Evaluation of breath-alcohol instruments. IV. Roadside tests with Alcolmeter pocket model

This paper reports results from a field trial with a breath-alcohol screening device--Alcolmeter pocket model. Breath tests were made with drivers apprehended during routine controls (road-blocks), for traffic violations and those involved in traffic accidents. Of 908 roadside breath tests made with chemical reagent tubes, 343 showed zero alcohol (no colour change) and these results were confirmed by Alcolmeter. Alcohol was detected in 191 tests but the level was judged as being below the legal limit of 0.50 mg/ml. The Alcolmeter results, however, ranged from 0 to 1.22 mg/ml (mean 0.21 mg/ml) and 15 individuals (7.8%) were above the legal limit. There were 373 positive chemical tube breath screening tests whereas in 5 cases (1.3%) Alcolmeter indicated a blood-alcohol level below 0.50 mg/ml. Duplicate determinations with the Alcolmeter device were highly correlated r = 0.93 +/- 0.02 (+/- S.E.), P less than 0.001. The standard deviation of a single breath-alcohol analysis under field conditions was +/- 0.10 mg/ml which corresponds to a coefficient of variation of 10%. The time interval between positive roadside breath test and blood-sampling ranged from 5 to 220 min (median 62 min). The results were therefore adjusted by 0.15 mg/ml per hour to compensate for ethanol metabolised between the time of sampling blood and breath. The corrected blood and breath values were well correlated r = 0.84 +/- 0.03, P less than 0.001 but the predictive power of the regression relationship was poor. The regression equation was y = 0.27 +/- 0.65x and the standard error estimate was +/- 0.21 mg/ml at the mean concentration of ethanol of 1.0 mg/ml.     

Evaluation of breath alcohol instruments II. In vivo experiments with Alcolmeter Pocket Model

The precision and accuracy of an Alcolmeter Pocket Model breath alcohol instrument have been investigated in experiments with human subjects under controlled conditions. The instrument response was zero in all tests with breath samples from alcohol-free subjects. The standard deviations of ethanol determinations in breath were ±0.0722 mg/ml during ethanol absorption and ±0.0416 mg/ml during ethanol elimination. The standard deviation during the elimination phase increased with ethanol concentration in the sample, being ±0.0416 mg/ml on average at a mean concentration of 0.420 mg/ml, corresponding to a coefficient of variation of 9.9%.The blood alcohol estimates using the Alcolmeter were somewhat too high during active absorption of ethanol, and too low during elimination, when a constant blood-breath alcohol ratio of 2100:1 was used to calibrate the instrument. During the elimination phase of ethanol kinetics and at a mean blood alcohol concentration of 0.50 mg/ml, the mean Alcolmeter result was 0.456 ± 0.169 mg/ml with 95% confidence, i.e. varying between 0.287 and 0.625 mg/ml 95 times out of 100 tests at this critical blood alcohol level.     

Evaluation of breath alcohol instruments I. In vitro experiments with Alcolmeter Pocket Model

An Alcolmeter Pocket Model breath alcohol device, based on an electrochemical (fuel cell) oxidation principle for ethanol analysis, has been evaluated under in vitro conditions. The result of a test is displayed on an analogue meter within 20 – 30 seconds after sampling; replicate tests may be made within 3 – 5 minutes. The electrochemical detector used was found to respond to acetaldehyde, methanol, isopropanol and n-propanol vapours besides ethanol, but it was insensitive to acetone vapour. The Alcolmeter response with a 0 – 2.0 mg/ml scale was linearly related to ethanol vapour concentration up to 1.0 mg/ml blood alcohol equivalent concentration; above this level the response was curvilinear, the Alcolmeter reading being too low. The standard deviation of an ethanol vapour determination in vitro was ±0.0175 mg/ml at a mean concentration of 0.902 mg/ml. The accuracy of the device expressed as percent recovery at 0.50, 1.0 and 1.4 mg/ml blood alcohol concentrations was 96.8%, 98.3%, and 88.3%, respectively. When the Alcolmeter was calibrated at 0.50 mg/ml and used occasionally each day over an 18-day period, the drop in initial calibration was 0.01 mg/ml per week.     

Relationship between the concentration of ethanol and methanol in blood samples from Swedish drinking drivers

Headspace gas chromatography was used to determine the concentration of ethanol and methanol in blood samples from 519 individuals suspected of drinking and driving in Sweden where the legal alcohol limit is 0.50 mg/g in whole blood (11 mmol/l). The concentration of ethanol in blood ranged from 0.01 to 3.52 mg/g with a mean of 1.83 +/- 0.82 mg/g (+/- S.D.). The frequency distribution was symmetrical about the mean but deviated from normality. A plot of the same data on normal probability paper indicated that it might be composed of two subpopulations (bimodal). The concentration of methanol in the same blood specimens ranged from 1 to 23 mg/l with a mean of 7.3 +/- 3.6 mg/l (+/- S.D.) and this distribution was markedly skew (+). The concentration of ethanol (x) and methanol (y) were positively correlated (r = 0.47, P less than 0.001) and implies that 22% (r2) of the variance in blood-methanol can be attributed to its linear regression on blood-ethanol. The regression equation was y = 3.6 + 2.1 x and the standard error estimate was 0.32 mg/l. This large scatter precludes making reliable estimates of blood-methanol concentration from measurements of blood-ethanol concentration and the regression equation. But higher blood-methanol concentrations are definitely associated with higher blood-ethanol in this sample of Swedish drinking drivers. Frequent exposure to methanol and its toxic products of metabolism, formaldehyde and formic acid, might constitute an additional health risk associated with heavy drinking in predisposed individuals. The determination of methanol in blood of drinking drivers in addition to ethanol could indicate long-standing ethanol intoxication and therefore potential problem drinkers or alcoholics.     

Observations on the specificity of breath-alcohol analyzers used for clinical and medicolegal purposes

This paper deals with the application of three kinds of breath-alcohol analyzer for clinical and medicolegal purposes. The limited specificity for analyzing ethanol in expired breath has given misleading information with potential serious consequences. Three different methods of alcohol analysis are reported: semiconductor sensing (Alcotest 7310), electrochemical fuel cell (Alcolmeter SM-1), and infrared (IR) absorptiometry (IR Intoximeter 3000). Methanol could not be distinguished from ethanol with any of these breath-test instruments. When nonspecific techniques of ethanol analysis are used, the results must be considered with caution when interfering substances expelled in breath cannot be excluded.     

Reliability of breath-alcohol analysis in individuals with gastroesophageal reflux disease.

Gastroesophageal reflux disease (GERD) is widespread in the population among all age groups and in both sexes. The reliability of breath alcohol analysis in subjects suffering from GERD is unknown. We investigated the relationship between breath-alcohol concentration (BrAC) and blood-alcohol concentration (BAC) in 5 male and 5 female subjects all suffering from severe gastroesophageal reflux disease and scheduled for antireflux surgery. Each subject served in two experiments in random order about 1-2 weeks apart. Both times they drank the same dose of ethanol (approximately 0.3 g/kg) as either beer, white wine, or vodka mixed with orange juice before venous blood and end-expired breath samples were obtained at 5-10 min intervals for 4 h. An attempt was made to provoke gastroesophageal reflux in one of the drinking experiments by applying an abdominal compression belt. Blood-ethanol concentration was determined by headspace gas chromatography and breath-ethanol was measured with an electrochemical instrument (Alcolmeter SD-400) or a quantitative infrared analyzer (Data-Master). During the absorption of alcohol, which occurred during the first 90 min after the start of drinking, BrAC (mg/210 L) tended to be the same or higher than venous BAC (mg/dL). In the post-peak phase, the BAC always exceeded BrAC. Four of the 10 subjects definitely experienced gastric reflux during the study although this did not result in widely deviant BrAC readings compared with BAC when sampling occurred at 5-min intervals. We conclude that the risk of alcohol erupting from the stomach into the mouth owing to gastric reflux and falsely increasing the result of an evidential breath-alcohol test is highly improbable.     

Minimum respiratory function for breath alcohol testing in South Australia.

The aim of this study was to determine if inability to complete a breath alcohol test successfully, using a Lion Alcolmeter SD-2 or Drager Alcotest 7110, was related to any of the standard parameters obtained from the lung function spirometry test. A total of 153 subjects referred to a clinical laboratory for routine lung function testing were tested using the Alcolmeter, 158 using the Alcotest, with 69 subjects completing tests on both instruments. Of the 153 patients who volunteered to use the Alcolmeter, 49 (32%) were unable to produce a valid test effort on this instrument. One subject failed to complete a satisfactory test using the Alcotest, and one was unable to master the technique. There was considerable overlap of the minimum value for each of the lung function parameters of those subjects who could or could not successfully complete the breath alcohol test. It is recommended that changes are made to both of the instruments, the techniques used and the legislation, to minimize the number of breath alcohol testing failures and to reduce the variability of the results.     

Studies in breath-alcohol analysis: biological factors.

Various biological factors affecting breath-alcohol analysis were studied experimentally. End-expiratory temperatures in 55 healthy subjects were found to range from 32.41 to 35.69 degrees C with a mean of 34.53 degrees C. Forced vital capacity in the same subjects ranged from 1825 to 6550 ml with a mean of 4038 ml, and maximum exhalation after normal inhalation ranged from 1180 to 4550 ml with a mean of 2730 ml. It was found that 65-70% of available breath must be discarded before the alveolar plateau is reached during expiration. End-expiratory (alveolar) carbon dioxide in 155 healthy subjects was 3.5-8.3% by volume (mean = 6.52). After oral alcohol intake, retained mouth-alcohol in 8 subjects had disappeared after 11 minutes without subsequent water-rinsing of the mouth, and after 8 minutes with rinsing. Water condensation in plastic mouthpieces/saliva traps during breath sampling yielded mean weight gains of 13.0, 8.6, and 4.6 mg., respectively, at initial mouthpiece temperatures of 3 degrees C, 22.5 degrees C, and 34.7 degrees C, respectively.     

Comparison of ethanol concentrations in venous blood and end-expired breath during a controlled drinking study

Concentration-time profiles of ethanol were determined for venous whole blood and end-expired breath during a controlled drinking experiment in which healthy men (n=9) and women (n=9) drank 0.40-0.65 g ethanol per kg body weight in 20-30 min. Specimens of blood and breath were obtained for analysis of ethanol starting at 50-60 min post-dosing and then every 30-60 min for 3-6 h. This protocol furnished 130 blood-breath pairs for statistical evaluation. Blood-ethanol concentration (BAC, mg/g) was determined by headspace gas chromatography and breath-ethanol concentration (BrAC, mg/2l) was determined with a quantitative infrared analyzer (Intoxilyzer 5000S), which is the instrument currently used in Sweden for legal purposes. In 18 instances the Intoxilyzer 5000S gave readings of 0.00 mg/2l whereas the actual BAC was 0.08 mg/g on average (range 0.04-0.15 mg/g). The remaining 112 blood- and breath-alcohol measurements were highly correlated (r=0.97) and the regression relationship was BAC=0.10+0.91BrAC and the residual standard deviation (S.D.) was 0.042 mg/g (8.4%). The slope (0.91+/-0.0217) differed significantly from unity being 9% low and the intercept (0.10+/-0.0101) deviated from zero (t=10.2, P<0.001), indicating the presence of both proportional and constant bias, respectively. The mean bias (BAC - BrAC) was 0.068 mg/g and the 95% limits of agreement were -0.021 and 0.156 mg/g. The average BAC/BrAC ratio was 2448+/-540 (+/-S.D.) with a median of 2351 and 2.5th and 97.5th percentiles of 1836 and 4082. We found no significant gender-related differences in BAC/BrAC ratios, being 2553+/-576 for men and 2417+/-494 for women (t=1.34, P>0.05). The mean rate of ethanol disappearance from blood was 0.157+/-0.021 mg/(g per hour), which was very close to the elimination rate from breath of 0.161+/-0.021 mg/(2l per hour) (P>0.05). Breath-test results obtained with Intoxilyzer 5000S (mg/2l) were generally less than the coexisting concentrations of ethanol in venous blood (mg/g), which gives an advantage to the suspect who provides breath compared with blood in cases close to a threshold alcohol limit.     

Effect of hyperthermia on breath-alcohol analysis

Mild hyperthermia to the extent of a 2.5 degrees C increase above normal body temperature was produced by immersion of ethanol-intoxicated subjects in a warm water bath. Hyperthermia did not influence the blood-alcohol decay curve of the subjects. Hyperthermia did cause a significant distortion of the breath-alcohol decay curve, up to as much as a 23% increase above blood-alcohol concentration. The magnitude of this distortion effect was calculated to be a 8.62% increase in breath-alcohol concentration over blood-alcohol concentration for each degree C increase in core body temperature. The forensic relevance of these results is that further support is given to previous recommendations that temperature monitoring be included in procedures for breath-alcohol analysis. This leads to the recommendation that mouth temperature be measured before breath sampling to screen for abnormal body temperature and to allow for potential use of a "temperature correction factor." This modification to existing analytical procedures would optimize the reliability of breath-ethanol analysis for prediction of blood-ethanol concentration.     

Breath alcohol concentration determined with a new analyzer using free exhalation predicts almost precisely the arterial blood alcohol concentration

A new breath alcohol (ethanol) analyzer has been developed, which allows free exhalation, standardizes measured exhaled alcohol concentration to fully saturated water vapor at a body temperature of 37 degrees C (43.95 mg/L) and includes a built-in self-calibration system. We evaluated the performance of this instrument by comparing standardized alcohol concentration in freely expired breath (BrAC) with arterial (ABAC) and venous (VBAC) blood alcohol concentrations in fifteen healthy volunteers who drank 0.6 g of alcohol per kg body weight. The precision (coefficient of variation, CV) of the analyzer based on in vivo duplicate measurements in all phases of the alcohol metabolism was 1.7%. The ABAC/BrAC ratio was 2251+/-46 (mean+/-S.D.) in the post-absorptive phase and the mean bias between ABAC and BrAC x 2251 was 0.0035 g/L with 95% limits of agreement of 0.033 and -0.026. The ABAC and BrAC x 2251 were highly correlated (r=0.998, p<0.001) and the regression relationship was ABAC = 0.00045 + 1.0069 x (BrAC x 2251) indicating excellent agreement and no fixed or proportional bias. In the absorption phase, ABAC exceeded BrAC x 2251 by at most 0.04+/-0.03 g/L when tests were made at 10 min post-dosing (p<0.05). The VBAC/BrAC ratio never stabilized and varied continuously between 1834 and 3259. There was a proportional bias between VBAC and BrAC x 2251 (ABAC) in the post-absorptive phase (p<0.001). The pharmacokinetic analysis of the elimination rates of alcohol and times to zero BAC confirmed that BrAC x 2251 and ABAC agreed very well with each other, but not with VBAC (p<0.001). We conclude that this new breath analyzer using free exhalation has a high precision for in vivo testing. The BrAC reflects very accurately ABAC in the post-absorption phase and substantially well in the absorption phase and thereby reflects the concentration of alcohol reaching the brain. Our findings highlight the magnitude of arterio-venous differences in alcohol concentration and support the use of breath alcohol analyzers as a stand-alone test for medical and legal purposes.     

Simulation of an assault with self-tying and vaginal insertion of metal objects

Usefulness of portable, handheld breath analysers equipped with electrochemical sensor was assessed. Breath- and blood-alcohol concentrations in drunken drivers were taken from 370 expert opinions elaborated at the Institute of Forensic Research between January 1st 2002 and February 28th 2007. The results of second and subsequent measurements were re-calculated using mean elimination rates. The readings of portable instruments were in very good agreement with the results of confirmatory analyses performed by stationary devices (r=0.978, p<0.001, y=0.969x-0.0002). The correlation with the results of blood analysis was weaker (r=0.940, p<0.001, y=1.722x+0.214), but comparable with the correlation between the readings of stationary devices and the results of blood analyses (r=0.936, p<0.001, y=1.790x+0.091). The readings of portable and stationary breath analysers were also compared by the Bland-Altman plots. The differences in results were independent of alcohol concentration (absolute difference (mg/L): r=0.054, p>0.1, y=0.011x+0.013; relative difference (%): r=0.020, p>0.1, y=0.90x+2.36).     

Oral fluid results compared to self reports of recent cocaine and heroin use by methadone maintenance patients

A novel breath-alcohol analyzer based on the standardization of the breath alcohol concentration (BrAC) to the alveolar-air water vapour concentration has been developed and evaluated. The present study compares results with this particular breath analyzer with arterial blood alcohol concentrations (ABAC), the most relevant quantitative measure of brain alcohol exposure. The precision of analysis of alcohol in arterial blood and breath were determined as well as the agreement between ABAC and BrAC over time post-dosing. Twelve healthy volunteers were administered 0.6g alcohol/kg bodyweight via an orogastric tube. Duplicate breath and arterial blood samples were obtained simultaneously during the absorption, distribution and elimination phases of the alcohol metabolism with particular emphasis on the absorption phase. The precision of the breath analyzer was similar to the determination of blood alcohol concentration by headspace gas chromatography (CV 2.40 vs. 2.38%, p=0.43). The ABAC/BrAC ratio stabilized 30min post-dosing (2089±99; mean±SD). Before this the BrAC tended to underestimate the coexisting ABAC. In conclusion, breath alcohol analysis utilizing standardization of alcohol to water vapour was as precise as blood alcohol analysis, the present "gold standard" method. The BrAC reliably predicted the coexisting ABAC from 30min onwards after the intake of alcohol.     

A rapid method for blood alcohol determination by headspace analysis using an electrochemical detector.

A method for the determination of blood alcohol concentration by headspace analysis using an electrochemical detector is described. A determination can be made within 2 min, and only 0.1 ml of blood is required for each analysis. The detector response was linearly related to ethanol concentrations up to 3.0 mg/ml. The standard deviation of a single determination was +/- 0.014 mg/ml. The accuracy of the method based on comparison with an enzymatic (alcohol dehydrogenase) technique was high, the mean recovery being 102.2% of the attributed concentration. The ease of the operation and fast analysis time make the method ideal for serial determinations, for example during mass screening of biological samples for ethyl alcohol in forensic and toxicology laboratories.     

Comparison of blood-ethanol concentration in deaths attributed to acute alcohol poisoning and chronic alcoholism

Ethanol concentrations were measured in femoral venous blood in deaths attributed to acute alcohol poisoning (N = 693) or chronic alcoholism (N = 825), according to the forensic pathology report. Among acute alcohol poisonings were 529 men (76%) with mean age 53 years and 164 women (24%) with mean age 53 years. In the chronic alcoholism deaths were 705 men (85%) with mean age 55 years and 120 women (15%) with mean age 57 years. The blood-ethanol concentrations were not related to the person's age (r = -0.17 in acute poisonings and r = -0.09 in chronic alcoholism). The distribution of blood-ethanol concentrations in acute poisoning cases agreed with a normal or Gaussian curve with mean, median, standard deviation, coefficient of variation, and spread of 0.36 g/100 mL, 0.36 g/100 mL, 0.086 g/100 mL, 24% and 0.074 to 0.68 g/100 mL, respectively. The corresponding concentrations of ethanol in chronic alcoholism deaths were not normally distributed and showed a mode between 0.01 and 0.05 g/100 mL and mean, median, and spread of 0.172 g/100 mL, 0.150 g/100 mL, and 0.01 to 0.56 g/100 mL, respectively. The 5th and 95th percentiles for blood-ethanol concentration in acute poisoning deaths were 0.22 and 0.50 g/100 mL, respectively. However, these values are probably conservative estimates of the highest blood-ethanol concentrations before death owing to metabolism of ethanol until the time of death. In 98 chronic alcoholism deaths (12%) there was an elevated concentration of acetone in the blood (>0.01 g/100 mL), and 50 of these (6%) also had elevated isopropanol (>0.01 g/100 mL). This compares with 28 cases (4%) with elevated blood-acetone in the acute poisoning deaths and 22 (3%) with elevated blood-isopropanol. We offer various explanations for the differences in blood-ethanol and blood-acetone in acute poisoning and alcoholism deaths such as chronic tolerance, alcohol-related organ and tissue damage (cirrhosis, pancreatitis), positional asphyxia or suffocation by inhalation of vomit, exposure to cold coupled with alcohol-induced hypothermia, as well as various metabolic disturbances such as hypoglycemia and ketoacidosis.     

Evaluation of methyl tert-butyl ether (MTBE) as an interference on commercial breath-alcohol analyzers.

Anecdotal reports suggest that high environmental or occupational exposures to the fuel oxygenate methyl tert-butyl ether (MTBE) may result in breath concentrations that are sufficiently elevated to cause a false positive on commercial breath-alcohol analyzers. We evaluated this possibility in vitro by establishing a response curve for simulated breath containing MTBE in ethanol. Two types of breath-alcohol analyzers were evaluated. One analyzer's principle of operation involves in situ wet chemistry (oxidation of ethanol in a potassium dichromate solution) and absorption of visible light. The second instrument uses a combination of infrared absorption and an electrochemical sensor. Both types of instruments are currently used, although the former method represents older technology while the latter method represents newer technology.The percent blood alcohol response curve was evaluated over a breath concentration range thought to be relevant to high-level environmental or occupational exposure (0-361 microg/l). Results indicate that MTBE positively biases the response of the older technology Breathalyzer when evaluated as a single constituent or in combination with ethanol. We conclude that a false positive is possible on this instrument if the MTBE exposure is very high, recent with respect to testing, and occurs in combination with ethanol consumption. The interference can be identified on the older technology instrument by a time dependent post-reading increase in the instrument response that does not occur for ethanol alone. In contrast, the newer technology instrument using infrared and electrochemical detectors did not respond to MTBE at lower levels (0-36 microg/l), and at higher levels (>72 microg/l) the instrument indicated an "interference" or "error". For this instrument, a false positive does not occur even at high MTBE levels in the presence of ethanol.     

The influence of sex hormones on the elimination kinetics of ethanol

The goal of the investigation was to research the influence of sex hormones on the elimination kinetics of ethanol. Forty-seven healthy men (average age 25+/-6.1 years) and 61 healthy women (average age 24+/-2.4 years) received 0.79-0.95g of ethanol/kg body weight in the form of an alcohol beverage of their choice. The target concentration for both sexes was a blood alcohol concentration (BAC) of 1.10g/kg. Blood samples for the determination of the ethanol concentration followed in the elimination phase in 10-20min intervals. The sex hormone levels (estradiol, progesterone and testosterone) were determined concomitantly from the serum. In men, the mean testosterone concentration was 5.3+/-1.6ng/ml, the mean estradiol concentration was 34.6+/-13.6pg/ml and the mean progesterone concentration was 0.9+/-0.3ng/ml. In women, the mean estradiol concentration was 47.6+/-52.6pg/ml and the mean testosterone concentration was 0.8+/-0.4ng/ml. Progesterone displayed a so-called dummy effect in women. In the high progesterone group (n=11), the mean concentration was 11.1+/-3.5ng/ml and in the low progesterone group (n=50) the mean was 0.6+/-0.3ng/ml. The mean hourly elimination rate (beta60) was 0.1677+/-0.0311g/kg/h in men. In women, the mean hourly elimination rate was 0.2044+/-0.0414g/kg/h in the high progesterone group and 0.1850+/-0.0276g/kg/h in the low progesterone group (p<0.05). The beta60 for women in the low progesterone group was significantly higher than that of the men, whose progesterone levels fell within a similar range (p>0.01). These results allow one to conclude that the gender differences in the pharmacokinetics of ethanol can partly, but not completely, be explained by progesterone levels.     

A large-scale study of the relationship between blood and breath alcohol concentrations in New Zealand drinking drivers

Blood alcohol concentrations (BAC) and corresponding breath alcohol concentrations (BrAC) were determined for 21,582 drivers apprehended by New Zealand police. BAC was measured using headspace gas chromatography, and BrAC was determined with Intoxilyzer 5000 or Seres Ethylometre infrared analysers. The delay (DEL) between breath testing and blood sampling ranged from 0.03 to 5.4 h. BAC/BrAC ratios were calculated before and after BAC values were corrected for DEL using 19 mg/dL/h as an estimate of the blood alcohol clearance rate. Calculations were performed for single and duplicate breath samples obtained using the Intoxilyzer (groups I-1 and I-2) and Seres devices (groups S-1 and S-2). Before correction for DEL, BAC/BrAC ratios for groups I-1, I-2, S-1, and S-2 were (mean+/-SD) 2320+/-260, 2180+/-242, 2330+/-276, and 2250+/-259, respectively. After BAC values were adjusted for DEL, BAC/BrAC ratios for these groups were (mean+/-SD) 2510+/-256, 2370+/-240, 2520+/-280, and 2440+/-260, respectively. Our results indicate that in New Zealand the mean BAC/BrAC ratio is 19-26% higher than the ratio of the respective legal limits (2000).     

Driving under the influence of chlormethiazole

This article describes a case of driving under the influence of the sedative-hypnotic-anticonvulsant drug chlormethiazole. The suspect, who was a physician, was driving dangerously on a busy highway and caused a traffic collision. When apprehended by the police, the man had bloodshot and glazed eyes and pupil size was enlarged. He could not answer the questions properly and his gait was unsteady. A roadside breath-alcohol screening test was positive but an evidential breath-alcohol test conducted about one hour later was below the legal limit for driving of 0.10 mg/L (10 microg/100 mL or 0.021 g/210 L). Because of the special circumstances of the traffic crash and the man's appearance and behaviour, the police suspected that drugs other than alcohol were involved and obtained a venous blood sample for toxicological analysis. The blood contained 0.23 mg/g alcohol, which is above the legal limit for driving in Sweden 0.20 mg/g (20 mg/100 mL or 0.020 g/100 mL), and codeine was also present at a therapeutic concentration of 0.02 mg/L. The conflict between the clinical signs of impairment and the toxicology report prompted a reanalysis of the blood sample with major focus on sedative-hypnotic drugs. Analysis by capillary GC-NPD identified chlormethiazole at a concentration of 5mg/L, the highest so far encountered in traffic cases in Sweden. In 13 other impaired driving cases over 10 years the mean (median) and range of concentrations of chlormethiazole were 1.6 mg/L (1.6 mg/L) and 0.3-3.3 mg/L. This case report underscores the need to consider clinical observations and the person's behaviour in relation to the toxicology report when interpreting and testifying in drug-impaired driving cases.     

Evaluation of the Analytical Performance of a Fuel Cell Breath Alcohol Testing Instrument: A Seven‐Year Comprehensive Study

Abstract: Between 2003 and 2009, 54,255 breath test sequences were performed on 129 AlcoSensor IV–XL evidential instruments in Orange County, CA. The overall mean breath alcohol concentration and standard deviation from these tests was 0.141 ± 0.051 g/210 L. Of these test sequences, 38,580 successfully resulted in two valid breath alcohol results, with 97.5% of these results agreeing within ±0.020 g/210 L of each other and 86.3% within ±0.010 g/210 L. The mean absolute difference between duplicate tests was 0.006 g/210 L with a median of 0.004 g/210 L. Of the 2.5% of duplicate test results that did not agree within ±0.020 g/210 L, 95% of these had a breath alcohol concentration of 0.10 g/210 L or greater and 77% had an alcohol concentration of 0.15 g/210 L or greater. The data indicate that the AlcoSensor IV–XL can measure a breath sample for alcohol concentration with adequate precision even amid the effects of biological variations.