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This reference book is written most specifically for use by clinical toxicologists, physicians, residents, nurses and medical students in the diagnosis and treatment of poisoning. It has some value to forensic toxicologists and pathologists, however, because of the broad range of toxic agents covered and detailed summaries of adverse and toxic effects.

A handbook should be portable, comprehensive and accessible to people on many levels, and in all respects this book succeeds. The topic of drug facilitated sexual assault (DFSA) has risen in our consciousness in the last few years, initially because of the scare propagated in the popular media about flunitrazepam (Rohypnol ®). While that drug turned out to account for only a handful of such cases, it brought attention to the larger problem of the use of alcohol and drugs to incapacitate a victim prior to sexual assault.

As the publisher's cover notes on this volume point out, the low dose benzodiazepines and gamma hydroxybutyrate (GHB) escape detection in many laboratories because of their low effective doses and rapid metabolism. This is an important shortcoming because of the forensic consequences of the use and misuse of these drugs. Edited by Dr. Salvatore Salamone, the book is a collection of seven papers, any of which would be at home in the pages of this Journal, and it will be a useful addition to the library of any laboratory looking to improve its performance in the areas discussed. Its focus, however, is on a few of the low dose benzodiazepines, (a fact not clear from the title), and includes only a single chapter on GHB.

3,4-Methylenedioxymethamphetamine, or MDMA, is increasing in popularity in the United States as a drug of abuse. It has stimulant and empathogenic mood altering properties with the potential to affect psychomotor skills and impact driving. This report reviews the literature relating to the relevant psychomotor effects of the drug, the relationship between dose and blood concentrations, and studies and case reports on specific effects of the drug on driving. The latter reports include both laboratory driving simulator studies and anecdotal reports, and case series. We also report details of eighteen cases of apparent MDMA impaired driving, including six drivers whose blood tested positive for MDMA alone. Most subjects displayed muscle twitching and body tremors, dilated pupils, slow pupillary reaction to light, elevated pulse and blood pressure, lack of balance and coordination, and most were perspiring profusely. Five of the six subjects were given field sobriety tests (one leg stand, walk and turn test), and all five performed poorly. There was no clear correlation between the blood concentration of MDMA and the specific demeanor of the subject. These findings are consistent with other reports, and lead to the conclusion that MDMA use is not consistent with safe driving, and that impairment of various types may persist for a considerable time after last use.

Gamma hydroxybutyrate (GHB) was identified in the blood of 13 subjects arrested for impaired driving. GHB concentrations ranged from 26 to 155 mg/L (mean 87 mg/L, median 95 mg/L). In eight cases, GHB was the only drug detected, and signs of impairment were consistent with those of a CNS depressant, including erratic driving (weaving, swerving, ignoring road signs), confusion, incoherent speech, unresponsiveness, lack of balance, unsteady coordination, poor performances on field sobriety tests, and varying states of wakefulness. Given the ability of GHB to induce sleep and unconsciousness, it is evident from these cases that recreational use of the drug has the potential to impair a person's driving ability.

The first book reached for by most forensic toxicologists practicing in the postmortem drug testing arena is Baselt's Disposition of Toxic Drugs and Chemicals in Man, currently in its fourth edition. Baselt has, with this new volume, provided those toxicologists practicing in the impaired driving arena with a similarly valuable resource. Covering most of the commonly prescribed, centrally acting drugs, and a wide range of illicit drugs, the book contains 140 monographs. The format will be familiar to users of Baselt's original work. Each section succinctly reviews the pharmacology of each drug, considering publications of clinical trial data, recommended doses and associated plasma concentrations of both the parent and metabolites, when they are known, the drug's metabolism, and the warnings contained in the Physicians Desk Reference for the drug with respect to its potential effects on driving, or psychomotor skills. This is followed by a review of laboratory studies, which have included assessment of psychomotor effects from the use of the drug. Review of these studies is made more intelligible by the inclusion of a glossary of technical terms. Further sections are included on driving studies (where they exist) and epidemiology. Finally, Baselt summarizes all the material in terms of whether, and in what circumstances, there is evidence of psychomotor impairment. He is careful, however, to stress when these conclusions are based on specific driving studies and when they are inferred from more primary effects.

For practicing postmortem forensic toxicologists there are a small number of undisputed first line texts, such as Baselt's Disposition of Toxic Drugs and Chemicals in Man, relied on daily for interpretive assistance. There are then the second line texts such as Ellenhorn and Barceleoux, and Goodman and Gilman, relied on for more specific pharmacological information, and clinical presentation, and in cases where there is no prior published data to assist in interpretation. Spencer and Schaumburg's text would fit well on the shelf beside these other volumes, as a resource for some of the specific neurotoxicological mechanisms that can be invoked to rationalize or explain the evident consequences of overdose with therapeutic or abuse drugs, or exposure to environmental, bacterial, animal, and fungal toxins.

Zolpidem, a non-benzodiazepine hypnotic, was identified in the blood of 29 subjects arrested for impaired driving. Zolpidem concentrations ranged from 0.05 to 1.4 mg/L (mean 0.29 mg/L, median 0.19 mg/L). In the subjects whose cases we reviewed where zolpidem was present with other drugs and/or alcohol, symptoms reported were generally those of CNS depression. Symptoms included slow movements and reactions, slow and slurred speech, poor coordination, lack of balance, flaccid muscle tone, and horizontal and vertical gaze nystagmus. In five separate cases, where zolpidem was the only drug detected (0.08-1.40 mg/L, mean 0.65 mg/L, median 0.47 mg/L), signs of impairment included slow and slurred speech, slow reflexes, disorientation, lack of balance and coordination, and "blacking out." Although no quantitative relationship between blood concentrations and degree of driving impairment is currently possible, it is reasonable to conclude that because of its specific activity as a sleep inducer, blood concentrations consistent with therapeutic doses of zolpidem have the potential to affect driving in a negative way, and that concentrations above the normal therapeutic range would further impair a person's level of consciousness and driving ability.

Deaths by homicidal poisoning, which are recognized as such, titute a very small fraction of all poisoning deaths in the United States representing, according to this book, 14 poisonings per 10 000 homicides. The caveat however is critical, since as the author points out, murder by poisoning can be among the most difficult murders to identify. Of the cases discussed in this book, the vast majority involve the use of a classical poison, such as arsenic, cyanide, or strychnine, which makes them easier to identify. Poisoning using a drug which a decedent has been prescribed or has had access to, however, certainly cannot be distinguished from a voluntary ingestion on the basis of the toxicology laboratory result, and the only people who know whether the diug was willingly ingested by the victim, or administered by a poisoner, are usually these two actors, one of whom is invariably dead.

While the value and accessibility of a print book will never be letely matched, this volume undoubtedly represents the shape hings to come in educational publishing. This is a CD ROM based, narrated slide show, with text and photographs, regarding lethal effects of illicit drug groups comprised of inhalants, marijuana, cocaine and amphetamine, LSD and hallucinogens, and in. It is not highly technical, and according to the author, is directed towards school students, drug awareness programs, and th care personnel, as well as parents with at risk children who wish to learn more about drug abuse. It is clearly intended to highlight the seamier side of recreational dmg use, and the unpleasant and not infrequently lethal consequences. The information is quite graphic, and likely to be upsetting to some, however, the product carries an appropriate warning.

Trazodone is a popular antidepressant medication that has been available for approximately 30 years. It has a reputation as a safe drug with relatively few reported fatalities attributed solely to it. We review the pharmacology and forensic toxicology of trazodone and report toxicology and cause and manner of death in a series of 37 deaths in which trazodone was detected. Although the normal upper therapeutic blood concentration for trazodone is about 2 mg/L, fatalities are rarely attributed solely to it at blood concentrations below 9 mg/L. Considering the pharmacology of the drug, potential interactions between other drugs with serotonin reuptake properties need to be considered, as does the increased susceptibility to the toxic effects in patients with pre-existing heart disease. In the cases reviewed, none were attributed solely to trazodone, although trazodone was frequently present together with other serotonergic drugs, such as the selective serotonin reuptake inhibitors like fluoxetine and sertraline. Ten cases had blood trazodone concentrations above 2 mg/L. Of these cases, trazodone played a primary role in the death of three subjects, with blood concentrations all greater than 9 mg/L. We confirm the conclusions of others that trazodone is a relatively safe drug except in massive overdose, although its toxicity may be influenced by the presence of other drugs and underlying pathophysiology.

This paper considers the pharmacology of the centrally acting muscle relaxant carisoprodol, and its metabolite meprobamate, which is also administered as an anxiolytic in its own right. Literature implicating these drugs in impaired driving is also reviewed. A series of 104 incidents in which these drugs were detected in the blood of drivers involved in accidents or arrested for impaired driving was considered, with respect to the analytical toxicology results, patterns of drug use in these subjects, the driving behaviors exhibited, and the symptoms observed in the drivers. Symptomatology and driving impairment were consistent with other CNS depressants, most notably alcohol. Reported driving behaviors included erratic lane travel, weaving, driving slowly, swerving, stopping in traffic, and hitting parked cars and other stationary objects. Drivers on contact by the police displayed poor balance and coordination, horizontal gaze nystagmus, bloodshot eyes, unsteadiness, slurred speech, slow responses, tendency to doze off or fall asleep, difficulty standing, walking or exiting their vehicles, and disorientation. Many of these cases had alcohol or other centrally acting drugs present also, making difficult the attribution of the documented impairment specifically to carisoprodol and meprobamate. In 21 cases, however, no other drugs were detected, and similar symptoms were present. Impairment appeared to be possible at any concentration of these two drugs; however, the most severe driving impairment and most overt symptoms of intoxication were noted when the combined concentration exceeded 10 mg/L, a level still within the normal therapeutic range.

This paper reviews the complex pharmacology of the new class of antidepressant medications exhibiting selective inhibition of serotonin reuptake. The four selective serotonin reuptake inhibitors (SSRIs) considered--fluoxetine, fluvoxamine, sertraline and paroxetine--can result in toxicity and death through contributing to serotonergic excess resulting in serotonin syndrome, inhibiting the metabolism of other centrally acting drugs, leading to accumulation of toxic concentrations, and exerting complex vasoactive effects on the vascular smooth muscle. This latter feature is of particular concern in patients with preexisting heart disease. An analytical method involving isolation of the drugs by liquid/liquid extraction at alkaline pH into n-butyl chloride, and analysis by gas chromatography/mass spectrometry (GC/MS) is described, together with some of its limitations. Toxicologic and cause and manner of death data were examined in 60 deaths involving fluoxetine, 5 involving fluvoxamine, 75 involving sertraline, and 28 involving paroxetine. Deaths involving drug toxicity were generally a result of ingestion of multiple drugs, and in only a small number of the cases was death attributed principally to the SSRI involved. The potential for drug interactions between members of this class of drugs is discussed as well as their metabolites and a variety of other therapeutic and abused drugs which can contribute to their toxicity. In the absence of other risk factors, the lowest concentrations determined to have resulted in death were 0.63 mg/L for fluoxetine, 0.4 mg/L for paroxetine, and 1.5 mg/L for sertraline. We had insufficient data to make even this crude assessment for fluvoxamine. Drug-induced elevation of serotonin concentrations may be a significant risk factor for patients with atherosclerotic cardiovascular disease (ASCVD). Other factors including preexisting disease and the presence of other drugs and their pharmacology need to be carefully considered before determining the appropriate cause and manner of death in these cases.

Beer consumption is commonly an issue in a medico-legal setting, requiring estimates either of a likely blood alcohol concentration (BAC) for a given pattern of consumption or vice versa. Four hundred and four beers and malt beverages available for sale in the State of Washington were tested by gas chromatography for their alcohol content. Considerable variability in the alcoholic strength was found, even within the same class. Overall the range of concentrations was 2.92%v/v to 15.66%v/v. The mean alcohol concentration for ales was 5.51%v/v (SD 1.23%v/v), and for lagers, 5.32% (SD 1.43%v/v). Some specialty brews had characteristically higher or lower mean concentrations: ice beers 6.07%v/v, malt liquor 7.23%v/v, light beer 4.13%v/v, seasonal ales 6.30%v/v. Six brands of lager and four light beers account for the majority of all beer sales in the United States, and the mean alcohol concentration for these products was measured as 4.73%v/v and 4.10%v/v respectively. Few of the beers (17%) were labeled with respect to alcohol content, and in some cases, there was a significant disparity between the concentration listed on the label, and the measured alcohol concentration. Toxicologists need to exercise caution when performing Widmark type calculations, using all available information to select the most appropriate estimate for alcoholic strength of a beer or malt beverage.

Defendants in several driving under the influence cases have asserted that the presence in the mouth of a metal stud through a hole pierced in the tongue invalidates the breath alcohol test because of the prohibition against foreign substances in the mouth, and because of the potential for the jewelry to retain alcohol and interfere with the breath test. Rates of mouth alcohol elimination were evaluated in two subjects with pierced tongues and in two control subjects. No differences in the mouth alcohol elimination patterns were observed. The 15 min alcohol deprivation period prior to the test ensures no effect from residual mouth alcohol. For the purposes of breath alcohol testing, oral jewelry should be treated in the same manner as dental work, and may be left in place during the test without affecting its outcome.

The effects of eight prescription and non-prescription asthma inhalers and four over-the-counter nasal decongestants on the DataMaster, an evidential breath alcohol instrument, were evaluated. Subjects self administered the medication, and breath alcohol tests were administered immediately after use and following a 15 min waiting period. The only preparation which produced any effect on the instrument was Primatene Mist which contains 34% ethyl alcohol. The alcohol was, however, eliminated from the breath in the usual pattern of mouth alcohol elimination, and after 5 min there was no longer any effect. The inclusion of a 15 min deprivation period prior to an evidential breath test, during which time nothing is introduced into the mouth, is an adequate safeguard against interference with the test caused by alcohol containing inhalers.

We reviewed a series of deaths in which methamphetamine was detected in the decedent's blood. Analysis of postmortem whole blood was performed by gas chromatography/mass spectrometry with a limit of quantitation of 0.05 mg/L. Methamphetamine was detected in 146 cases; 52 were drug caused, i.e., a death in which the direct toxic effects of the drug caused or contributed to the death, 92 were classified as drug related, i.e., a death in which the drug was demonstrated in the blood, but did not directly cause death. A large proportion of the deaths resulted from homicidal (27%) or suicidal (15%) violence. An examination of methamphetamine concentrations in drug related deaths (n = 92), suggests that the range of concentrations in the recreational abusing population is substantial (0.05-9.30 mg/L) but with a median concentration of 0.42 mg/L, and with 90% of that population having concentrations less than 2.20 mg/L. There was substantial overlap in methamphetamine concentration between drug related deaths and drug caused deaths, although the highest concentrations were seen in the unintentional (accidental or undetermined) drug caused deaths. Methamphetamine related traffic deaths (n = 17) showed patterns of driving behavior consistent with reports elsewhere, and showed blood methamphetamine concentrations ranging from 0.05-2.60 mg/L (median 0.35 mg/L). The data show that most methamphetamine deaths occur with blood concentrations greater than 0.5 mg/L, but can occur with levels as low as 0.05 mg/L, though usually in conjunction with other drugs or significant natural disease. Neither apparently toxic nor therapeutic concentrations should be used in isolation to establish conclusively whether a death was caused by methamphetamine; proper classification of deaths involving methamphetamine requires complete death investigation, including investigation of the scene and circumstances of death, and a complete autopsy.

Blood and/or urine from fatally injured drivers in Washington State were collected and tested for the presence of drugs and alcohol. Drug and/or alcohol use was a factor in 52% of all fatalities. Among single vehicle accidents, alcohol use was a factor in 61% of cases versus 30% for multiple vehicle accidents. Drugs most commonly encountered were marijuana (11%), cocaine (3%), amphetamines (2%), together with a variety of depressant prescription medications. Trends noted included an association of depressant use with higher blood alcohol levels, while marijuana use was associated with lower blood alcohol levels. Marijuana use was noted to be most prominent in the 15-30 year age group, stimulant use in the 21-40 year old group, and prescription depres- sant use was more prevelant in the 45+ age group. Drug use demographics in this population are consistent wi~ those noted in other jurisdictions.

Following a review of the effects of methamphetamine on human performance, actual driving and behavior were evaluated in 28 cases in which drivers arrested or killed in traffic accidents had tested positive for methamphetamine. The circumstances surrounding the arrest or accident were examined, together with any observations by the arresting officer regarding behavioral irregularities. The investigators also made a determination of culpability. Most of the arrests resulted from accidents in which the driver was determined to be culpable. Typical driving behaviors included drifting out of the lane of travel, erratic driving, weaving, speeding, drifting off the road, and high speed collisions. Behavioral manifestations of methamphetamine use in arrestees included rapid or confused speech, rapid pulse, agitation, paranoia, dilated pupils, violet or aggressive attitude. Combined alcohol and methamphetamine use was uncommon, however use of marijuana was evident in about one third of the cases. In addition to impairing judgment and increasing risk taking, the effects of withdrawal from methamphetamine use including fatigue, hypersomnnolence, and depression are likely contributors to many of these accidents. A consideration of the literature and the cases discussed here, leads to the conclusion that methamphetamine at any concentration is likely to produce symptoms that are inconsistent with safe driving.

This study evaluated both site dependent differences and time dependent changes in postmortem morphine concentrations in man. In 32 deaths involving morphine, left ventricular blood, femoral blood, and cisternal cerebrospinal fluid, were collected as soon after death as possible (T1), and collected again together with iliac blood at the time of autopsy (T2). Samples were analyzed for morphine by radioimmunoassay. No evidence was found for changes in morphine concentration with respect to time at either central or peripheral sites, or in the cerebrospinal fluid. Ventricular blood morphine concentrations were however consistently higher than those in the peripheral compartment, represented by either femoral or iliac blood. This was particularly true when the ventricular morphine concentration exceeded 0.300 mg/L. At peripheral sites, femoral and iliac blood morphine concentrations were well correlated with each other, making either an appropriate site for collection of peripheral blood for toxicological testing.

A subject who apparently swallowed a baggie containing "crank" (methamphetamine) while being arrested, was admitted to hospital and then experienced a massive overdose of the drug. The subject went through a seizure with associated fixed dilated pupils, and a depressed pulse and blood pressure. His cardiac and respiratory problems could not be stabilized, and he died. Methamphetamine levels in central and peripheral blood, liver, bile, vitreous, gastric and urine were determined. Blood levels of greater than 60 mg/L, were found together with even higher levels in the bile, urine and gastric. These levels are discussed in terms of other fatal, non-fatal and recreational methamphetamine use.

This study evaluated the reliability of Widmark calculations, based on breath ethanol reading (BrACs), for estimating the amount of alcohol consumed. A standard ethanol dose (males 0.51 g/kg; females 0.43 g/kg) was given to 115 college seniors, and BrACs were measured for two hours. Calculations of ethanol dose were performed using BrACs taken at 60, 75, 105, and 125 minutes after drinking. Mean calculated ethanol doses were lower than actual doses at each time point (P < 0.001). Mean underestimates were 13, 12, 15, and 14 mL of 100 proof vodka at 60, 70, 105, and 125 min after drinking. Calculated doses overestimated actual doses in 11, 10, 3, and 3 subjects at 60, 75, 105, and 125 min after drinking. The maximum overestimates were 13, 11, 6, and 8 mL of vodka at 60, 75, 105, and 125 min after drinking. At the 95% confidence level, the calculated dose at 105 and 125 min did not overestimate the true dose, but could underestimate it by as much as 30 mL vodka.

Gas chromatography is the most widely used method for the analysis of ethanol and other low molecular weight volatiles for forensic applications. Many laboratories use only a single analytical method for this analyte. Concern over the possible misidentification of acetonitrile as ethanol, and our experience in a case where we misidentified diethyl ether as acetone using a single method approach, led us to develop and adopt the dual column method described herein. Two columns, 5% carbowax on 60/80 Carbopak B, and 0.8% THEED on 80/100 carbopak C, were used for the complementary analysis of 32 common volatile organic compounds.

The presence of interfering substances, particularly acetone, has historically been a concern in the forensic measurement of ethanol in human breath. Although modern infrared instruments employ methods for distinguishing between ethanol and acetone, false-positive interferant results can arise from instrumental or procedural problems. The case described gives the analytical results of an individual arrested for driving while intoxicated and subsequently providing breath samples in two different BAC Verifier Datamaster infrared breath alcohol instruments. The instruments recorded ethanol results ranging from 0.09 to 0.17 g/210 L with corresponding interferant results of 0.02 to 0.06 g/210 L over approximately three hours. Breath and venous blood specimens collected later were analyzed by gas chromatography and revealed in the blood: isopropanol 0.023 g/100 mL, acetone 0.057 g/100 mL and ethanol 0.076g/100 mL. Qualitative analysis of the breath sample by GCMS also showed the presence of all three compounds. This individual had apparently consumed both ethanol and isopropanol with acetone resulting from the metabolism of isopropanol. An important observation is that the breath test instruments detected the interfering substances on each breath sample and yet they did not show tendencies to report false interferences when compared with statewide interferant data.

Morphine analysis was performed using a variety of immunoassay methods in blood, urine and the cisternal cerebrospinal fluid (CSF) from 23 patients dying opiate-related deaths. Of these, 16 were a result of intravenous morphine or heroin use. The blood and CSF morphine concentrations were determined using both fluorescence polarization immunoassay (FPIA) and radioimmunoassay (RIA), while urine was analyzed by enzyme multiplied immunoassay technique (EMIT). Urine morphine concentrations were greater than 0.300 µg/mL in all but one case. Blood and CSF morphine concentrations were found to be poorly correlated, and it was concluded that one should not be used to predict the other. Following intravenous administration. CSF morphine concentrations of greater than 0.02 µg/mL were however found to be consistent with death from morphine related respiratory depression. As intrathecal or epidural administration of morphine can greatly influence the CSF concentration without inducing respiratory depression, the site of collection of the CSF must be known, as must the route of administration in order to properly interpret CSF morphine concentrations.

In March 1991, four cyanide poisonings were identified in Washington State. Three of these, one nonfatal and two fatal, were directly linked to the consumption of capsules of Sudafed-12 hour cold relief capsules. This article presents the details of these cases including the chronology, causes of death, autopsy and toxicological findings. The fourth case, also fatal, occurred after extensive publicity surrounding the poisonings, and was determined to be a copy-cat case intended to mimic the consumption of tainted Sudafed. The investigation and distinguishing features of this case are also discussed. A further cyanide poisoning occurred in Canada shortly after these incidents and had similar features to the copy-cat case.

A rapid procedure is described for the extraction and analysis of brain samples for cocaine and benzoylecgonine. Human brain tissue was sectioned at autopsy, and samples were subjected to a lipase digestion, subsequent to solid-phase extraction. The distribution of cocaine and benzoylecgonine throughout different regions of the brain was determined by high-performance liquid chromatography.

A sample concentration technique was adapted for the determination of cocaine and benzoylecgonine (BE) concentrations in vitreous humor. Vitreous humor (0.5 mL) was diluted 1:1 with water and applied through a filter onto a 3-cm preconcentration column. Following a simple wash step, the analytes were flushed directly onto a reversed-phase analytical high-performance liquid chromatography (HPLC) system. Absolute recoveries were high (above 90%) and the chromatograms were free from interference. Analysis for the drug and its breakdown product was performed using ultraviolet (UV) visible photodiode array detection, which allowed confirmation of peak identity. Recognizable UV spectra could be measured with as little as 20 ng on column. Comparison of the drug levels in 27 blood and vitreous humor samples showed that, while there was only a low correlation between the blood and vitreous concentrations (R = 0.70), vitreous cocaine and BE determinations were good indicators of antemortem cocaine use. In almost all cases, the vitreous BE concentrations were higher than the cocaine concentrations. The technique was easy to perform and the vitreous samples were especially compatible with this low-labor analytical procedure.

A method for the determination of morphine is post-mortem blood by HPLC with electrochemical detection is described. Blood morphine levels in post-mortem cases are reported and the importance of these in causing death is discussed. These post-mortem levels are compared further with morphine levels in the blood of patients receiving morphine as an analgesic.

A method is described for the rapid HPLC analysis of a number of anticonvulsant drugs in vitreous humour by injection directly onto a preconcentration column without the need for prior extraction. The conditions for optimum precision and accuracy were investigated and the method was subsequently applied to the analysis of phenytoin in a number of overdose cases. Sensitivity was 0.05 μg/ml on a 0.5 ml vitreous sample. The mean blood/vitreous ratio for phenytoin was found to be 2.8 (range: 1.4–5.1). The relationship between blood and vitreous levels had a correlation coefficient of 0.85. Vitreous was found to be a very clean, stable sample, ideally suited to this technique.

An enforcement emphasis project, "Operation Trucker Check," was established in order to determine the extent to which commercial tractor-trailer drivers were operating their vehicles while impaired by drugs. A total of 1079 drivers and their vehicles were assessed for driver and equipment violations, and drivers additionally underwent preliminary field sobriety tests conducted by drug recognition expert (DRE) officers. Anonymous urine specimens for drug analysis were requested, and 822 urine specimens were obtained in total. Compliance with the drug-testing portion was voluntary, and there was a 19% refusal rate. Overall, 21% of the urine specimens tested positive for either illicit, prescription, and/or over-the-counter drugs, and 7% tested positive for more than one drug. Excluding caffeine and nicotine, the largest number of positive findings (9.5%) were for CNS stimulants, such as methamphetamine, amphetamine, phentermine, ephedrine/pseudoephedrine, and cocaine. The second most frequently encountered drug class were the cannabinoids, with 4.3% of drivers testing positive for marijuana metabolites. Only 11 drivers (1.3%) were positive for alcohol. Sixteen truck drivers (1.6%) were charged with driving under the influence of drugs after a full DRE evaluation was conducted. The results indicate that in spite of comprehensive drug testing in the trucking industry, some tractor-trailer drivers are continuing to take illicit and other drugs with the potential of having a negative effect on their driving ability. On the other hand, only a few drivers were, in fact, deemed to be under the influence of drugs at the time of driving when evaluated by DRE officers.

Absorption extraction on diatomaceous earth was examined and found to be compatible with typical postmortem blood specimens encountered in forensic toxicology. The effects of solvent, solvent volume, eluate flow rate, and pH on drug recovery and extract quality were investigated. It was concluded that the best method was not necessarily that with the highest recoveries, but that considerations of extract quality were also required. The optimized method was compared with a single-step liquid/liquid extraction method and found to be superior in terms of ease of operation, extract quality, and absolute recovery. The results indicated also that although useful for screening, quantitative methods using liquid/solid extraction may be prone to error.

The authors describe a simple chemical test to determine whether a suspect specimen contains cocaine and if so whether it is present as free base cocaine or in a salt form. The distinction is based on the relative solubility of the two compounds in aqueous or organic solvent. The test, based on the widely accepted cobalt thiocyanate color reaction, is performed in three stages to make the interpretation as complete as possible.