Impairment due to alcohol, tetrahydrocannabinol, and benzodiazepines in impaired drivers compared to experimental studies.

OBJECTIVE: In some countries, per se laws for other drugs than alcohol are used to judge drunk and drugged drivers. These blood concentration limits are often derived from experimental studies on traffic relevant behavior of healthy volunteers. Knowledge about how results from experimental studies could be transferred to a real-life setting is missing. The aim of this study was to compare impairment seen in experimental studies to the impairment seen at equivalent concentrations in apprehended drunk and drugged drivers. METHODS: Results from previously performed meta-analyses of experimental studies regarding impairment from alcohol, tetrahydrocannabinol (THC), and benzodiazepines were compared to impairment in apprehended drunk and drugged drivers as judged by a clinical test of impairment. Both experimental studies and real-life cases were divided into 4 groups according to increasing blood drug concentration intervals. The percentage of impaired test results in experimental studies was compared to the percentage of impaired subjects among drivers within the same blood drug concentration window. RESULTS: For ethanol, the percentage of impaired drivers (n = 1,223) increased from 59% in the lowest drug concentration group to 95% in the highest drug concentration group, compared to 7 and 72% in the respective groups in experimental studies. For THC, the percentage of impaired drivers (n = 950) increased from 42 to 58%, the corresponding numbers being 11 and 42% for experimental studies. For benzodiazepines, the percentage of impaired drivers (n = 245) increased from 46 to 76%, the corresponding numbers being 16 and 60% for experimental studies. The increased odds ratio for impairment between 2 concentration groups was comparable for experimental studies and impaired drivers. CONCLUSIONS: Fewer test results indicated impairment in experimental studies compared to impaired drivers in real life when influenced by similar blood concentrations of either ethanol, THC, or benzodiazepines. In addition, a comparable relationship between drug concentration and impairment was seen for both experimental studies and real-life cases. We believe that the present study strengthens the background for using experimental studies to establish fixed concentration limits for drunk and drugged drivers, but experimental studies in an impaired driver population could further expand our knowledge.

Evaluation of the hip-flask defence by determination of ethyl glucuronide and ethyl sulphate concentrations in blood.

INTRODUCTION: The hip-flask defence (i.e. claiming ethanol intake after an incident) is difficult to refute by the use of ethanol analyses alone, as these may show decreasing concentrations shortly after intake of alcohol. The non-oxidative metabolites of ethanol, ethyl glucuronide (EtG) and ethyl sulphate (EtS) have a different pharmacokinetic profile, with peak concentrations in blood around 4h after intake. The aim of this study was to describe a method for using EtG-analysis for the purpose of estimating the time point of ethanol intake and to report cases in which this method is used. METHODS: Previously published studies are summarised. Also, in expert witness cases where the hip-flask defence is claimed, EtG and EtS were analysed in selected cases. Twelve such cases are reported. RESULTS: In previous studies, about 70 healthy volunteers have been included in different kinetic studies, demonstrating maximal individual concentrations of EtG always below 0.5 mg/L after 1 h, below 1 mg/L after 2 h and somewhat above 1 mg/L 4 h after a moderate alcohol intake (up to 80 grams of ethanol). Twelve cases are reported in the present study, where the suspect claimed no alcohol intake before driving, only intake after driving. In all 12 cases, ethanol concentration was lower in the second sample (taken approximately 30 min after the first). The median EtG concentration in the first sample was 4.13 mg/L (range 2.0-7.4) and 4.34 mg/L (range 2.1-7.2) in the second sample. One case showed an increase in EtG concentrations of 15% from first to second sample (the time difference between the samples was 32 min, with the first sample taken 41 min after driving). For the remainder of the cases, EtG concentrations were relatively stable. CONCLUSIONS: In all the presented cases, the levels of EtG were substantially higher than what would be expected only about 1-2h after a very recent alcohol intake. The relatively stable concentrations between the first and second sample also indicated that the high EtG concentrations were not caused by a rapid formation after a recent intake, as this would have demonstrated increasing concentrations over a time period of 30 min. In conclusion, EtG and EtS in blood could be a helpful tool in assessment of the hip-flask defence, in cases where the detected ethanol is claimed to be caused solely by a single intake after driving.