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Background Hydrogen sulfide is a toxic gas about which much has been written. We discuss here several issues we believe would benefit from further clarification. Conclusions We conclude that: 1) Certain neurotoxic effects of exposure are probably due to a direct toxic effect on the brain, while others are almost certainly a result of hypoxia secondary to H2S-induced respiratory insufficiency; 2) pulmonary edema is a common consequence of poisoning and there is suggestive evidence of hyperactive airway responses in some individuals following brief H2S-induced unconsciousness (knockdown); 3) criteria for acceptable community levels are very different than those governing occupational standards; 4) urinary thiosulfate determinations can be useful for monitoring occupational exposure; and 5) determination of sulfide ion concentrations in blood or major organs can be useful in corroborating a diagnosis of fatal H2S toxicity, but there are many pitfalls in collecting, storing, and analyzing tissue and fluid samples. Am. J. Ind. Med. 35:192–195, 1999. © 1999 Wiley-Liss, Inc.

Eighteen male subjects participated in a clinical study to examine a skin patch method of monitoring drug use. On the first day of each of two periods, 14 Band-aid type collection devices (sweat patches) were applied to a subject's torso, biceps, and back. On the following day, the subject took 50 or 126 mg cocaine hydrochloride intranasally. A 1-week interval separated treatment periods, and the order of dose levels was counterbalanced. On the days subjects received cocaine, one patch was removed before treatment, and five were removed after treatment. Subjects then returned over the next 7 days for removal of the remaining patches. They provided urine samples immediately after each patch removal. A group of 18 nondrug users also wore patches for up to 12 days. Analysis of the patch content yielded cocaine levels from the cocaine subjects that accurately reflected usage. Mean levels for 16 subjects were significantly different for the two treatment doses. However, given the between-dose and between-subject variability, the data cannot be used to determine either dose or time of use. The data do indicate, however, that the patch technology can be used to diagnose a single episode of cocaine use as far back as 7 days.

Serum and urine specimens of 31 patients with suspected lysergic acid diethylamide (LSD) intoxication were analyzed for LSD by both radioimmunoassay (RIA) and high-pressure liquid chromatography (HPLC). The RIA assay, using 0.1 ng/mL as the limit of detection instead of the manufacturer's recommendation of 0.5 ng/mL, was positive for LSD in 13 blood and urine specimens from 14 patients. Results were compared to HPLC analysis using methysergide instead of lysergol as the internal standard and a limit of detection of 0.5 ng/mL. HPLC detected LSD in 9 of 13 serum specimens and 11 of 13 urine specimens that had tested positive by RIA. Of 18 patients with a final clinical diagnosis of LSD intoxication, LSD was detected by RIA in 14 patients and by HPLC in 11 patients. For 13 other cases in which the final diagnosis was a condition other than LSD intoxication, serum and urine assays for LSD were negative in all cases by both techniques. LSD assays have not been generally available in clinical laboratories. We conclude that the qualitative determination of LSD in either serum or urine by a commercially available radioimmunoassay has made it possible to provide reliable laboratory confirmation of LSD intoxication.

We have become aware of several commercial products that, when orally ingested, will purportedly not only eliminate "toxins" from a person's system, but will also correct any urinary imbalances caused by excessive water consumption.Unblinded study of one volunteer subject, tested weekly x 4 for 24-hour urine elimination of test drug under conditions of control, control plus 1200 mL water, Quick Flush', and Eliminator.Each of the treatment protocols studied caused reductions of drug or metabolite concentrations as measured by gas chromatography-mass spectrometry in urine specimens collected up to 24 hours after ingestion of amphetamine, 9-carboxy-11-nor-delta-9-THC, benzoylecgonine, or codeine, yet the radioimmunoassay screening results demonstrated very little effect. Water alone was approximately as effective as the two commercial products in reducing the metabolite level. None of the treatment protocols employed in this study altered urinary pH, specific gravity, or creatinine concentration outside the normally accepted physiological range.Attempts to conceal drug abuse by water dilution are most likely to play a substantial role when concentrations are at or near the detection threshold for a particular assay such as the terminal stages of drug eliminations.

A driver was found asleep behind the steering wheel of his car, and the vehicle was at rest in a traffic lane with the engine running. His manifestations included horizontal and vertical gaze nystagmus, muscle flaccidity, and severe ataxia. He admitted ingesting a white powder, which he identified as an amino acid, about 1 hour prior to discovery by police. A urine specimen collected approximately 1 hour after the traffic stop contained 1975 mg/L of gamma-hydroxybutyrate (GHB). We tentatively conclude that GHB may cause impairment of the psychomotor skills required for safe operation of a motor vehicle. Language: en

With γ-hydroxybutyrate (GHB) becoming popular as a drug of abuse in the US and elsewhere (1), we are receiving increasing requests for the analytical determination of GHB in blood or urine in criminal investigations, especially in sexual assault cases. In a recent report of a fatal poisoning with GHB, the victim had a postmortem blood GHB concentration of 27 mg/L (2), and another three GHB-related fatalities were reported with postmortem …

A study was undertaken to determine if a relatively minor modification of our existing specimen collection tubes could enhance the long-term stability of blood cocaine. We added cocaine, benzoylecgonine (BE) and ethanol to whole sheep blood in glass tubes that were prepared to contain one of several combinations of preservatives and anticoagulant. On day 1 and at intervals of up to one year, the drugs were measured by gas chromatography-mass spectrometry (cocaine and BE) or headspace gas chromatography (ethanol). Storage of blood containing 200 ng/mL cocaine at 4 degrees C for one year resulted in 100% loss of the drug using our normal 10 mL specimen collection tubes containing 100 mg sodium fluoride and 20 mg potassium oxalate. The substitution of oxalic acid for potassium oxalate reduced this loss to 76% without any significant effect on the benzoylecgonine or ethanol concentrations. Further addition of 10 mg echothiophate iodide, a quaternary ammonium compound, brought the cocaine loss down to 60% of the original concentration by one year. Further work will be required to determine if oxalic acid and/or echothiophate iodide could be used in blood collection vials intended for forensic toxicological purposes without any detrimental effect on other assays.

This volume continues in the same vein as the first 4 volumes of this reference set, which were issued in 1987. Volumes 1–3 contain alphabetical listings for approximately 1200 drugs, showing for each drug on two pages the reference spectra by ultraviolet, infrared, nuclear magnetic resonance and mass spectrometry analysis. Volume 4 contains an index and several appendices, with sequential page numbering of all 4 volumes for a total of 2682 pages.

The theme of the 25th International Meeting of the International Association of Forensic Toxicologists (TIAFT) was “Interpretation of Analytical Results.” A number of the 52 papers included in these proceedings do address themselves to this topic and provide much useful information. Most of the other articles cover either general or specific analytical techniques: immunoassay and gas chromatography/mass spectrometry are equally well represented, and there appears to be more emphasis on high-performance liquid chromatography methods than in past TIAFT proceedings. The preface by the editors provides a welcome overview, and a delightful commentary by Dr. V. Spiehler presents a more personalized profile of the attendees, their scientific interests, and the social functions included in the program.

A method is presented for the routine determination for toxicological purposes of the common benzodlazepines In biological fluids and tissues. The procedure makes use of flameionization gas-liquid chromatography without prior derlvatlzation of the drugs, and it employs prazepam as an Internal standard. Diazepam, nordlazepam, flurazepam, desalkylflurazepam, chlordiazepoxide, and oxazepam may be Identified and quantitated at concentrations of 0.2 ug/ml or greater. A thin-layer chromatographic technique has been Included for the purposes of confirming the Identity of the drugs analyzed with this procedure.

Human blood, plasma, or serum concentrations of drugs important to the analytical toxicologist are tabulated, as an aid to interpretation of analytical toxicological results. Significant pharmacological factors are included such as dosage, route and frequency of administration, number and weight of subjects, and time of sampling.

Methadone, administered subcutaneously to rats once daily for 12 days, nearly doubled the bile flow rate in isolated perfused livers. The increase in bile flow was accompanied by an increase in the biliary excretion rate of metabolites of 3 H-methadone, which was added to the perfusion system at a dose of 1 mg/kg body weight. To determine whether an alteration of the rate of methadone metabolism accounted for this effect, Phenol-3,6-dibromphthalein disulfonate (DBSP), an analogue of BSP which is excreted unchanged in the bile, was added (80 mg/kg) to the perfusion system. It was also excreted at an enhanced rate by the livers of the methadone pretreated rats. Neither the plasma disappearance rate of methadone or DBSP nor the pattern of biotransformation of methadone was significantly affected by the methadone pretreatment. It is concluded that chronic methadone treatment of rats stimulates bile flow via an unknown mechanism, resulting in increased biliary excretion of methadone metabolites and possibly of other compounds which undergo elimination in the bile.

The case of a 55-year-old woman who died following the Ingestion of 300 mg of tranylcypromine and several other drugs is presented. High concentrations of tranylcypromine were found in blood, brain, liver, and urine by gas-liquid chromatography. Monoamine oxidase activity in liver was markedly diminished from that of the control case, although the cerebral cortical activity of this enzyme did not differ significantly from the control. Pathological findings were limited to pulmonary edema and congestion of the liver, spleen, and kidneys.

The concentrations of thioridazine in body fluids and tissues, as measured by a spectrophotofluorometric method, have been compared in thioridazine-induced fatalities and in deaths of patients on thioridazine therapy that were otherwise unrelated to drugs. A distinct overlap of blood concentrations was apparent for the two groups, although a substantial difference between liver concentrations was observed. We believe that postmortem blood and liver concentrations determined by a fluorometric technique may be used to reach a conclusion as to the cause of death in thioridazine-related fatalities. When parenchymatous tissue is not available, a diagnosis of thioridazine poisoning would best be made on the basis of case history and data obtained with a highly specific analytical technique.

The toxicologic findings in eight cases of death due primarily to codeine overdosage are presented. Blood codeine concentrations ranged from 1.4 to 5.6 mug/ml as determined by gas-liquid chromatography. Morphine was found in only two of the blood samples, at concentrations of 0.2 and 0.6 mug/ml, and may have resulted from heroin usage rather than codeine metabolism. A case of death of a codeine user by violent means is also presented in which the blood codeine concentration was 2.6 mug/ml.

Paired serum and saliva samples, obtained from 100 emergency department patients suspected of phencyclidine (PCP) intoxication, were analyzed using a specific PCP radioimmunoassay (RIA). Seventy-four of the 100 saliva samples and 75 of the paired serum samples were positive for PCP. The final clinical diagnosis was PCP intoxication in 79 cases. Of these, both serum and saliva tests were positive in 70 cases, only serum was positive in two cases, and both serum and saliva samples were negative in seven cases. The concentration of PCP in the samples did not correlate with the severity of PCP intoxication. In the remaining 21 cases, with no clinical evidence of PCP intoxication, PCP assays were negative in both serum and saliva in 17 cases, three patients had positive saliva and serum tests, and one other patient had a positive PCP saliva assay. Thus, saliva would appear to be as reliable as serum as a specimen for PCP analysis.

Exposure of pregnant rats to inhalation of nickel carbonyl on days 7 or 8 of gestation frequently causes the progeny to develop ocular anomalies, including anophthalmia and microphthalmia. The incidence of extraocular anomalies is very low. The specificity of nickel carbonyl for induction of ocular anomalies in rats appears to be unique among known teratogenic agents.

This is the twelth volume in a series entitled “Methodological Surveys in Biochemistry and Analysis,” edited by Dr. Eric Reid of the University of Surrey; it is the second such volume discussed by this reviewer (see JournalofAnalytical ToxicologyK, Vol. 3, 1979, p. 224). while Dr. Reid has “cleaned up” his literary act significantly over the years, having recently refrained from using wraparound sentences and footnotes to footnotes, he was apparently unable to restrain entirely his double-jointed typist in the latest volume. The result, a collection of 30 articles by some 52 contributors (including our own Rokus de Zeeuw), is a multifaceted, perhaps eclectic, presentation of approaches to drug analysis in biological fluids that is occasionally marred by the cryptic editorial style that hag become the trademark of this series.

Thirty-two postmortem blood specimens, with and without sodium fluoride as preservative, were analyzed for cholinesterase activity by the Michel method. The fluoridated specimens, which contained from 0.7 to 31 mg/mL (average 6.3) of sodium fluoride, were found to exhibit cholinesterase activities that were 5 to 59% (average 25%) lower than the duplicate unfluoridated specimens. We concluded that, while this decrease is quite significant, a fluoridated postmortem blood specimen may be used for the measurement of cholinesterase activity when a non-fluoridated specimen is unavailable.