even protective [Terhune et al, 1992; Williams et al, 1985]. Assessment of risk for other drugs or drug groups has not been studied in any detail.

We have used a method based on establishing the responsibility of a driver using strict scoring guidelines [Robertson & Drummer, 1994]. We have used this approach to investigate the involvement of drugs in over 1000 fatal accidents.


Information of drivers killed in motor vehicle accidents were obtained from records kept either at the Victorian Institute of Forensic Pathology and the State Coroner's Office (Victoria), numerous Coroner's courts in NSW or the Western Australian Police (WA). Accidents occurred from January 1990 to December 1993.

Drivers were scored for responsibility as described by Robertson and Drummer [1994]. Cases in which insufficient information was available to allow an assessment of culpability were omitted from the analysis. Toxicology data relating to drivers scored for responsibility were only assessed after the responsibility analysis was conducted.

Toxicological analysis was conducted for a large range of drugs including the drugs of abuse, the benzodiazepines and other prescription drugs. Drugs administered in hospital were excluded. Only cases which had both alcohol and a full range of drug tests were used in the study.

The proportion of drivers deemed to be responsible in a drug-free group were compared to drivers with target drugs found in their blood stream. Accident risk is defined as the odd's ratio of a drug group over the drug-free control group.

Means and 95% confidence intervals are shown in the text and Tables. Data were analysed by smoothed logistic regression. Odd's ratios were adjusted for age and sex [Schleselman, 1982]. EGRET statistical software was used to evaluate these data.


Drugs (including alcohol) were detected in 49% of the drivers. Alcohol was detected in 36% of the cases, whilst drugs were detected in 22%. 13% had only drugs detected. The remaining 9% of the population involved a combination of drugs and alcohol.

The most common drugs detected are shown in Table 1. Over forty drugs were represented in these cases. Illegal drugs were found in 12.9% of the drivers. The most common illegal drugs were marijuana and the stimulants (This group represents the amphetamines, the ephedrines and the slimming drugs such as phentermine etc). However four cases involved heroin and only one case involved cocaine.

Table 1
Type and Abundance of Drugs


DrugAbundance (%)
Cannabis 10.5
Stimulants 3.3
Benzodiazepines 3.2
Opiates 3.2
Analgesics 2.0
Anti-depressant drugs 1.0
Anti-convulsant drugs 0.6
Anti-inflammatory drugs 0.6


Odd's ratios and statistical significance for drug groups are shown in Table 2. Drivers in whom opiates, stimulants or benzodiazepines were detected gave odd's ratio of 2.0 compared to an age and sex matched drug free group, but neither drug group were significant statistically. Marijuana cases provided an odd's ratio of 0.6, but again this was not significant statistically. By contrast the odd's ratio for alcohol was 7.6.

Table 2
Adjusted Odd's Ratios for Selected Drugs


DrugOdd's Ratio*P-value
Alcohol 7.6 (4.6-12) <0.001
Any Drug 1.4 (0.9-2.2) 0.130
Cannabis 0.6 (0.3-1.0) 0.065
Stimulants 2.0 (0.7-5.6) 0.217
Benzodiazepines 2.0 (0.6-7.0) 0.295
Opiates 2.0 (0.7-6.3) 0.220
Misc. Drugs 2.8 (1.1-7.3) 0.040


* 95% confidence interval in parentheses

Drivers with higher than therapeutic concentrations detected represented 22 drivers (2.1%). Most of these drivers were found to be responsible. Multiple drug cases (alcohol excluded) were found in 24 cases (2.3%). Most of these cases were responsible. For example, of the 24 drivers in whom more than one psychoactive drug was detected (alcohol excluded), 22 were deemed culpable, 2 were contributory and 2 were not culpable.


The use of responsibility rates of drivers has been used to establish that alcohol increases accident risk [Terhune et al, 1992; Williams et al, 1985]. This is again confirmed in this study. The prevalence of alcohol at over 30% in the Australian fatally-injured driver population reinforces the magnitude of alcohol-related trauma which still exist on Australian roads.

The contribution of drug use on road trauma and accident risk is less well defined. While most common drug type detected were the illegal drugs, marijuana, certain stimulants and certain opiates, their effect individually and collectively were small compared to alcohol.

Drivers with higher than therapeutic drug concentrations and drivers involving multiple drug use tended to be responsible. If cases involving alcohol were excluded, then such cases represented 2.6% of the driving population. This contrasts to ~30% of the population involving alcohol over 0.05 gram/100 mL (general legal limit in Australia).

It was of some interest that cannabis tended to show a negative effect on relative risk when other drug groups showed an increase. This phenomenon has also been seen elsewhere [Terhune et al, 1992; Williams et al, 1985]. The most likley reason probably relates to the over compensation of marijuana-using drivers on their driving skills. Over compensation may be caused simply by slowing down and avoiding adverse driving situations. These observations do not seem to be related to whether delta-9-THC or 11-carboxy-THC are measured in blood [Terhune et al, 1992; Williams et al, 1985].

In conclusion, these findings show that the contribution of drugs to accident causation is much lower than for alcohol. While more cases are required before any definitive conclusions can be made on the effect of specific drug types on driving risk, cases involving multiple drug use and higher than therapeutic drug concentrations tended to be culpable in fatal accidents.


There were many persons and/or organisations who provided valuable assistance to various parts of this project;. Ms. Lynette Kornmehl; Ms Maryanne Maisey; the staff of the Victorian Institute of Forensic Pathology and the State Coroners Office; Dr. Phillip Swann of Vic Roads; members of the Advisory Group on Drugs and Driving (AGODD); Dr. Peter Vulcan of the Accident Research Centre, Monash University; NSW State Coroners; staff of the NSW Institute of Forensic Medicine; staff of the NSW Division of Analytical Laboratories; Dr. David Saffron of the Road Safety Unit of the NSW Roads and Traffic Authority; the Federal Office of Road Safety; WA Police; the WA Coroner; staff of the Toxicology Section of the Western Australian Department of Mines, and Professor John McNeil and Dr. Andrew Forbes of the Department of Social and Preventative Medicine, Monash University.


H. Jick, J. R. Hunter, B. J. Dinan, S. Madsen and A. Stergachis. Sedating drugs and automobile accidents leading to hospitalization. Am. J. Pub. Health 7: 1399-1400 (1981).

Lagier et al, Benzodiazepine/Driving Collaborative Group. Are benzodiazepines a risk factor for road accidents. Drug and Alcohol Dependence, 33: 19-23 (1993).

M. D. Robertson and O. H. Drummer. A methodology to study the effect of drugs in driving. Accid. Anal. and Prev. 26: 243-7 (1994).

J. J. Schleselman. In: "Case-control studies". New York Oxford University Press (1982).

D. C. G. Skegg, S. M. Richards and R. Doll. Minor tranquillisers and road accidents. Br. Med. J. 1: 917-9 (1979).

K.W. Terhune, C. A. Ippolito, D. L. Hendricks, J. G. Michalovic, S. C. Bogema, P. Santinga, R. Blomberg and D. F. Preusser . The incidence and role of drugs in fatally injured drivers. US Department of Transportation, National Highway Traffic Safety Administration, Report DOT HS 808 065; (1992).

A. F. Williams, M. J. Peat, D. J. Crouch, J. K. Wells and B. S. Finkle. Drugs in fatally injured young male drivers. Public Health Reports. 100: 19-25 (1985).

Aus. Govt's view of Medical Cannabis

The medicinal use of cannabis in the ancient world has been well documented (Abel 1980). In the United States, cannabis was first mentioned as a medicinal drug in 1843 and by 1852 it was included in the US dispensatory list of medicines. It was thought to be beneficial in the treatment of 'neuralgia, gout, tetanus, hydrophobia, cholera, convulsions, chorea, hysteria, depression and insanity' (Wood & Bache 1854, cited in Abel 1980, p182). In Australia, tincture of cannabis was used in medicine until the 1960s, when it was declared a prohibited drug (Cartwright 1983).

Since the introduction of legislation prohibiting the recreational use of cannabis, its use for medicinal purposes has, in most Western countries, not been popular. However, recently the therapeutic benefits of cannabis have received close attention in the United States. In 1991, Doblin and Kleiman conducted an anonymous survey of the members of the American Society of Clinical Oncology measuring the attitudes and experiences of American oncologists concerning the use of cannabis to treat nausea in cancer chemotherapy patients. They found that, of those oncologists who replied to the survey (43 per cent), more than 44 per cent of them reported recommending the illegal use of cannabis for the control of nausea to at least one cancer patient. Some 48 per cent said that they would prescribe cannabis to some of their patients if it were legal (Doblin & Kleiman 1991).

Cannabis has been used as an anti-emetic in the treatment of AIDS patients and as a painkiller for those suffering from chronic pain (Grinspoon 1991). It has also been regarded by some medical practitioners as being effective in reducing intra-ocular pressure in glaucoma patients (Caswell 1992) and in treating epilepsy (Cartwright 1983), Huntington's chorea (Moss et al. 1989) and Parkinsonian tremor (Frankel et al. 1990).

Despite the attention that the medical use of cannabis has received in recent times, legislation in the United States does not permit the medical use of marijuana. In the Federal Controlled Substances Act, cannabis is categorised as a Schedule 1 drug, and as such is described as having a high potential for abuse, no currently accepted medical use and no acceptable safe level of use under medical supervision. In 1989, organisations such as the (US) National Organization for Reform of Marijuana Laws (NORML), the Alliance for Cannabis Therapeutics (ACT) as well as various individuals,20 applied to have cannabis rescheduled so that it could be used for medical purposes. The Administrator of the Drug Enforcement Administration rejected these claims and stated that:

It is clear that cannabis cannot meet the criteria ... for safety under medical supervision. The chemistry of cannabis is not known and reproducible. The record supports a finding that marijuana plant material is variable from plant to plant. The quantities of the active constituents, the cannabinoids, vary considerably. In addition, the actions and potential risks of several of the cannabinoids have not been studied ... (US Government, Federal Register, vol. 54, no. 249, 29 December 1989, p53,734).

This position has recently been restated by Robert C. Bonner, a later Administrator of the US Drug Enforcement Agency, when he responded to a subsequent petition lodged by NORML (US Government, Federal Register, vol. 57, no. 59, 26 March 1992, pp10,499-10,508).

Those in favour of rescheduling the drug argue that, for some, the denial of cannabis as a medicine is particularly cruel. Grinspoon argues that 'sick people are forced to suffer anxiety about prosecution in addition to their anxiety about the illness ... Doctors are afraid to recommend what they know to be the best treatment because they might lose their reputation or even their licence' (Grinspoon 1991).

The Australian medical community has not been as enthusiastic about the therapeutic benefits of cannabis although many argue that where the drug has been demonstrated to be effective its use should be permitted. A study done at the Royal Children's Hospital in Melbourne found that THC (the psychoactive ingredient in cannabis) was an effective anti-emetic for some children undergoing chemotherapy (Cartwright 1983). Dr Lorna Cartwright, a lecturer in Pharmacology at Sydney University stated:

I think there are probably better drugs for medical uses. The point is, though, I think it should be allowed to be used for conditions in which it has been shown to have effect, such as for glaucoma, for children having chemotherapy and for epilepsy. I always feel that if something is good even for a small percentage of patients, it should be allowed to be used (cited in Caswell 1992, p498).

Another pharmacologist, Dr Greg Chesher, argues that cannabis clearly has therapeutic benefits but that research into the possible uses of the drug is being hampered by the fact that cannabis is a prohibited drug (cited in Caswell 1992).

The position in Australia is different from that in the USA in that in this country there is no legislation or binding administrative ruling specifically stating that no medical use exists for cannabis.21 Neither does the United Nations Single Convention on Narcotic Drugs, to which Australia is a party, specifically forbid the medical use of cannabis. In fact the Convention recognises that some otherwise illicit drugs may have medical purposes and states that cannabis use should be 'subject to the provisions of this Convention, to limit exclusively to medical and scientific purposes the...use and possession of drugs' (Article 4(1) (c)).

Given that the United Nations Conventions do not specifically proscribe the medical uses of cannabis, introducing legislation that allowed the use of the drug for medical purposes in Australia would be relatively simple. Clauses authorising the therapeutic use of the drug could simply be inserted into relevant drug legislation and therapeutic products scheduling. Politically, however, such a change in policy could be difficult. As an illicit drug, cannabis has a negative image and is seen as an being an inherently dependence producing, damaging drug that has no possible benefits. Recognition of the medical benefits of the drug may challenge this dominant view of cannabis.


Abel, E. 1980, Marihuana: The First Twelve Thousand Years, Plenum Press, New York.

Cartwright, L. 1983, 'Marihuana', Current Affairs Bulletin, vol. 59, no. 10, pp19-31.

Caswell, A. 1992, 'Marijuana as medicine', The Medical Journal of Australia, vol. 156, pp497-498.

Doblin, R. E. & Kleiman, M. 1991, 'Marijuana as anti-emetic dedicine: A survey of oncologists experiences and attitudes, Journal of Clinical Oncology, vol. 9, pp1314-1319.

Frankel, J.P., Hughes, A., Lees, A.J. & Stern, G.M. 1990, 'Marijuana for Parkinsonian Tremor', Journal of Neurological Neurosurgical Psychiatry, vol. 53, pp436-442.

Grinspoon, L. 1991, 'Marijuana in a time of psychopharmalogical McCarthyism' in Searching for Alternatives: Drug Control Policy in The United States, eds M.B. Krauss & E.PLazear, pp379-389, Hoover Institution Press, Stanford, California.

Moss, D.E., Manderscheid, P.Z. & Montgomery, S.P. 1992, 'Nicotine and cannabinoids as adjuncts to neuroleptics in the treatment of Tourettes Syndrome and other motor disorders', Life Science, 1989, vol. 44, pp1521-1525.