Background
Medical cannabis use is increasingly common in Australia. Patients and physicians need to be aware of the important implications that such use may have for driving.
Objective
The aim of this article is to briefly review the scientific evidence regarding cannabis and driving impairment and discuss current legal issues affecting patients, as well as to update physicians on relevant issues and the best guidance to offer their patients.
Discussion
Delta-9-tetrahydrocannabinol (THC) impairs driving performance and can increase crash risk. These effects are more pronounced in people who use THC occasionally and can last for up to eight hours with oral THC products. There is no evidence that cannabidiol (CBD) impairs driving. Patients using THC-containing products should avoid driving and other safety-sensitive tasks (eg operating machinery), particularly during initiation of treatment and in the hours immediately following each dose. Patients may test positive for THC even if they do not feel impaired, and medical cannabis use does not currently exempt patients from mobile (roadside) drug testing and associated legal sanctions.
Legal access to medical cannabis is increasingly common in Australia, with the Therapeutic Goods Administration (TGA) having approved >100,000 Special Access Scheme Category B applications for patient access to cannabinoid products as of March 2021.1 It is important for physicians and their patients to understand the driving-related risks that medical cannabis use may confer.
The aim of this article is to briefly review the scientific evidence around cannabis and driving impairment and discuss current legal issues affecting patients, as well as to update physicians on relevant issues and the best guidance to offer their patients.
The two major cannabinoids: THC and CBD
Of the hundreds of bioactive molecules in the cannabis plant, Δ9-tetrahydrocannabinol (THC) and cannabidiol (CBD) are the most abundant and the best characterised. THC is responsible for the intoxicating effects of cannabis, and current evidence supports its efficacy in treating chronic pain, chemotherapy-induced nausea and vomiting, and spasticity in multiple sclerosis.2–4
In contrast, CBD is non-intoxicating and has current regulatory approval in Australia for certain rare forms of childhood epilepsy as a 100 mg/mL oral formulation (Epidyolex). There is also emerging evidence of CBD efficacy in treating anxiety, psychosis, chronic pain and neurological disorders.5–7 There is some limited evidence that CBD can counteract negative THC-related side effects such as anxiety and paranoia.8,9 There is a rapidly growing worldwide market for CBD ‘wellness’ products. Such products typically contain very low CBD doses (eg 5–50 mg) that are of uncertain therapeutic value.10,11
With the exception of the oral THC/CBD spray nabiximols (Sativex) and the CBD oil Epidyolex, medical cannabis products in Australia are all unregistered medicines as they have not been formally assessed by the TGA for safety, quality or efficacy. These are predominantly oral preparations, oromucosal sprays and capsules; they can be THC dominant, CBD dominant or contain a specific mix of THC and CBD.12 Cannabis plant material is also available but less commonly prescribed. Therapeutic THC doses are typically in the range of 5–20 mg, while CBD doses tend to be higher (eg 50–1500 mg).
The TGA has recently announced that CBD products meeting certain specifications will be down-scheduled from Schedule 4 to Schedule 3 and therefore available in pharmacies as over-the-counter products. Such products will be limited to a maximum dose of 150 mg/day and for oral or sublingual administration. At present, there are no CBD products that have obtained regulatory approval under Schedule 3,13 although there likely will be within the next 12–24 months once companies have had products approved by the TGA for registration on the Australian Register of Therapeutic Goods.
Cannabis pharmacokinetics
Smoking or vaporising cannabis produces a rapid and transient peak in blood and oral fluid THC concentrations. When taken orally, cannabis is absorbed more slowly through the gastrointestinal tract, producing far lower blood THC concentrations. THC is highly lipophilic and is readily absorbed into fatty tissue, from where it can slowly re-enter the bloodstream days or even weeks following cannabis consumption. Blood THC concentrations are therefore not necessarily indicative of recent cannabis consumption or the amount of cannabis consumed. The mere presence of THC in blood or oral fluid THC does not reliably predict impairment, although current mobile drug testing methods and associated laws rely entirely on this.14
Cannabis and crash risk: Evidence from epidemiological studies
Epidemiological studies aim to quantify the impact substances have on road safety by estimating relative crash risk. This is an odds ratio describing the likelihood of a driver who tests positive for a drug or alcohol being involved in a crash relative to a sober driver.
The most recent and authoritative meta-analyses in this field suggest that cannabis-positive drivers are approximately 1.1–1.4 times more likely to be involved in a crash than sober drivers15,16 and are also more likely to be culpable for a crash.17 Notably, however, there have also been major recent studies in which no increases in crash or culpability risk were detected,18 particularly when drivers had low blood THC concentrations (<5 ng/mL).19 Overall, the increase in crash risk associated with THC is similar to that associated with a low-range blood alcohol concentration (BAC; 0.01–0.05 g/L),20 although some analyses suggest that crash risk and culpability with cannabis may be greater with higher blood THC concentrations.17,19 Table 1 shows relative crash risk and culpability estimates for cannabis, alcohol and other drug classes.
Table 1. Crash risk and crash culpability estimates for different drug classes | ||
Drug class | Crash risk estimate | Crash culpability estimate |
Alcohol (BAC = 0.02) | 1.03–1.1918,46 | 1.3618 |
Alcohol (BAC = 0.05) | 1.38–1.7518,46 | 2.1918 |
Alcohol (BAC = 0.08) | 2.69–2.9218,46 | 3.6318 |
Cannabis | 1.11–1.4215,16,47–49 | 1.20–1.4215,16,47 |
Antidepressants | 1.35–1.4048,50 | N/A |
Antihistamines | 1.1248 | N/A |
Benzodiazepines and Z-hypnotics | 1.17–2.3048,51 | 1.4151 |
Opiates | 1.68–2.2948,52 | 1.4752 |
BAC, blood alcohol concentration; N/A, not available |
Cannabis and driving: Evidence from experimental studies
Experimental driving studies typically administer drugs to volunteers and then examine effects on driving using a driving simulator or, less frequently, during real-world highway driving (called on-road studies). The most common outcome measure in these studies is the standard deviation of lateral position (SDLP), a measure of lane weaving (Figure 1) that is highly sensitive to the effects of alcohol and other sedative drugs and indicates reduced vehicular control.21,22
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