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A W Jones

Publications and source records attributed to A W Jones.

At least 37 records · Page 2Linked to original sources
PubMed2003

Evaluating alleged drinking after driving--the hip-flask defence. Part 2. Congener analysis.

The second part of this review describes the principles and practice of forensic congener analysis as an alternative way to evaluate claims of drinking alcohol after driving. Congener analysis was developed, perfected and practised in Germany as a way to evaluate hip-flask defences. This kind of defence challenge arises frequently when the drunk driving suspect is not apprehended at the wheel and especially after hit-and-run incidents. Besides ethanol and water, alcoholic beverages contain trace amounts of many other low-molecular substances, known collectively as the congeners, which impart the characteristic smell and taste to the drink. Importantly, the congener profile can be used to identify a particular kind of alcoholic beverage. Forensic congener analysis entails making a qualitative and quantitative analysis of ethanol, methanol, n-propanol and the isomers of butanol in blood and urine from the apprehended driver and comparing the results with the known congener profile of the alcoholic beverage allegedly consumed after driving. Interpreting the results of congener analysis requires knowledge about the absorption, distribution and elimination pattern of the congener alcohols, including their oxidation and conjugation reactions, and any metabolic interactions with ethanol. Complications arise if drinks with widely different congener profiles are consumed or if the same beverage was ingested both before and after driving. Despite these limitations, congener analysis can furnish compelling evidence to challenge or support claims of drinking alcohol after driving.

1-Propanol↗
PubMed2003

Blood analysis by headspace gas chromatography: does a deficient sample volume distort ethanol concentration?

This study was prompted by a recent judgment in the Royal Courts of Justice (Gregory v. Director of Public Prosecutions, 2002) in a case of driving a motor vehicle after consuming too much alcohol (Road Traffic Act 1988). An expert witness for the defence alleged that a deficient volume of blood in the tube sent for analysis meant an excess amount of sodium fluoride (NaF) preservative, which would increase the concentration of ethanol, determined by headspace gas chromatography (HS-GC), owing to a salting-out effect. The prosecution did not produce expert evidence to rebut this argument and the drunk driving suspect was acquitted. A small volume of blood and excess sodium fluoride might have increased the concentration of ethanol in the air-space in the tube sent for analysis but this does not mean that the result of the HS-GC analysis would be higher. This follows because prior to analysis an aliquot of blood is removed and diluted (approximately 10 times) with n-propanol as the internal standard. The dilution lowers the concentration of NaF in the blood and for quantitative analysis the ratio of the ethanol to n-propanol response is measured. The use of a ratio also helps to compensate for any salting-out effect of ethanol. Our experiments showed that a deficient volume of blood and excess NaF actually lowered the concentration of ethanol by 2-3% compared with heparinised blood. Seemingly, n-propanol (n-PrOH) a 3-carbon straight chain alcohol is salted out slightly more effectively than the 2-carbon ethanol (EtOH) causing a lower peak area ratio (EtOH/n-PrOH) and a lower apparent concentration of ethanol. In a separate study, we showed that the concentration of ethanol was lowered even more when a 4-carbon alcohol (t-butanol) was used as the internal standard.

Alcoholic Intoxication↗
PubMed2003

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.

2-Propanol↗
PubMed2003

Coexistence and concentrations of ethanol and diazepam in postmortem blood specimens: risk for enhanced toxicity?

Both ethanol and diazepam are classified as depressants of the central nervous system and exert their effects via the GABAA receptor complex. We report the coexistence and concentrations of ethanol, diazepam, and its primary metabolite nordiazepam in a case series of 234 forensic autopsies collected over a ten-year period. Diazepam, nordiazepam, and ethanol were determined in femoral venous blood by highly selective gas chromatographic methods. The mean (median) femoral blood concentrations were ethanol 0.24 g/100 mL (0.25 g/100 mL), diazepam (D) 0.23 microg/g (0.10 microg/g), nordiazepam (ND) 0.24 micro/g (0.20 microg/g), sum (D + ND) 0.43 microg/g (0.30 microg/g), and the ratio D/ND was 1.19 (1.0). When cause of death was attributed to alcohol and/or drug intoxication (N = 50), the mean and median blood-ethanol concentration was higher, being 0.36 g/100 mL and 0.38 g/100 mL, respectively, whereas the mean (median) and range of blood-diazepam concentrations were about the same, 0.23 microg/g (0.10 microg/g) and 0.05 to 1.2 microg/g. The femoral-blood concentrations of diazepam and nordiazepam were highly correlated (r = 0.73), but there was no correlation between the concentrations of ethanol and diazepam (r = -0.15). In another 114 fatalities (all causes of death) with diazepam and/or nordiazepam as the only drugs present, the mean (median) and range of blood-diazepam concentrations were 0.22 microg/g (0.10 microg/g) and 0.03 to 3.5 microg/g. The pathologists report showed that none of these deaths were classed as drug intoxications. The impression gleaned from this study of ethanol-diazepam deaths is that high blood-ethanol concentration is the major causative factor. We found no evidence that concurrent use of diazepam enhanced the acute toxicity of ethanol, although interpretation is complicated by the high blood-ethanol concentration (median 0.38 g/100 mL), making it difficult to discern an added effect of diazepam.

Central Nervous System Depressants↗
PubMed2002

Faster absorption of ethanol and higher peak concentration in women after gastric bypass surgery.

AIMS: To investigate the absorption, distribution and elimination of ethanol in women with abnormal gut as a result of gastric bypass surgery. Patients who undergo gastric bypass for morbid obesity complain of increased sensitivity to the effects of alcohol after the operation. METHODS: Twelve healthy women operated for morbid obesity at least 3 years earlier were recruited. Twelve other women closely matched in terms of age and body mass index (BMI) served as the control group. After an overnight fast each subject drank 95% v/v ethanol (0.30 g kg-1 body weight) as a bolus dose. The ethanol was diluted with orange juice to 20% v/v and finished in 5 min. Specimens of venous blood were taken from an indwelling catheter before drinking started and every 10 min for up to 3.5 h post-dosing. The blood alcohol concentration (BAC) was determined by headspace gas chromatography. RESULTS: The maximum blood-ethanol concentration (Cmax) was 0.741 +/- 0.211 g l-1 (+/- s.d.) in the operated group compared with 0.577 +/- 0.112 g l-1 in the controls (mean difference 0.164 g l-1, 95% confidence interval (CI) 0.021, 0.307). The median time to peak (tmax) was 10 min in the bypass patients compared with 30 min in controls (median difference -15 min (95% CI -10, -20 min). At 10 and 20 min post-dosing the BAC was higher in the bypass patients (P < 0.05) but not at 30 min and all later times (P > 0.05). Other pharmacokinetic parameters of ethanol were not significantly different between the two groups of women (P > 0.05). CONCLUSIONS: The higher sensitivity to ethanol after gastric bypass surgery probably reflects the more rapid absorption of ethanol leading to higher Cmax and earlier tmax. The marked reduction in body weight after the operation might also be a factor to consider if the same absolute quantity of ethanol is consumed.

Adult↗
PubMed2002

Reference limits for urine/blood ratios of ethanol in two successive voids from drinking drivers.

Specimens of venous whole blood and two successive urinary voids were collected from 450 individuals apprehended for driving under the influence of alcohol in Sweden. The first specimen of urine (UAC-1) was obtained as soon as possible after arrest, and the second void (UAC-2) was collected about 60 min later (mean 66 min, range 30-130). A specimen of venous blood was drawn approximately 30 min after the first urine sample was collected. Ethanol was determined in blood and urine by headspace gas chromatography, a method with high analytical precision (coefficient of variation approximately 1%). The mean UAC for the first void was 2.60 g/L (range 0.21-5.35) compared with 2.40 g/L (range 0.16-5.50) in the second void. The mean concentration of alcohol in venous blood (BAC) was 1.97 g/L (range 0.08-4.57). The concentrations of ethanol in the two voids of urine were highly correlated (r = 0.97, residual standard deviation [SD] 0.22 g/L). The UAC and BAC results were also highly correlated; r = 0.958 (residual SD 0.28 g/L) for the first void and r = 0.978 (residual SD 0.21 g/L) for the second void. The concentration of ethanol in the first void (UAC-1) was higher than the second void (UAC-2) in 383 (87%) instances, decreasing by 0.23 g/L/h on average. In 57 instances (13%), UAC-1 was less or equal to UAC-2 with a mean increase of 0.19 g/L. When BAC exceeded 0.5 g/L (N = 429), the mean UAC-1/BAC ratio was 1.345 with 95% reference limits of 0.968 and 1.72, which agreed well with median (2.5th and 97.5th percentiles) of 1.325 (0.938 and 1.79). For the second void, the mean UAC-2/BAC ratio was 1.221 with 95% reference limits of 0.988 and 1.45 and with a median (2.5th and 97.5th percentiles) of 1.226 (0.997 and 1.46). These reference limits are appropriate to use when a person's venous BAC needs to be estimated with reasonable scientific certainty from the concentration determined in specimens of urine.

Alcoholic Intoxication↗
PubMed2002

Evaluating alleged drinking after driving--the hip-flask defence. Part 1. Double blood samples and urine-to-blood alcohol relationship.

This two-part article examines the strengths and weaknesses of various ways of investigating claims of drinking alcohol after driving, commonly known as the hip-flask or glove-compartment defence. In many countries the onus of proof in hip-flask cases rests on the prosecution. With good co-operation from the police and timely sampling of body fluids, such as blood and urine for forensic analysis of ethanol, useful evidence can be mustered to support or challenge the truthfulness of alleged drinking after driving. The person's blood-alcohol concentration (BAC) can be compared with values expected on the basis of the amount of alcohol consumed after driving, according to theoretical Widmark calculations. The actual BAC measured is then adjusted for the additional amount of alcohol consumed in the after-drink. Double blood samples, that is, taking two specimens of venous blood about 30-60 minutes apart and looking at the magnitude and direction of change in BAC provides little or no more information than a single blood specimen. However, the relationship between alcohol in blood and urine is very useful in hip-flask cases whereby the concentration expected in the primary urine is compared with the concentration in the bladder urine voided. The concentration of alcohol determined in a second urine sample collected 30-60 min later gives supporting evidence in hip-flask cases. A graphical method, which entails plotting ethanol concentrations in blood and urine as a function of time provides a robust and practical way to investigate hip-flask defences. In the second part of the review, congener analysis is presented, which entails comparing the concentrations of n-propanol, isobutanol and occasionally other congeners in the alcoholic beverage allegedly consumed after driving with the volatiles present in the suspect's blood and urine determined by headspace gas chromatography.

Alcohol Drinking↗
PubMed2001

Characterization of an NBTI-sensitive equilibrative nucleoside transporter in vascular smooth muscle.

Adenosine plays a significant role in various physiological and regulatory processes including coronary vasodilatation. In the current study, a high-affinity adenosine transporter in freshly dissociated porcine coronary smooth muscle (PCSM) cells and cultured human coronary smooth muscle (HCSM) cells was characterized. Kinetic analysis of the transport process revealed a V(max) of 82+/-17 pm/mg protein/min and a K(m) of 4.3+/-2.1 microm for PCSM cells, whereas a K(m) of 4.8 microm and V(max) of 254 pm/mg/min was observed for cultured HCSM. Concentration-dependent inhibition of adenosine uptake by S-(4-nitrobenzyl)-6-thioinosine (NBTI) was observed in both PCSM (IC(50), 0.08 microm) and HCSM (0.1 microm) cells. Both cell types also demonstrate a high-affinity, single binding site for NBTI (PCSM, B(max) 144.8+/-23 fmol/mg protein and K(d) 1.1+/-0.35 nm; HCSM, B(max) 672+/-62 fmol/mg protein and K(d) 0.45+/-0.14 nm). Adenosine uptake in these cells was not affected by extracellular sodium concentration. RT-PCR analysis of mRNA from individually selected PCSM and HCSM cells demonstrated expression of an NBTI-sensitive equilibrative transporter. Smooth muscle cells isolated from porcine brachial and femoral arteries also transported adenosine at levels similar to that of coronaries. These data demonstrate that vascular coronary smooth muscle possess an NBTI-sensitive equilibrative transporter for adenosine which could function in regulation of vasodilation.

Adenosine↗
PubMed2001

Albumin supplementation during the first week after a burn does not mobilise tissue oedema in humans.

OBJECTIVE: To measure water balance and changes in distribution, and the effect of giving supplementary albumin, early after a burn injury. DESIGN: Consecutive patients (matched groups) and healthy controls. SETTING: National burn unit in a Swedish university hospital. PATIENTS AND SUBJECTS: Eighteen patients with 18%-90% total burned surface area and 16 healthy male control subjects. INTERVENTIONS: The patients were given an intravenous infusion of ethanol over 1 h, 0.35-0.60 g/kg body weight, and a bolus of 3.3 to 6.5 g of iohexol. The control subjects were given the same amounts of either ethanol or iohexol. Patients were subdivided into two groups according to whether or not they received supplementary albumin starting 12 h post-burn. MEASUREMENTS AND RESULTS: Blood samples were drawn at 20-30 min intervals over 4 h after the start of the infusion. Serum ethanol was measured by headspace gas chromatography, and iohexol with high-pressure liquid chromatography (HPLC). Distribution volume was calculated from the concentration-time profiles. Total body water (TBW) was measured by the ethanol tracer and bioelectric impedance (BIA) techniques, and estimated extracellular water (ECWest) by iohexol tracer. They were all significantly increased after a burn. Excess water was accumulated mainly in the extracellular compartment. It declined towards normal values (those of volunteers) at the end of the week. Albumin supplementation did not influence the amount or distribution of the excess fluid. CONCLUSION: Body water increases after a burn. Excess water is mainly deposited in the extracellular space. Tissue oedema fluid is not mobilised by albumin supplementation.

Adult↗
PubMed2001

Do ethanol and deuterium oxide distribute into the same water space in healthy volunteers?

BACKGROUND: The volume of distribution at steady state for ethanol (Vss) is thought to be identical to the total body water (TBW). We compared a two-compartment pharmacokinetic model with parallel Michaelis-Menten and first-order renal elimination with the classical one-compartment zero-order elimination model. Ethanol concentration-time profiles were established for breath, venous blood, and urine. The values of Vss obtained for ethanol were compared with TBW determined by deuterium oxide dilution. METHODS: Sixteen healthy volunteers each received a 30-min intravenous infusion of ethanol on two occasions. Ethanol was measured in breath by a quantitative infrared analyzer and in blood and urine by headspace gas chromatography. Deuterium oxide was given as an intravenous injection and measured in serum by isotope-ratio mass spectrometry. Components of variation were calculated by ANOVA to determine the precision of the estimates of Vss and TBW. RESULTS: Mean TBW, determined by deuterium oxide dilution, was 44.1 +/- 3.9 liters (+/-SD) for men, corresponding to 0.61 liters/kg, and 37.4 +/- 3.2 liters for women, or 0.54 liters/kg. Estimates of Vss from blood-ethanol pharmacokinetics were 87.6% of TBW according to isotope dilution and 84.4% for breath analysis with the two-compartment model. This compares with 95.1% and 95.4% for blood and breath alcohol, respectively, when the classical zero-order kinetic analysis is used. The precision of the estimates of Vss and TBW was between +/-1.56 and +/-2.19 liters (95% confidence interval). CONCLUSIONS: Ethanol does not distribute uniformly into the TBW. The precision of measuring Vss by ethanol dilution was comparable to estimates of TBW by isotope dilution. Results of noninvasive breath ethanol analysis compared well with use of venous blood for estimating Vss. The sophisticated two-compartment model was much superior to the classical one-compartment model in explaining the total concentration-time course of intravenously given ethanol.

Adult↗
PubMed2001

Uncertainty in estimating blood ethanol concentrations by analysis of vitreous humour.

AIMS: To determine the concentrations of ethanol in femoral venous blood (FVB) and vitreous humour (VH) obtained during forensic necropsies. The ratios of ethanol concentrations in VH and FVB, the reference interval, and the associated confidence limits were calculated to provide information about the uncertainty in estimating FVB ethanol concentrations indirectly from that measured in VH. METHODS: Ethanol concentrations were determined in specimens of FVB and VH obtained from 706 forensic necropsies. The specimens were analysed in duplicate by headspace gas chromatography (HS-GC), with a precision (coefficient of variation) of 1.5% at a mean ethanol concentration of 500 mg/litre. The limit of detection of ethanol in body fluids by HS-GC in routine casework was 100 mg/litre. RESULTS: In 34 instances, ethanol was present in VH at a mean concentration of 154 mg/litre, whereas the FVB ethanol concentration was reported as negative (< 100 mg/litre). These cases were excluded from the statistical analysis. The concentration of ethanol in FVB was higher than in VH in 93 instances, with a mean difference of 160 mg/litre (range 0 to 900). The mean concentration of ethanol in FVB (n = 672) was 1340 mg/litre (SD, 990) compared with 1580 mg/litre (SD, 1190) in VH. The arithmetic mean VH/FVB ratio of ethanol was 1.19 (SD, 0.285) and the 95% range was 0.63 to 1.75. The mean and SD of the differences (log VH - log FVB) was 0.063 (SD, 0.109), which gives 95% limits of agreement (LOA) from -0.149 to 0.276. Transforming back to the original scale of measurement gives a geometric mean VH/FVB ratio of 1.16 and 95% LOA from 0.71 to 1.89. These parametric estimates are in good agreement, with a median VH/FVB ratio of 1.18 and 2.5th and 97.5th centiles of 0.63 and 1.92. CONCLUSIONS: The ethanol distribution ratios (VH/FVB) show wide variation and this calls for caution when results of analysing VH at necropsy are used to estimate the concentration in FVB. Dividing the ethanol concentration in VH by 2.0 would provide a very conservative estimate of the ethanol content in FVB, being less than the true value, with a high degree of confidence.

Autopsy↗
PubMed2001

Interaction of gender and exercise training: vasomotor reactivity of porcine skeletal muscle arteries.

The purpose of the present study was to test the hypothesis that gender influences exercise training-induced adaptations of vascular reactivity of porcine arteries that provide blood flow to skeletal muscle and femoral and brachial arteries. Male and female Yucatan miniature swine were exercise trained on a motor-driven treadmill or cage confined for 16-20 wk. Contractile responses of arterial rings were evaluated in vitro by determining concentration-response curves for endothelin-1 (ET-1; 10(-10) to 10(-7) M) and norepinephrine (NE; 10(-10) to 10(-4) M). Relaxation responses of arteries precontracted with 30 microM PGF(2alpha) were examined for endothelium-dependent agents [bradykinin (BK; 10(-11) to 10(-6) M), ACh (10(-10) to 10(-4) M), and a Ca(2+) ionophore, A-23187 (10(-6) M)] and a endothelium-independent agent [sodium nitroprusside (10(-10) to 10(-4) M)]. Arteries from female pigs developed greater contractile force in response to ET-1 than arteries from male pigs, whereas contractile responses to NE and KCl were similar in arteries from both genders. Femoral arteries from females exhibited greater endothelium-mediated vasorelaxation (BK and ACh) than did those from males. In contrast, brachial arteries of males were more responsive to BK and ACh than brachial arteries of females. Exercise training increased ET-1-induced contractions in arteries from males (without endothelium) but not in arteries from females. Training had no effect on endothelium-dependent relaxation in arteries from males but increased relaxation responses in brachial arteries from females. We conclude that both gender and anatomic origin of the artery influence exercise training-induced adaptations of vascular reactivity of porcine skeletal muscle conduit arteries.

Animals↗
PubMed2001

Influence of age, sex, and Helicobacter pylori infection before and after eradication on gastric alcohol dehydrogenase activity.

BACKGROUND: Gastric alcohol dehydrogenase may contribute to the metabolism of orally ingested ethanol and decrease the bioavailability of the drug. The aims of this study were to assess the impact of Helicobacter pylori infection and its eradication on gastric alcohol dehydrogenase activity and to relate the findings to gastric histology. Furthermore, the role of age- and sex-related differences in gastric alcohol dehydrogenase activity were studied. METHODS: A total of 76 subjects (39 women and 37 men) underwent upper gastrointestinal endoscopy, and biopsies were obtained from the corpus and antrum. The specimens were used for determining gastric alcohol dehydrogenase activity, histological examination, and urease testing. Subjects with H. pylori infection (n = 36) received medication to eradicate the infection, and repeat biopsies were taken 2 and 12 months later. RESULTS: No significant difference in gastric alcohol dehydrogenase activity was found between men and women (p > 0.05). Gastric alcohol dehydrogenase activity did not differ significantly between the subjects older than 50 years (n = 39) and those 50 years or younger (n = 37). In subjects with H. pylori infection, gastric alcohol dehydrogenase activity was significantly reduced in the antrum (p < 0.05). After eradication of H. pylori, alcohol dehydrogenase activity in the antrum increased significantly within 2 months (p < 0.01). Antral biopsies with the most pronounced inflammation and histological changes had significantly decreased alcohol dehydrogenase activity (p < 0.05). In contrast, no significant differences were found in corpus. CONCLUSIONS: H. pylori infection is associated with decreased antral alcohol dehydrogenase activity, which seems to be related to the severity of the inflammatory changes in the mucosa. Eradication of H. pylori normalizes antral alcohol dehydrogenase activity within 2 months.

Adult↗
PubMed2001

Concentration ratios of morphine to codeine in blood of impaired drivers as evidence of heroin use and not medication with codeine.

BACKGROUND: Both the illicit drug heroin and the prescription drug codeine are metabolized to morphine, which tends to complicate interpretation of opiate-positive samples. We report here the concentrations of morphine and codeine, the morphine/codeine ratios, and 6-acetylmorphine (6-AM) in blood specimens from individuals arrested for driving under the influence of drugs (DUID) in Sweden. The results were compared with positive findings of 6-AM in urine as evidence of heroin intake. METHODS: In 339 DUID suspects, both blood and urine specimens were available for toxicologic analysis. In another 882 cases, only blood was available. All specimens were initially analyzed by immunoassay, and the positive results were verified by isotope-dilution gas chromatography-mass spectrometry. In routine casework, the limits of quantification (LOQs) for unconjugated opiates were 5 ng/g for blood and 20 microg/L for urine. RESULTS: The median concentration of morphine in blood was 30 ng/g with 2.5 and 97.5 percentiles of 5 and 230 ng/g, respectively (n = 979). This compares with a median codeine concentration of 20 ng/g and 2.5 and 97.5 percentiles of 5 and 592 ng/g, respectively (n = 784). The specific metabolite of heroin, 6-AM, was identified in only 16 of 675 blood specimens (2.3%). This compares with positive findings of 6-AM in 212 of 339 urine samples (62%) from the same population of DUID suspects. When 6-AM was identified in urine, the morphine/codeine ratio in blood was always greater than unity (median, 6.0; range, 1-66). In 18 instances, 6-AM was present in urine, although morphine and codeine were below the LOQ in blood. The morphine/codeine ratio in blood was greater than unity in 85% of DUID cases when urine was not available (n = 506), and the median morphine and codeine concentrations were 70 ng/g and 10 ng/g, respectively. When morphine/codeine ratios in blood were less than unity (n = 76), the median morphine and codeine concentrations were 10 ng/g and 180 ng/g, respectively. CONCLUSIONS: Only 2.3% of opiate-positive DUID suspects were verified as heroin users on the basis of positive findings of 6-AM in blood. A much higher proportion (62%) were verified heroin users from 6-AM identified in urine. When urine was not available for analysis, finding a morphine/codeine concentration ratio in blood above unity suggests heroin use and not medication with codeine. This biomarker indicated that 85% of opiate-positive DUID blood samples were from heroin users.

Automobile Driving↗