Effects of Alcohol and Other Drugs on Driver Performance

Abstract

In the past century we have learned that driving performance is impaired by alcohol even in low dosage, and that many other drugs are also linked to impairment. This paper is a summary of some of the more relevant studies in the past fifty years – an overview of our knowledge and unanswered questions.
There is no evidence of a threshold blood alcohol (BAC) below which impairment does not occur, and there is no defined category of drivers who will not be impaired by alcohol. Alcohol increases not only the probability of collision, but also the probability of poor clinical outcome for injuries sustained when impaired by alcohol. This review samples the results of the myriad studies that have been performed during the last half century as experiments have moved from examination of simple sensory, perceptual and motor behaviours to more complex measures of cognitive functioning such as divided attention and mental workload. These more sophisticated studies show that significant impairment occurs at very low BACs (<0.02 gm/100 ml).
However, much remains to be determined regarding the more emotional aspects of behaviour, such as judgment, aggression and risk taking. Considering that the majority of alcohol related accidents occur at night, there is a need for increased examination on the role of fatigue, circadian cycles and sleep loss.
The study of the effects of drugs other than alcohol is more complex because of the number of substances of potential interest, the difficulties estimating drug levels and the complexity of the drug/subject interactions. The drugs of current concern are marijuana, the benzodiazepines, other psychoactive medications, the stimulants and the narcotics. No one test or group of tests currently meets the need for detecting and documenting impairment, either in the laboratory or at the roadside.

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Effects of Alcohol and Other Drugs on Driver
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E. J.D. OGDEN & H. MOSKOWITZ
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Traffic Injury Prevention, 5:185–198, 2004
Copyright C
 2004 Taylor & Francis Inc.
ISSN: 1538-9588 print / 1538-957X online
DOI: 10.1080/15389580490465201
Effects of Alcohol and Other Drugs on Driver
Performance
E. J. D. OGDEN
Centre for Drugs and Driving, Swinburne University of Technology, Australia
H. MOSKOWITZ
Southern California Research Institute, Encino, California, USA
In the past century we have learned that driving performance is impaired by alcohol even in low dosage, and that many other
drugs are also linked to impairment. This article is a summary of some of the more relevant studies in the past fifty years—an
overview of our knowledge and unanswered questions.
There is no evidence of a threshold blood alcohol concentration (BAC) below which impairment does not occur, and
there is no defined category of drivers who will not be impaired by alcohol. Alcohol increases not only the probability of
collision, but also the probability of poor clinical outcome for injuries sustained when impaired by alcohol. This article
samples the results of the myriad studies that have been performed during the last half century as experiments have moved
from examination of simple sensory, perceptual, and motor behaviors to more complex measures of cognitive functioning,
such as divided attention and mental workload. These more sophisticated studies show that significant impairment occurs at
very low BACs (<0.02 gm/100 ml).
However, much remains to be determined regarding the more emotional aspects of behavior, such as judgment, aggression,
and risk taking. Considering that the majority of alcohol-related accidents occur at night, there is a need for increased
examination on the role of fatigue, circadian cycles, and sleep loss.
The study of the effects of drugs other than alcohol is more complex because of the number of substances of potential
interest, the difficulties estimating drug levels and the complexity of the drug/subject interactions. The drugs of current
concern are marijuana, the benzodiazepines, other psychoactive medications, the stimulants, and the narcotics. No single
test or group of tests currently meets the need for detecting and documenting impairment, either in the laboratory or at the
roadside.
Keywords Alcohol Impairment; Drug Impairment; Alcohol; Drugs; Driver Performance; Traffic Safety; Driving Skills;
Impairment Tests
Few people in developed countries can imagine life without
their car. While most drivers would know the economic cost of
their vehicle, how many of them stop to count the social cost, or
to consider the associated morbidity and mortality? Collisions
involving vehicles have left countless people crippled, maimed,
or bereaved. Road trauma is the most common cause of prema-
ture death among young adults in most countries not embroiled
in war. Although transport safety continues to be improved by
better engineering of roads and vehicles, the most prominent
causal factor in collisions remains the human element.
Transport mishaps related to alcohol impairment are not new.
It was common knowledge in the pre-industrial age that drunk-
Received 4 February 2004; accepted 7 April 2004.
Address correspondence to H. Moskowitz, Southern California Research
Institute, 4138 Royal Crest Place, Encino, CA 91436. E-mail: herbmosk@ucla.
edu
ards were at increased risk when riding horses or driving horse-
drawn vehicles, but to a limited extent a good horse could share
the responsibility for safe transport with an incompetent driver,
compensate for human impairment, and plod homeward in rel-
ative safety. The advent of the horseless carriage brought the
era of forgiving transportation to an end. The consequences of
combining recreational drug usage and transportation became
more serious.
One of the most remarkable features about vehicle driving
is that a very large fraction of the human race can master the
basic concepts and acquire rudimentary skill at the task relatively
quickly and without expending large amounts of time or energy
(Evans, 1991). Yet the complexity of the man-machine-traffic
interaction can make the tasks of driving complex and hazardous.
Although the increased injury toll associated with motor
transportation became apparent soon after the beginning of the
twentieth century, there was only limited research on driving
185

186 E. J. D. OGDEN AND H. MOSKOWITZ
behavior in general, or driving under influence of drugs or alcohol
in particular. It was perhaps the massive increase in private mo-
tor vehicle ownership after World War II (WWII) that led to
the increasing research concern with the human costs of mass
private transportation. Prior to the 1950s, for example, although
there were frequent prevalence studies on alcohol in driving ac-
cidents, there was only one primitive case-controlled study. The
1950s saw the beginning of a major spurt in epidemiological
studies of driving accidents and the influence of alcohol.
The growth in motor vehicle usage was matched by growth
in research into the behavioral effects of alcohol. A series of
large case-controlled epidemiological studies after WWII pro-
vided the evidence for the close association between increased
BAC and increased accident, injury, and fatality rates. These pio-
neering studies included Lucas et al. (1955) in Toronto, Canada,
Vamosi (1960), in Bratislava, Czechoslovakia, McCarroll and
Haddon (1962) in New York City, and Borkenstein et al. (1964)
in Grand Rapids, Michigan. These studies were highly influen-
tial in making the public aware of the real accident frequency
associated with alcohol.
At the same time the nature of the impairment that under-
lies the increased crash rate was subjected to research at several
levels: studies of the individual components of the driving task,
studies of simulated driving, and studies of on-road driving. This
article has its major focus on alcohol because alcohol is associ-
ated with as many fatal collisions as all other drugs combined.
For instance, Drummer et al. (2004) describe the toxicological
analysis of 3,398 collisions in which the driver died. Of these,
1,704 cases (50.1%) screened negative for alcohol and drugs.
Alcohol was present in 29% of cases (n =990), drugs were
present in 27% of cases (n =907).
Unfortunately, there have been only a few studies that have
examined the nature of the driving impairment from an epi-
demiological perspective. This is partly because of the difficulty
in assigning a particular driving deficit to an associated behav-
ioral failure, since the same driving error could be due to many
behaviors.
Police descriptions of crashes are typically assigned to the
cause of current interest. For example, Moskowitz (2004) exam-
ined a series of crashes at T-intersections where drivers drove
through into the wooded area beyond the junction where the
road no longer existed. From the 1950s through the 1980s the
majority of police reports characterized this as “loss of control.”
Nowadays “inattention”has become a favorite explanation, al-
though there is no evidence that driver behavior has changed.
There have only been a few multi-disciplinary accident investi-
gation studies with professional human-factors personnel aware
of research in cognitive psychology. More studies of this type
would help enlighten the epidemiological record.
Moskowitz and Robinson (1988) and Moskowitz and
Fiorentino (2000) have extensively reviewed the experimental
literature on alcohol and driving. Jones et al. (2003) have re-
viewed the literature on drugs. This article does not purport to
be a comprehensive literature review, so much as an overview
of the field and the directions research has taken.
ALCOHOL
Alcohol is a drug whose main acute effect is on the cen-
tral nervous system. Unlike anesthetic agents that depress all
brain functions, the effects of alcohol are first manifest in the
brain centers involved in highly integrated functions, such as
skilled performance. The analysis of sensory information, the
control of intricate movement patterns and short-term memory
are especially sensitive to alcohol. The effects on human skills
and performance commence at the lowest measurable BACs
and increase in a roughly dose-related manner (Moskowitz &
Robinson, 1988).
There is no evidence of a threshold effect for alcohol because
some impairment of performance occurs at the lowest levels that
can be measured; nor is there a level at which a sudden transition
from unimpaired to impaired can be expected: whatever the level
of BAC examined, at least some skills can be demonstrated to be
significantly impaired. The effects of alcohol are dependent both
on the quantity consumed and the nature of the performance re-
quired. There is no evidence that low BACs improve any human
skill (Moskowitz, 1985).
The variation in individual performance at BACs below
0.10% is sufficiently broad that uncertainties must attach to any
prediction of the precise effects of a given quantity of alco-
hol on an individual. All individuals are impaired at any level
of alcohol and the impairment increases as the BAC increases.
Individual psychomotor abilities vary at the no-alcohol base-
line, so that viewing an individual behavior at low BAC can
give only limited information about the BAC. Conversely, as
impairment can be demonstrated at all levels of BAC there is
general agreement that the skills relating to driving can be pre-
sumed to be adversely affected below 0.10% (the limit in many
jurisdictions) and many of the skills related to driving are sig-
nificantly impaired below 0.05% (Dunbar et al., 1987; Mitchell,
1985; Moskowitz, 1985; Starmer et al., 1988). Moskowitz and
Robinson (1988) concluded: “The legislature is free to pro-
hibit driving at any B.A.C., since such a limit would not con-
tradict the scientific data demonstrating no lower limit to
impairment.”
Subjective Measures of Impairment
For the purpose of this article, impairment has been defined as the
occurrence of a change for the worse in the performance required
for safe driving. Impairment is not the same as intoxication.
Dictionaries give multiple definitions of intoxication using terms
like “drunk,”“inebriation,”and “stupefaction,”which are not
scientific concepts and have no relevance to the driving task.
When the layman thinks of impairment, he probably envis-
ages the obvious signs of lack of judgment, poor self-control,
and loss of gross motor skills. Widmark (1981) reported on
the experience in Sweden of testing drivers arrested on sus-
picion of being under the influence of alcohol. Swedish law
required these drivers to be examined by physicians at a po-
lice station using a standard seven-item behavioral test battery.
At 0.15 g/100 ml physicians assessed only 50% of the arrested

ALCOHOL EFFECTS ON DRIVERS 187
drivers as being under the influence and only assessed every-
one over 0.26 g/100 ml as intoxicated. Perper (1986) describes
87 patients entering an alcohol treatment program with positive
BACs. Twenty-four percent of the subjects over 0.20 g/100 ml
showed no evidence of intoxication and 26% of those over 0.30 g/
100 ml passed many behavioral tests. Physicians fared little bet-
ter when grading patients in an emergency room. Those patients
evaluated as being sober were found to have a mean BAC of
0.272 g/100 ml. One patient declared not to be intoxicated had
a BAC of 0.54 g/100 ml (Urso, 1981).
The probability of a police officer detecting drivers on the
road with a BAC above the legal limit is estimated to less than 1%
(Borkenstein et al., 1963). Wells (1997) examined the ability of
police to detect impairment at the roadside. When police cleared
drivers from a sobriety checkpoint as “not under the influence,”
researchers requested breath samples for confidential analysis.
Eighty-seven percent of drivers between 0.05 and 0.079 g/100 ml
were not arrested, 62% of those between 0.08–0.99 g/100 ml;
64% of those between 0.10 and 0.119 g/100 ml; and, 62% of
those at or above 0.12 g/100 ml were not arrested. Whether
contemporary education of police has improved this detection
rate has not been tested.
The gross intoxication that the layman associates with being
“drunk”bears no relationship to the impairment that is signifi-
cant for road safety.
PERFORMANCE MEASURES
Skills Related to Driving
The 1988 review by Moskowitz and Robinson of the effects
of low levels of alcohol on driving-related behavior summa-
rized studies on reaction time, tracking, concentrated attention,
divided attention, information processing, visual functions, per-
ception, psychomotor skills, and performance in simulators and
on the road.
They obtained more than 500 studies from a sampling of
the literature. From these 500 studies, 177 were selected for
incorporation in the report because they met their criteria of
adequate statistical analysis, sufficient information that the BAC
at the time of behavioral testing could be determined, and the
presence of placebo treatment. Of the 177 studies 158 reported
impairment of one or more behavioral skills at one or more BACs
ranging from 0.01g/100 ml to 0.10 g/100 ml and above. Only
19 studies failed to report impairment at the levels examined.
A more recent review of the literature summarized 112 stud-
ies published from 1981 to 1997 and screened using similar
criteria (Moskowitz & Fiorentino, 2000). In this review 27% of
the studies reported finding impairment by .039 g/100 ml, 47%
by 0.049 g/100 ml and 92% by .079 g/100 ml. The greater sensi-
tivity of the later studies may be accounted for by improvements
in methodology, better instrumentation, and more frequent ex-
amination of multiple BACs. Some studies reported impairment
at BACs less than 0.01 g/100 ml. The studies showing greatest
sensitivity to alcohol impairment were on-the-road and simula-
tor studies of driving, divided attention tasks, and measures of
drowsiness. The least sensitive tests were simple reaction time
and studies of critical flicker fusion. In between were tasks such
as vigilance, tracking, perception, visual functions, and cogni-
tive tasks. There is strong evidence that some driving-related
skills were impaired with any departure from zero BAC. By
0.05 g/100 ml the majority of studies reported impairment of
some skill by alcohol.
Reaction Time
Although reaction time is adversely affected by alcohol, the level
at which significant effects are noted depends on the complexity
of the reaction demanded and the complexity of the stimulus.
Some studies have demonstrated deterioration at levels as low
as 0.02%, but a level of 0.07% is needed to produce significant
deficit with common tasks (Starmer, 1989). The nature of the
stimulus and the reaction required are complicating factors in
interpreting the reported results. In a complex task such as driv-
ing at night deterioration of reaction time is observed at low
levels. Tiredness is an important factor in increasing reaction
time (Corfitsen, 1982).
Simple reaction time is the only experimental variable that
has failed to consistently and overwhelmingly demonstrate im-
pairment by alcohol (Moskowitz et al., 2000). No systematic
study of the variation in results from reaction time experiments
has been undertaken to explain this variability. However, reac-
tion time experiments involving complex situations tend to show
more impairment at lower levels than simpler experiments with
fewer demands. Since the driving task is intrinsically a complex
task, studies on simple reaction time under the influence of al-
cohol appear less relevant than studies that are more analogous
to the complexity of real driving.
Tracking
The ability to follow a complex path under the influence of
alcohol was one of the earliest performance measures studied.
Tracking is analogous to car control because the subject uses a
control device, such as a steering wheel, to follow a target that
moves on a screen or (in actual driving) to follow the contours
of the road. Tracking is the essence of what most people have in
mind when they conceive of car control.
Thirty years ago, Moskowitz (1973) reviewed tracking under
the influence of alcohol and concluded that there was variability
in alcohol effects depending on whether the tracking task was
compensatory or pursuit. A compensatory tracking task has the
operator observing only the difference between the desired po-
sition and the actual position of a controlled element and acting
to reduce the error. A pursuit-tracking task has the observer at-
tempting to follow a moving target on a course. Compensatory
tracking tasks performed alone have generally failed to find al-
cohol impairment, except at very high BACs.
There is marked impairment of tracking at quite low alco-
hol levels if tracking is not the only task. The Moskowitz and
Robinson report examined 28 tracking studies, where the track-
ing was accompanied by some additional task, and found that

188 E. J. D. OGDEN AND H. MOSKOWITZ
the BAC at which impairment occurs is as low as 0.02 g/100 ml
(Moskowitz & Robinson, 1988).
Vigilance
Concentration is not particularly sensitive to alcohol and no ef-
fects are demonstrated below 0.05%. However, when the task
also involves speed and accuracy, such as clerical tasks, impair-
ment can be demonstrated in the range of BAC from 0.005% to
0.009% (Nash, 1962). The most consistent finding is an increase
in error rates (Starmer, 1989). Low doses of alcohol interfere
with learning and adaptation to unfamiliar tasks (Ogden et al.,
1995).
Divided Attention Tasks
Any experiment that requires subjects to do more than one thing
at a time is highly sensitive to drug effects (Moskowitz, 1984).
Deterioration is detected on some tests at levels below 0.02% and
many studies show deterioration below 0.05%. Small quantities
of alcohol impair the ability to perform a secondary task while
driving, long before the effect on the mechanics of driving are
demonstrable (Brown, 1970).
It has been suggested that one of the reasons for this deterio-
ration in performance is that the alcohol-affected brain processes
information more slowly (Moskowitz & Austin, 1983). Since the
mental workload required to divide attention is a component of
nearly all studies, the challenge is to isolate the effects of alcohol
on divided attention from the effects on the constituent compo-
nents of the task. A study by Moskowitz, Burns, and Williams
(1985) demonstrated that divided attention performance was im-
paired for all subjects at a BAC of 0.015 g/100 ml.
Visual Functions
Vision is peculiarly sensitive to sedatives including alcohol caus-
ing abnormal eye movements, difficulty in accurate eye track-
ing of moving objects, impaired color discrimination, tunnel vi-
sion, and even temporary blindness (Colson, 1940; Grant, 1974;
Thompson-Crawford & Slater, 1971; Wallgren & Barry, 1970;
Wilkinson et al., 1974).
Alcohol may impede recovery from glare and impair visual
acuity, although the studies have produced conflicting results.
Moskowitz, Wilkinson, and Burg (1993) reviewed 112 studies
of visual performance under alcohol, and suggested that the dis-
crepancy in findings resulted from experimental techniques that
confounded alcohol effects on glare and acuity with concomitant
presence of other visual functions, such as search behavior, that
have also been demonstrated to be impaired by alcohol. Alco-
hol effects on visual performance are most marked for moving
objects or when there is a simultaneous demand to process other
information (Adams et al., 1978; Zeidman et al., 1980).
Eye movement control is the most sensitive of the various
components of eye function and is affected at very low BACs. A
BAC of 0.04% is enough to induce nystagmus (Aschan
et al., 1956; Grant, 1974; Katoh, 1988; Stapleton et al., 1986).
Moskowitz and Robinson (1988) reviewed 28 studies of opto-
metric vision tasks such as saccade velocity, nystagmus, track-
ing, and acuity, and reported impairment at low BACs but esti-
mated that the magnitude of the impairments were unlikely to be
important for the driving tasks. More cognitive visual functions
exhibit impairment at even lower BACs and are more likely to
influence driving.
Alcohol changes the way that the subject uses vision. Belt
(1969) used eye movement recordings in drivers on the road
to demonstrate that BACs as low as 0.04 g/100 ml produced
changes in the distribution of eye fixation. Similar results have
been found by other investigators including a form of tunnel
vision with fewer visual excursions to the periphery and a shift
in the distribution and duration of eye fixation (Buikhuisen &
Jongman, 1972; Moskowitz et al., 1976).
It seems that alcohol slows processing of visual information
requiring longer time spent fixed on an object in order to perceive
its nature. One consequence of this slower visual processing is
that fewer fixations are possible in any given time, which in
turn means that fewer things can be seen. Drivers are literally
looking less, because each look takes longer under the influence
of alcohol (Moskowitz et al., 1976). Alcohol-affected drivers are
unable to discern the meaning of road signs until they are closer
to the sign compared to driving when unimpaired (Davis W.,
1998). This difficulty is even more evident with poor lighting
(Hicks, 1976).
Driving Skills
The actual skills required for driving have been studied in sim-
ulators, on the road in instrumented cars and as a cause of epi-
demic disease. The complexity of the task and the number of
variables to be considered in “safe driving”make simple mod-
els impossible.
Driving simulators have been used because of the inherent
safety advantage of simulated driving. The more complex the
driving challenge, the lower the BAC at which errors occur.
Steering errors are noticed at an alcohol concentration of 0.03%
and collision frequencies rise. Subjects tend to ignore rules and
instructions before reaching 0.05%. Subjects are more sluggish
to correct positional errors and steering control responsiveness
deteriorates after low to moderate doses of alcohol (Starmer,
1989). Drinking experience does not make any difference to
driving ability (Laurell et al., 1990). Prior driving skill does not
reduce impairment (Beirness & Vogel-Sprott, 1982).
Closed driving course assessments are also used as a model
of on-the-road driving tasks. In common with the results of sim-
ulator testing, the more complex the task required when actually
driving, the greater the deficit produced by alcohol. Increasing
blood alcohol levels result in progressive impairment of driv-
ing performance. This impairment is clearly demonstrated in
non-competitive drivers at 0.05% and in competition drivers
at 0.08% (Starmer, 1989). The alcohol-impaired driver may use
past experience and learning to cope with normal routine driving
demands, but cannot do so in an emergency situation (Lovibond
& Bird, 1971).

ALCOHOL EFFECTS ON DRIVERS 189
EPIDEMIOLOGY OF VEHICULAR ACCIDENTS
Driving Survey Data
One way of studying the drinking driver is to study those people
apprehended for driving offenses. Such surveys cannot provide
information about the general population because they are, by
definition, studies of a selected subgroup. Excluding “random
breath-testing,”police officers do not apprehend drivers ran-
domly and police are not randomly distributed in time or place.
Police patrol known “trouble spots”and select individuals be-
cause of their driving style, vehicle, or other attributes. The re-
sults of such studies are as much a measure of policing biases
as of driver characteristics.
Post Accident Surveys
Post-accident studies have similar limitations except that the
driver is selected by involvement in a collision. Several con-
trolled epidemiological studies have been performed.
Borkenstein et al. (1964) performed an influential study in Grand
Rapids, Michigan. They compared breath alcohol levels in
roughly 6,000 crash-involved drivers with 7,600 control drivers
who had not crashed. The probability of involvement in a col-
lision was determined for each BAC by comparing the relative
number of collision-involved drivers at each BAC in the crash
group with the relative number of non-collision-involved drivers
at the same BAC in the control group.
The Grand Rapids study indicated that the probability of caus-
ing an accident was a sharply rising exponential function of the
driver’s blood alcohol concentration. At 0.10 g/100 ml there was
a roughly six-fold increase in crashes compared with the crash
rate for drivers with no alcohol. At 0.15 g/100 ml the odds ratio
was 25 to 1. Young drivers (16 and 17 years) had a five-fold
increase in crashes with BACs below 0.04 g/100 ml. At every
blood alcohol concentration, drivers under 21 years and over
70 years of age had greater crash rate than drivers age 25 to
45 years.
The original Grand Rapids report created some confusion
with its J-shaped curve. It not only showed no increase in overall
crashes for alcohol levels below 0.04 g/100 ml, it even suggested
that drivers might do better with low levels of alcohol rather than
none!
Many researchers have since argued that the Grand Rapids
study failed to compensate for factors other than alcohol that
influence crash rate. For valid comparison, the control group
should have shared the characteristics that influenced outcome.
The Grand Rapids study was biased by a zero BAC group with
a greater proportion of both younger and older drivers than the
“crash”group. Both younger and older drivers have higher crash
rates with no alcohol present than drivers aged 25 to 55 years.
Other variables that affect crash rates that were not equally dis-
tributed among the various groups in the study include educa-
tional level, number of miles driven, occupation, and frequency
of drinking. Determining the relationship between BAC and
crash probability requires controlling for these other variables.
The Grand Rapids data has subsequently been analysed by
several groups using more sophisticated statistical methods re-
vealing some apparent paradoxes (Allsop, 1966; Hurst, 1973).
Daily drinkers had the lowest accident rate compared to weekly,
monthly, or yearly drinkers. The youngest and oldest drivers,
who tend not to drink daily, have higher crash rates than 25–
55-year-olds who might be drinking daily. Once the variable
“drinking frequency”is controlled, the probability of involve-
ment in collision increases with any departure from zero BAC
and the rate of increase is greatest for the least frequent drinkers.
The curve loses its J shape.
The US Department of Transportation sponsored another epi-
demiological study of alcohol and crash probability, collecting
data from drivers involved in crashes in Long Beach, California,
and Fort Lauderdale Florida for more than a 12-month period
(Moskowitz et al., 2000, 2002). This study represented an im-
provement over prior study designs by sampling control drivers
at the same site, time, and direction of travel as the original crash
drivers. Two control drivers were obtained for each crash driver
one week after the collision. Extensive efforts were made by the
police to capture as many hit-run drivers as possible. BAC esti-
mates were obtained from drivers who refused to participate by
passive breath sampling techniques. These factors proved im-
portant since more than 69% of the apprehended hit-run-drivers
had positive BACs, typically in the higher ranges. Almost 50%
of the crash drivers who refused to participate had positive BACs
in contrast to fewer than 16% of the control drivers who refused
to participate.
Had it not been for the apprehension of some 20% of the
hit-run drivers and the use of the passive alcohol sensors to de-
termine alcohol presence in drivers who refused to participate,
it was estimated that more than 46% of all drivers involved in
crashes who had positive blood alcohol would not have been
detected. The study used logistic regression analysis to adjust
the control and crash samples for variation in age, sex, drink-
ing practice, and other variables. This improved analysis of the
probability of crash involvement as a function of BAC indicated
that crash probability increased for alcohol involved drivers at
all levels from 0.01 g/100 ml, and the probabilities for crash
involvement were considerably greater than in any other prior
study.
Single-Vehicle Collisions
The Grand Rapids study reported that the probability, of a sin-
gle vehicle collision at various BACs was greater than that of
a multiple-vehicle collision. That finding was supported by re-
ports in the 1950s and 1960s that roughly 70% of fatally injured
drivers in single-vehicle collisions had alcohol present (NHTSA,
1997).
Zador (1991) argues that single-vehicle crashes provide the
only true measure of the contribution of alcohol to increasing
the rate of crash involvement. Non-impaired drivers may be
able to compensate for the impairment of other drivers and so
avoid becoming involved in collisions. When Zador examined

190 E. J. D. OGDEN AND H. MOSKOWITZ
the probability of fatal single-vehicle crashes involving alcohol
as a function of driver age and sex using data from the Na-
tional Highway Traffic Safety Administration, he determined
that 0.02–0.04 g/100 ml BAC increased fatal crash involve-
ment by 40%; BACs between 0.05 and 0.09 g/100 ml increased
fatal crash involvement by 1,100%; BACs between 0.10 and
0.14 g/100 ml increased fatal collision probability by 4,800%;
and at levels of 0.15 g/100 ml or higher, the fatal collision rates
increased by 38,000%. Thus the role of alcohol in fatal crashes
is even more significant than the Grand Rapids report suggested
for all collisions.
Stein (1990) looked at drivers at 0.10% or above and found
their chances of being involved in a fatal collision were 100 times
greater than the sober driver regardless of time of day. However
the sober driver’s chances of being in a fatal collision with such
a driver rose dramatically between 1 A.M. and 3 A.M. because of
the increased concentration of drunk drivers in the early hours
of the morning.
RATE OF ALCOHOL CONSUMPTION
The rate at which consumption of alcohol has been under-
taken influences the outcome. Moskowitz and Burns (1976)
studied four groups of subjects who drank alcohol at different
rates to achieve a peak BAC of 0.10 g/100 ml, and a control
group with a placebo beverage. The 40 subjects were tested on
a performance battery that included measures of information
processing, motor control, hand steadiness, and body sway. The
duration over which they drank ranged from 15 minutes to four
hours. The group that consumed the greatest amount of alcohol
was the group that took the longest period of time to achieve
0.10 g/100 ml, since they were eliminating alcohol as they were
consuming it. Nevertheless, the most impaired individuals were
in the group that drank the fastest, even though they drank the
least total amount, and the least impaired were in the group that
drank the greatest amount at the slowest rate.
ALCOHOL AND FATIGUE
Sleep disorders have become a recognized medical speciality,
and the last decade has seen increased interest in the effects
of alcohol on sleepiness (Lyznicki, Doege, Davis, & Williams,
1998), particularly the effects after the BAC has dropped to zero.
Roehrs et al. (1994) compared subjects given sufficient alco-
hol to produce a peak level of 0.06 g/100 ml at 7.30 A.M., alcohol
sufficient to reach a peak at 0.04 g/100 ml given at 10.30 A.M.,or
placebo. By 3:30 P.M., all subjects were at zero BAC. Subjects
were tested for sleep latency (time to fall asleep) at two-hour
intervals from 9:30 A.M. until 9:30 P.M . Subjects displayed a
shortened time to fall asleep throughout the entire period when
alcohol was present and even when the BAC had dropped to
zero, compared with the placebo treatment day.
Taking a nap normally combats fatigue and increases the time
required to fall asleep. A dose of alcohol that produces a peak
level of 0.04 g/100 ml counteracts the effect of the nap (Roehrs
et al., 1989).
These laboratory studies are relevant to real-life driving sit-
uations. In New Mexico there was an increase in the num-
ber and proportion of alcohol-related traffic crashes during the
seven days following the change to and from daylight-saving,
compared with the week before and the second week after the
changes (Hicks et al., 1998).
HANGOVER
The after effects of alcohol intoxication have been shown
to persist after the BAC has fallen to zero. Many people with
a hangover report feeling unwell and impaired. Measurable ef-
fects of hangover include hormonal changes, depression of brain
activity, difficulty with judgment of space-time relationships, ir-
ritability, and poor concentration.
The degree of “hangover”is not easily measured, but impair-
ment has been demonstrated in driving simulators, flight simu-
lators, skiing, and administrative tasks. The impairment persists
for at least three hours after all the alcohol has been metabolized
(Collins & Chiles, 1980; Delin & Lee, 1992; Lemon et al., 1993;
Yesavage et al., 1986; York & Regan, 1988).
ALCOHOL AND AGGRESSION
The last decade has seen increasing concern about aggressive
driving and the phenomenon the media call “road rage.”There
is no hard epidemiological evidence linking aggressive driving
and alcohol consumption, but there is extensive laboratory ev-
idence showing increased aggressive behavior under alcohol.
Bushman and Cooper performed a meta-analysis of thirty ex-
perimental studies and concluded that the evidence supported
the conclusion that alcohol causes aggression in male “social
drinkers”(Bushman & Cooper, 1990).
There is a vast literature in sociology, criminology, and psy-
chology linking alcohol to acts of violence, as well as the indi-
vidual characteristics that may predispose some individuals to
violence and the situations that promote its expression (Brain,
1986). It has been suggested that alcohol reduces inhibition and
unmasks underlying aggressive tendencies. The extent to which
this is reflected in crash statistics is not yet known.
ALCOHOL AND DEGREE OF INJURY
Alcohol not only reduces performance and affects behavior,
but the “use of alcoholic beverages predisposes to more severe
and extensive injury than would be experienced by non-drinkers
given impact of the same severity”(Committee on Trauma Re-
search, 1985). There is an extensive trauma literature on this
subject, which is beyond the scope of this article.
Animals subjected to a standardized force with and without
alcohol demonstrate increased trauma with alcohol (Brodner
et al., 1981). Humans experiencing trauma have altered hor-
monal responses when alcohol is present that may influence
outcome (Woolf et al., 1990), and alcohol affected trauma vic-
tims are likely to have sustained more injuries (Fabbri et al.,
2001).

ALCOHOL EFFECTS ON DRIVERS 191
Waller et al. (1986) examined over a million collision reports
in North Carolina from 1979 to 1983. When they controlled for a
wide variety of factors such as crash severity, type and weight of
vehicle, speed, driver age and sex, and seatbelt use, they found
that the presence of alcohol increased the probability of being
killed in an collision 225% over that of a matched non-alcohol
involved driver.
Evans and Frick (1993) used fatal crash data for two-car
crashes where at least one driver was killed and controlled for
factors such as relative weight and impact areas. They deter-
mined that the presence of a BAC of 0.10 g/100 ml roughly
doubled the risk of death from a given impact and a BAC of
0.25 g/100 ml tripled the probability of death.
DRUGS OTHER THAN ALCOHOL
Epidemiology of Drugs and Crashes
While alcohol remains the dominant drug causing impairment
of driving performance, other drugs, especially in combina-
tion with alcohol, increase collision risk. Reviewing the his-
tory of 43,000 outpatients, Skegg et al. (1979) found that the
53 crash-involved drivers in that sample were 4.9 times more
likely than their matched controls to have been using a tranquil-
lizer. The relative risk of a driver being killed in a traffic crash
(assessed by odds ratio analysis) shows a significant increase for
drivers consuming alcohol alone, alcohol with other psychoac-
tive drugs, combinations of psychoactive drugs, and cannabis
(Alvarez et al., 1992a, 1992b; Alvarez et al., 1997; Drummer &
Gerostamoulos, 1998; Drummer et al., 1998).
Impairment can be predicted from known or expected effects
of medication on:
•Alertness (e.g., sedation, stimulation)
•Vision (e.g., visual blurring, delayed recovery from glare)
•Function (e.g., impaired coordination or movement)
•Performance (e.g., impaired performance on skills testing)
•Psycho-social (e.g., changes in behaviour, risk taking)
•Cognition (e.g., changes in processing information)
This information is available from the pharmacology of certain
substances, reports of adverse drug reactions, epidemiological
data, and specific testing (Ogden & Brous, 1999).
Major Problems in Interpreting Data on Drugs and Driving
There are many major problem areas that need to be considered
when attempting to show the correlation between drug consump-
tion and road trauma.
Proof That the Drug Has Been Consumed. Proof of drug
consumption requires analysis of a body fluid to identify the
drug. There is a large number of potential drugs that could be
screened, and many of the drugs of interest may only be present
in minute quantities while having significant effects.
Could the Amount of Drug Detected Produce Impairment?
The fact that a substance is found does not mean that it caused
impairment. It is necessary to ask a series of questions: Does
this substance cause impairment of human skills? If so, is such
impairment universal or idiosyncratic? Does the impairment oc-
cur in normal dosages or only when the drugs is used in excess?
The presence of a drug may not necessarily mean the driver is
impaired (Maki & Linn¨oila, 1976). There is considerable in-
formation on the clinical use of some drugs and on the normal
levels expected and on what constitutes a “toxic”concentra-
tion (Baselt et al., 1975; Uges, 2004). The clinical concepts
of “therapeutic”and “toxic”do not necessarily correlate with
impairment. Some individuals will be impaired with levels of
a drug normally considered therapeutic (e.g., sedatives), while
dangerously toxic levels of other drugs may have no effect on
driving skills (e.g., paracetamol) (Pearl et al., 1989). There is no
critical level of most drugs above which impairment is present
or below which no impairment can be demonstrated (Starmer
et al., 1988).
While we are interested in the behavioral effects of drugs,
presumably due to activity at some site in the brain, we are
limited to taking samples from peripheral sites in the body. The
drug levels in blood, urine, saliva, hair, etc., may be
1. quite different from that in the CNS and
2. not well correlated over time as levels change at the central
and peripheral sites.
Could This Amount of Drug Have Contributed to the Crash?
There are a number of individuals whose behavior and function-
ing is considerably improved by prescription medications, and
without which they would not be fit to hold a drivers licence, such
as anti-convulsants for epilepsy. Withdrawal of such drugs may
produce a considerable deterioration in driving performance.
The alcohol literature has relied heavily on the utility of mea-
suring the blood alcohol concentration. Alcohol is a relatively
easy drug to study: it is taken in large quantities; it is water-
soluble; the concentration is easy to measure; and impairment
is effectively dose-related. This paradigm does not translate to
other drugs that may be impairing in miniscule doses; be protein
bound or sequestered into fat; be hard to quantify; and the blood
levels may have no correlation with impairment.
THC is a good example of the problems understanding the
relationship between drug usage and impairment. When mari-
juana is smoked, THC in the inhaled smoke is absorbed within
seconds. Peak blood levels appear about the time smoking is
finished. The cannabinoids are rapidly distributed into fat and
blood levels fall within minutes. Maximum impairment is ob-
served an hour after smoking, when THC levels are about 5 to
10% of the peak (Tzambasis, 2001). The half-life of THC is
estimated to be as long as 10 days and metabolic products can
be found for several weeks after exposure. The presence of THC
metabolites is evidence of drug exposure and not of impairment.
The work of Terhune in the United States (Terhune et al.,
1992) and Drummer’s group in Australia (Drummer &
Gerostamoulos, 1998; Drummer et al., 1998; Robertson &
Drummer, 1994) has examined the culpability of fatally injured

192 E. J. D. OGDEN AND H. MOSKOWITZ
Table I Risk of culpability for fatal collision
Culpability
Drug(s) Percentage of cases odds ratio
Alcohol alone 24 9.1
Alcohol plus drugs 9 11
Psychoactive drugs 2 3.4
Drug combinations 3 4.6
THC >5 ng/ml 1 3.0
Benzodiazapines 4 2.4
All psychotropics 13 1.5
Stimulants 3 1.4
drivers. They have each used the odds ratio to indicate the rel-
ative importance of various drugs in fatal collision causation.
Drummer summarized this work in Table I (Drummer, 2002).
These results must be taken cautiously, because epidemio-
logical studies to evaluate the role of drugs such as cannabis in
live drivers are fraught with difficulties. First, the rate at which
subjects agree to participate in providing body fluid samples for
drug testing is far below that found in alcohol studies. The re-
sults of studies where voluntary participation rates are only in
the 80% range may suffer considerable bias.
Second, relative risks for death may be very different from the
risk of injury or non-injury collision. Studies of fatal collision
may not be comparable with studies of injured or non-injured
drivers.
Third, the probability of crash involvement is also a function
of non-drug factors including geographic area, traffic conditions,
vehicle characteristics, and the individual characteristics of the
driver. Few studies have obtained data that would permit the
separation of the possible effects of a drug in collision causation
from all the other factors that determined the event.
For example, in the United States the National Highway Traf-
fic Safety Administration estimates that alcohol is present in 8%
of all motor collisions. Even if one assumes that alcohol was the
sole cause of all of those crashes, it leaves 92% of the crashes as
due to other causes. How do we determine the degree to which
those other causes are also present in alcohol-related crashes?
How are the contributions of the various factors to be separated
or proportioned? The difficulty of performing epidemiological
studies even with respect to cannabis, the most frequently stud-
ied drug other than alcohol, can be seen in two recent reviews
of the literature that reached differing conclusions. Bates and
Blakely, (1999) concluded that “.. . there is no evidence that
consumption of cannabis alone increases the risk of culpability
for traffic crash fatalities or injuries for which hospitalization
occurs, and may reduce those risks.”Ramaekers et al. (2004)
concluded that drivers who had recently used cannabis were
“about three to seven times more likely to be responsible for
their crash as compared to drivers that had not used drugs or
alcohol.”
Impairment Tests
Given the difficulty of obtaining appropriate biological samples,
getting timely analysis, and interpreting the result, law enforce-
ment measures aimed at drug-impaired driving have been de-
pendent on behavioral tests to demonstrate impairment (Ogden,
1995). There is worldwide interest in roadside testing for drugs
and the establishment of per se definitions of impairment.
The probability of being arrested for driving while impaired
by alcohol was estimated to be extremely low with a risk es-
timated at 0.001 per trip made while intoxicated. This led the
US Department of Transportation to commission work during
the late 1970s to develop a standardised field sobriety test bat-
tery that would facilitate the accurate recognition of intoxicated
drivers in the field.
Burns and Moskowitz carried out two large research projects
involving over 500 subjects (Burns & Moskowitz, 1977; Tharp
et al., 1981). Police officers tested laboratory subjects who had
consumed alcohol to simulate intoxicated drivers. They identi-
fied three tests (Horizontal Gaze Nystagmus, Walk and Turn,
One-Leg Stand) that reliably identified alcohol intoxication (de-
fined BAC >0.10%). This battery of three relatively straight-
forward tests was recommended for adoption by police as a
roadside screen for sobriety, The three tests became collectively
known as the Standardised Field Sobriety Test (SFST).
In the laboratory studies, police officers’estimates of BAC
differed from the measured concentration by an average 0.03%.
They were able to correctly classify subjects above or below
0.10 g/100 ml, 81% of the time.
Anderson et al. (1983) found that different police departments
had predictive accuracy between 76% and 96%, suggesting that
reliability may be related to training and careful adherence to
protocol rather than inherent test validity. Drugs other than al-
cohol may have contributed to the apparent over-classification.
At the roadside, “No decision”is not an option for operational
police (Burns, 1991): a decision must always be made. It seems
natural that police will err on the side of caution when making
roadside assessments: better to make an incorrect release than
make an incorrect arrest. “It is apparent that the ‘arrest’crite-
rion is lower in the laboratory. The penalties for mistakes in a
laboratory setting are, of course, fairly trivial when compared
to a real world setting”(Burns & Anderson, 1995). A Finnish
study with more than 5,000 subjects found that observations of
nystagmus combined with tests of balance and walking was the
best screening tool for alcohol (Pentilla et al., 1974).
Evidence of drug impairment traditionally relied on physi-
cians with the appropriate experience and interest. The Los An-
geles Police Department pioneered the training of police officers
to perform these field evaluations and give expert evidence on
drug effects. The program allowed prosecution for drug impaired
driving in three discrete steps:
1. The arresting officer establishes impairment and calls for a
Drug Recognition Expert.
2. The drug recognition officer establishes that the impairment
is likely to be due to a drug in a particular class.
3. The laboratory confirms that a drug in that class is present in
blood or urine.

ALCOHOL EFFECTS ON DRIVERS 193
Enthusiasm for the abilities of the police trained Drug Recogni-
tion Expert (DRE) performance should be restrained. There are
no scientific studies utilizing adequate blind controls to examine
the ability of DRE trained officers to correctly identify an indi-
vidual as drug impaired, and/or identify the drug classification.
The studies performed have been primarily field observational
studies. It is interesting to note that when one examines the
ability of police officers to detect and identify the presence of
alcohol beverage on an individual’s breath (with adequate con-
trols) how much the results vary from commonly held police
opinions as to their ability to detect whether a person has been
drinking (Moskowitz et al., 1999).
The DRE program has been refined and renamed Drug Eval-
uation and Classification (DEC). SFST procedures remain at
the core of this process with the addition of some physiological
data (pupil reaction, pulse, blood pressure, finger-nose test) to
aid drug classification.
No battery has been standardized against the broad range of
drugs that are implicated in driving impairment. Tzambasis has
shown that observation of head movements and jerks improves
the discrimination of SFST for impairment due to marijuana
(Tzambasis, 2001; Tzambazis et al., 2000, 2001), but similar
work has not yet been done with other substances.
SPECIFIC DRUGS
There are many ways to look at the literature on drugs and
driving. The alcohol review was arranged according to experi-
mental methodology and performance variables. A similar ap-
proach to other substances would give a coherent overview of
the research methodologies, but make it difficult for the reader
to appreciate the specific effects of individual substances. We
have chosen to present the data by drug because of the practical
implications, acknowledging that this is done at the expense of
presenting a somewhat disjointed overview.
Marijuana
Marijuana is the common term given to the leaves of the plant
cannabis sativa. It has been used for centuries in various parts of
the world, and has become a popular recreational drug through-
out the western world.
Of the many chemical compounds in its leaves, delta-9
tetrahydrocannabinol (9 THC or THC) has been identified as
the major psychoactive component. THC has significant effects
on the human brain in tiny concentrations both at the time of
consumption and long term.
The most frequently detected metabolite of THC is 11-nor-
carboxy-delta-9-THC (often called THC-carboxylic acid),
which is inactive. THC-carboxylic acid can be detected in blood,
urine, and other tissues for an extended period. It has a metabolic
half-life of 33–40 hours, but its half-life in fatty tissues is sig-
nificantly longer because of its affinity for fat. It can take up to
a month to be eliminated beyond the detection limits of modern
toxicological techniques. The detection of the metabolite in a
biological sample is therefore evidence of the consumption of
cannabis within the last month, but does not enable a more ac-
curate estimate of when it was consumed nor quantification of
the dose consumed.
There is no biological measurement of cannabinoid concen-
tration that allows direct estimate of cannabis-induced impair-
ment of driving skills as exists for alcohol (Chesher et al., 1986).
Tzambasis’s (2001) observation that impairment was greatest 70
minutes after smoking when THC levels had fallen to 5 to 10%
of peak level demonstrates this point.
Drivers under the combined influence of marijuana and al-
cohol have an increased likelihood of initiating a crash and the
combination produces an additional decrement in performance
of driving related tasks (Burns & Moskowitz, 1980; Chesher
et al., 1986; Drummer, 2002; Drummer & Gerostamoulos, 1998;
Drummer et al., 1998; Klonoff, 1983; Perez-Reyes et al., 1988;
Ramaekers et al., 2004).
Early studies on the effects of marijuana on simulated driv-
ing performance established that some driving variables are im-
paired by the consumption of marijuana. In particular subjects
appeared to have delayed or inappropriate reactions, attention
deficits, poor speed and distance judgment, and poor hazard per-
ception. People affected by cannabis tend to travel slowly and
avoid risk. It is unclear to what extent this is due to conscious
recognition of impairment rather than distortion of judgement
of time and distance.
More recent studies in more realistic driving simulators show
that marijuana increases the variability of speed control and road
position. Marijuana-affected participants tend to hit obstacles,
miss signs, have delayed responses to the need to change speed
(both braking and accelerating are inappropriate), and drive
more slowly than when unaffected (Drummer, 2002; Drummer
& Gerostamoulos, 1998; Drummer et al., 1998; Tzambasis,
2001; Tzambazis et al., 2000, 2001).
There have been several on-road driving studies examining
the effects of cannabis on driving performance. Results showthat
marijuana results in poor car handling, with drivers exposed to
high doses of marijuana five times more likely to strike cones
on a driving task than when not affected by the drug (Klonoff,
1974, 1983; McBay & Owens, 1981; Ramaekers et al., 2000).
There does not appear to be a “hangover effect”of the sort
seen with alcohol and long-acting sedatives (Chait, 1990; Chait
et al., 1985), however there is some prolonged impairment of
skilled performance. Leirer et al. (1991) studied nine experi-
enced licensed pilots performing a simulator flight with numer-
ous response variables before and after smoking a cigarette con-
taining 20 mg of delta 9-tetrahydrocannabinol (THC). Marijuana
impaired performance at 0.25, 4, 8, and 24 hours after smoking.
At 24 hours, only one pilot reported awareness of drug effects.
THC levels greater than 5 ng/ml are associated with a three-
fold increase in the risk of being responsible for a fatal colli-
sion (Drummer, 2002). Yet several other epidemiological stud-
ies have failed to find above baseline fatality rates for use of
cannabis alone (Bates & Blakely, 1999). The combination of
marijuana and alcohol severely impairs performance (NHTSA,
2000).

194 E. J. D. OGDEN AND H. MOSKOWITZ
Anti-Anxiety Drugs
The benzodiazepine group of drugs includes minor tranquil-
lizers, sedatives, anticonvulsants, and hypnotics. Representative
members of the group are diazepam, oxazepam, nitrazepam, and
flunitrazepam. These drugs have largely taken the place of the
barbiturates in the treatment of anxiety and insomnia because of
their efficacy and safety even with overdose.
Different members of the class depress the central nervous
system to varying degrees and in qualitatively different ways.
Some are better at relieving pathological anxiety and agitation
and are classified as tranquillizers. Others are more sedating and
hence are used to treat insomnia. Some members of the group
are primarily used in epilepsy as anticonvulsants. There is no
sharp distinction between any of these effects and higher doses
of any of the benzodiazepines may induce sedation and coma.
Berghaus and Grass (1997) reviewed over 500 experimental
studies of driving related tasks. They showed that the serum level
of each of the benzodiazepines studied was related to the degree
of impairment in the laboratory.
The data suggest that there is an increased risk of personal
injury crashes among drivers using anti-anxiety drugs compared
with the rest of the population (Skegg et al., 1979) and this is ex-
acerbated by alcohol (Sepp¨al¨a et al., 1976a). There is a hangover
effect and a small dose of alcohol the following day can potenti-
ate the effect. There is a decrement in tasks requiring vigilance
at low doses and tolerance is only occasionally noted. The oppo-
site effect, exaggerated impairment, has also been documented
(Kolega, 1989).
The benzodiazepine group has been shown to impair driv-
ing skills to a similar degree and in similar ways to alcohol.
Thomas (1998) concluded that the risk of collision was dou-
bled for patients taking benzodiazepines. The impairment and
collision risk are greatest in the first two weeks of treatment
(de Gier et al., 1981). The ICADTS working group concluded
that patients should be warned not to drive in the first two weeks
of treatment (Alvarez & de Gier, 2002). However,not all research
has found an association between sedative use and collision risk
(Jick et al., 1981). de Gier (1993) reported that clinically anxious
patients are also poor drivers. Although treatment with benzodi-
azepine tranquillizers will improve clinical anxiety, there is no
improvement in their driving ability.
Psychoactive Medication
The untreated psychiatric patient is a potentially hazardous driver
either because of the underlying illness and the consequent dis-
order of the mind, or of the associated psychomotor impairment.
Once stabilized on medication, patients are better on their medi-
cation and a greater risk without it (Sepp¨al¨a et al., 1976b; Smiley
et al., 1981). There is some question about the generality of this
conclusion (de Gier et al., 1981) as it has been based primarily
on subjective clinical judgment without adequate research back-
ing. There is some interaction with alcohol generally related to
the sedative effects of some psychoactive drugs (Bauer, 1984;
Hindmarch, 1984).
Different members of each class of psychoactive medication
have quite different effects on driving. For instance, the tricyclic
antidepressants are quite impairing of driving skill, while the se-
lective serotonin reuptake inhibitor (SSRI) antidepressants have
lesser effect on driving and little or no interaction with alcohol
(Pullen, 1999). Starmer and Mascord (1994) have stated that
tricyclic anti-depressants, which are intrinsically sedative in na-
ture and cause driving impairment in normal individuals, will
improve the driving ability of depressed patients.
Stimulants—Amphetamine/Cocaine
There are laboratory studies showing that small doses of stim-
ulants can improve cognitive performance (De Wit et al., 2002;
Wachtel & de Wit, 1999) and improve reaction time (Fleming
et al., 1995; Halliday et al., 1994). On the other hand, am-
phetamines cause deficits in divided attention tasks and per-
ception in the peripheral visual fields (Easterbrook, 1955; Mills
et al., 2001).
Amphetamine variants (dexamphetamine, methamphetamine,
and methylenedioxymethamphetamine (MDMA, or Ecstasy))
have been implicated in traffic fatalities (Drummer, 1994, 2002;
Drummer & Gerostamoulos, 1998, 1999; Drummer et al., 1998).
A review of the epidemiological evidencein 1987 by Hurst found
little to support such a relationship.
There’s been little laboratory work with driving simulators or
on-the-road performance under amphetamines. However, using
a driving simulator, Silber et al. (2004) found that 0.42 mg/kg
dexamphetamine significantly impaired overall performance for
daytime but not night-time driving, possibly because the visual
field is restricted in the night-time simulation and peripheral
cues are less important. During the daytime simulation, drivers
signalled incorrectly and failed to stop at red traffic lights more
frequently.
Laboratory studies are required that replicate the conditions
under which the amphetamines are frequently used. Thus, for ex-
ample, long-distance drivers often take methamphetamine repet-
itively and so the drug should be examined experimentally under
similar conditions. Finally, it is known that methamphetamine
depresses neurotransmitters in the brain for extended periods
over a week or more, even following single-dose treatments.
During that period subjects exhibit depressed behavior that
should be examined for impairment.
Opioid Analgesics
The opiate drugs—heroin, methadone, codeine, and related
compounds—are used for pain relief and the suppression of
cough. They have a high addiction potential. Acute sedation
and impairment is observed in a dose-related manner and there
is a deleterious interaction with alcohol, although the effects
are slight compared with alcohol (Chesher, 1989). Methadone
is used for the long-term maintenance therapy of narcotic ad-
dicts. Long-term methadone maintenance is not associated with
an increase in collision risk after the initial stabilization period

ALCOHOL EFFECTS ON DRIVERS 195
(Chesher et al., 1995; Friedel & Berghaus, 1995; Friedrich et al.,
1991; Moskowitz & Robinson, 1985).
Minor Analgesics and Anti-Arthritics
There are few central side effects of the common minor pain-
killers (aspirin, paracetamol) or of the non-steroidal anti-
inflammatory agents that are used for the treatment of arthritis.
SUMMARY
Alcohol, the substance most frequently found in crash-
involved drivers, has been extensively examined in experimen-
tal and epidemiological studies. While behavioral areas such as
judgment, emotion, cognition, and sleep requires further work,
the existing large literature describes numerous behaviors im-
paired by alcohol and their role in traffic safety.
Other drugs have been shown to impair human performance,
or have been implicated in epidemiological studies as increasing
the risk of crashes. None have been examined in the same detail
as alcohol over the wide range of possible behaviors. Such ex-
amination would enhance the ability to evaluate the role of these
drugs in traffic. The increasing sophistication of behavioral mea-
sures examining cognitive processes and judgment will assist
researchers in estimating drug safety.
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