Cannabis produces euphoria and relaxation, alters perception, distorts time, and intensifies ordinary sensory experiences, such as, eating, watching films, appreciating nature, and listening to music. Users' short-term memory and attention, motor skills, reaction time and skilled activities are impaired while they are intoxicated (Hall & Pacula, 2003; Iversen, 2007). These effects develop rapidly after smoking cannabis and typically last for 1 to 2 hours (Iversen, 2007). Their onset is delayed for 1 to 4 hours after oral use (Iversen, 2007).
Cannabis users are typically seeking one or more of these effects when they use. But use can also result in unsought and adverse effects. The most common unpleasant effects of acute cannabis use are anxiety and panic reactions (Hall & Pacula, 2003; Kalant, 2004). These may be reported by naive users and they are a common reason for discontinuing use. More experienced users may also report these effects after receiving a much larger than usual dose of THC (Hall & Pacula, 2003). Recent research suggests that CBD can moderate the psychotogenic effects of THC (Morgan & Curran, 2008), but it remains to be tested whether cannabis products with lower THC:CBD ratios also produce fewer anxiety and panic reactions.
THC appears to produce its effects by acting on specific cannabinoid (CB1 and CB2) receptors on the surfaces of cells (Pertwee, 2008). The CB1 receptor is widely distributed in brain regions that are involved in cognition, memory, reward, pain perception and motor coordination (Iversen, 2007; Murray et al., 2007). These receptors also respond to a naturally-occurring (or endogenous) cannabinoid ligand, anandamide, which produces similar effects to THC but is less potent and has a shorter duration of action (Pertwee, 2008). Neuroimaging studies of the acute effects of cannabis in humans using positron emission tomography (PET) methods confirm findings in animals that THC increases activity in the frontal and paralimbic regions of the brain and in the cerebellum (Chang & Chronicle, 2007).
The acute toxicity of cannabinoids is very low by comparison with other psychoactive drugs, because they do not depress respiration like the opioids, or have toxic effects on the heart and circulatory system like cocaine and other stimulants (Gable, 2004; Kalant, 2004). There have been two reported human deaths from cannabis poisoning in the world medical literature (Gable, 2004), but it is not clear that THC was responsible for these deaths (Kalant, 2004). The dose of THC required to produce 50% mortality in rodents is extremely high by comparison with other commonly used drugs; the estimated fatal human dose is in the range of 15 (Gable, 2004) to 70 g (Iversen, 2007), many times greater than the dose that even heavy users could consume in a day (Gable, 2004).
Cannabis increases heart rate and produces complex changes in blood pressure (Chesher & Hall, 1999). There have been reported deaths from myocardial infarction after cannabis use in young adults (e.g. Bachs & Morland, 2001), but these have been rare and they may have occurred in persons with pre-existing, undiagnosed heart disease (Kalant, 2004; and see below).
The greatest public health concern about the acute effects of cannabis is that intoxicated drivers may cause motor vehicle crashes (Hall & Pacula, 2003). In laboratory studies, cannabis produces dose-related decrements in cognitive and behavioural performance that may affect driving (Ramaekers et al., 2004; Robbe,
1994). Specifically, it slows reaction time and information processing, and impairs perceptual-motor coordination, motor performance, short term memory, attention, signal detection, and tracking behaviour (Ramaekers et al., 2004; Solowij, 1998). These effects increase with THC dose, and are larger and more persistent in tasks requiring sustained attention (Solowij, 1998).
Surveys find that drivers who report using cannabis are twice as likely to report being involved in accidents as drivers who do not (e.g. Asbridge et al., 2005; Hingson et al., 1982 b). It has been difficult to decide how much of the relationship reflects the effects of cannabis on accident risk, the effects of concurrent alcohol use, and the risk behaviour of heavier cannabis users. One recent study found that the association disappeared after controlling for these factors (Fergusson & Horwood, 2001), while another (Blows et al., 2005) found that "habitual" cannabis users had a nine-fold higher crash risk that persisted after controlling for confounding factors including blood-alcohol concentration (BAC).
Studies of the effects of cannabis upon on-road driving performance have reported more modest impairments than comparable doses of alcohol (Smiley, 1999). This appears to be because cannabis-intoxicated drivers drive more slowly and take fewer risks than alcohol-intoxicated drivers (Smiley, 1999). More recent studies of the effects of cannabis on driving performance on the road that have used doses closer to typical recreational doses (Robbe, 1994) have found small but consistent decrements in driving performance.
Cannabis is the illicit drug most often detected in the bodily fluids of drivers who have been injured or killed in motor vehicle crashes (see Kelly et al., 2004 for a review). It has been uncertain for a number of reasons whether cannabis has played a causal role in these accidents (Hall et al., 2001). Firstly, earlier studies measured inactive cannabinoid metabolites in blood and urine, which only indicated that cannabis had been used within the past few days; they did not establish that the driver was intoxicated at the time of the accident (see Bates & Blakely, 1999; Hall et al., 2001; Kelly et al., 2004 for reviews). Secondly, many drivers with cannabinoids in their blood also had high blood alcohol levels (Bates & Blakely, 1999; Hall et al., 2001).
Better-controlled epidemiological studies have recently provided better evidence that cannabis users who drive while intoxicated are at increased risk of motor vehicle crashes. Gerberich et al. (2003) found that current cannabis users had higher rates of hospitalisation for injury from all causes than former cannabis users or non-users in a cohort of 64,657 patients from a Health Maintenance Organization. The relationship for motor vehicle accidents (relative risk (RR) = 1.96) persisted after statistical adjustment among men but not among women. Women in the cohort also had much lower rates of cannabis use and accidents. Mura et al. (2003) found a similar relationship in a study of THC in the serum of 900 persons hospitalised for motor vehicle injuries and 900 age-and-sex matched controls in France. They did not, however, statistically adjust for blood-alcohol level which was found in 40% of cases with THC present.
Drummer et al. (2004) assessed THC levels in blood in 1420 Australian drivers killed in accidents. They found cannabis users were more likely to be culpable for accidents (odds ratio (OR) = 2.5) and there was a higher accident risk (OR = 6.6 [95% CI: 1.5, 28.0]) among those with THC levels greater than 5 nanograms per millilitre. Their findings differed from those of another Australian study (Longo et al., 2000) that did not find a relationship between THC and culpability. However, this study involved injuries rather than fatalities, there were longer delays between these accidents and drug testing, and the average levels of THC detected in blood were much lower than those reported by Drummer et al. (2004).
Laumon et al. (2005) compared blood THC levels in 6,766 culpable and 3,006 nonculpable drivers in France between October 2001 and September 2003. There was an increased culpability for drivers with THC detected in their blood at levels of greater than 1 ng/ml (OR = 2.87) compared to a 15.5 increase for drivers with BAC greater than 0.05 g/l. There was a dose-response relationship between THC and culpability that persisted after controlling for BAC, age and time of accident. On these data, 2.5% of fatal accidents in France could be attributed to cannabis and 29% to alcohol (with a BAC of greater than 0.05%).
Bedard et al. (2007) examined the relationship between cannabis use and accident risk in 32,543 drivers killed in the USA between 1993 and 2003. They found a dose response relationship between BAC and culpability and a more modest association (OR = 1.39 [99% CI: 1.21-1.59]) between culpability and cannabis use assessed in a variety of ways, including inactive metabolites. The association was attenuated but still significant after adjustment for crash history, age, convictions for drink driving and BAC (OR = 1.29).
A convergence of fallible evidence thus suggests that cannabis use increases the risk of motor vehicle crashes 2-3 times (Ramaekers et al., 2004). The size of the effect on driving risks is much more modest than that of alcohol (with ORs for cannabis ranging from 1.3-3, compared with 6-15 for alcohol). The relationship may be attenuated because impairment is not as directly related to blood THC levels as is BAC. The estimated contribution of cannabis use to accident deaths has been much smaller than that of alcohol (2.5% vs. 29%). This probably reflects a combination of the lower crash risks in cannabis-impaired drivers and the lower prevalence of cannabis-impaired drivers.
The motor vehicle crash risks of cannabis use are of public health significance because of the high rates of cannabis use among young adults at highest risk of injury and death from car crashes. An additional concern is that the combined use of cannabis and alcohol (which is in some countries more common that cannabis use alone) probably increases the crash risk over that of either drug used on its own (Ramaekers et al., 2004). The policy challenge is to define a level of THC in blood that can be used by courts to define impairment (Grotenhermen et al., 2007).
Cannabinoid CB2 receptors are found in the immune system, (Roth et al., 2002), and animal studies suggest that high doses of cannabis extracts and of THC impair immune functioning. A number of studies in mice and guinea pigs suggest that high doses (200 mg/kg) of cannabinoids decrease resistance to infection with Lysteria monocytogenes (Morahan et al., 1979) and herpes simplex type 2 virus (e.g. Cabral & Pettit, 1998). There have, however, been very few epidemiological studies of immune system functioning and disease susceptibility in heavy cannabis users to assess how serious these immunological risks may be (Cabral & Pettit, 1998; Klein et al., 2001; Roth et al., 2002).
Several epidemiological studies have examined the effects of self-reported cannabis use on progression to AIDS among HIV positive homosexual men. Kaslow et al. (1989) reported a prospective study of progression to AIDS among 4954 HIVpositive homosexual and bisexual men. Cannabis use did not predict increased progression to AIDS, and it was not related to changes in immunological functioning. There was also no relationship between marijuana use and progression to AIDS in HIV-seropositive men in the San Francisco Men's Health Study (N=451) over 6 years (DiFranco et al., 1996). There was an increased risk of progression to AIDS among cannabis users in the Sydney AIDS Project, but the Institute of Medicine (1999) has described this finding as "less reliable" than those of Kaslow et al. and DiFranco et al. because the study had a short follow-up period, and many of the "HIV-positive cases" already had AIDS. A study of mortality among a cohort enrolled in a health insurance plan (Sidney et al., 1997 a) did find an association between cannabis use and death from AIDS, but this was attributed to confounding of cannabis use and sexual preference (which was not assessed in the study).
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