Evaluation of an onsite alcohol testing device for use in postmortem forensic toxicology.

The disposable QED saliva alcohol test provides a very simple, fast, and reliable means for quantitative onsite alcohol detection. The purpose of this study was to determine if the QED test would be a useful tool for the determination of postmortem ethanol levels in cases where a rapid result was needed. QED results were compared with ethanol levels determined by headspace GC analysis. Both saliva and vitreous humor specimens were used for the evaluation. QED tests were initially attempted using the oral fluid from 50 individuals. Of these cases, 17 of the tests were valid with 8 positive results. For 23 cases the oral fluid was not attainable, and for 10 cases, the sample was contaminated with blood making the tests invalid. The correlation between the oral fluid results and the blood headspace GC analysis was poor (r = 0.8345) over the range of 0.01-0.29 g/dL. Vitreous specimens were found to be the matrix of choice for analyzing postmortem cases using the QED. Only 6 of 171 specimens were found to be unsuitable. The QED results correlated well with the headspace GC analysis (r = 0.9931, n = 165). When using ethanol levels > 0.02 g/dL (n = 126), an average vitreous (GC)/blood ratio of 1.16 correlated well with the average QED/blood ratio of 1.22. Although the QED saliva alcohol test does not appear to be useful in determining postmortem saliva ethanol levels, it does provide accurate results when using postmortem vitreous humor as the testing matrix.

Detection of drugs of abuse in nails.

Postmortem toenail samples were used for the detection of cocaine (COC), benzoylecgonine (BZE), norcocaine (NCOC), cocaethylene (CE), morphine (MOR), 6-monoacetylmorphine (6-MAM), codeine (COD), and hydrocodone (HDC). After the toenail clippings were washed with methanol, they were solubilized in 0.1 M potassium phosphate (pH 5.0). The drugs of interest, along with internal standards, were isolated by solid-phase extraction followed by derivatization with N-methyl-N-trimethylsilyl-trifluoroacetamide. The derivatized products were analyzed by gas chromatography-mass spectrometry operated in the selective ion monitoring (SIM) mode. The limit of quantitation for all analytes was 0.3 ng on column. The quantities of drugs found in toenails of each of 46 decedents were compared with those of their corresponding postmortem fluids. The toenails of the 46 decedents were tested for COC, BZE, NCOC, and CE, and 34 of the collected samples were also tested for opiates. COC and BZE concentrations ranged from 0.20 to 140.17 (n = 20) and 0.30 to 315.44 ng/mg (n = 21), respectively. NCOC concentrations of 6.78 and 0.66 ng/mg and CE concentrations of 2.60 and 0.73 ng/mg were detected in two of the decedents' toenails. MOR and 6-MAM were detected in three sets of toenails at average concentrations of 0.37 and 0.89 ng/mg, respectively. COD was detected in two sets of specimens at concentrations of 3.07 and 1.02 ng/mg. HDC (0.62 ng/mg) was found in only one set of specimens.

Diltiazem and pentoxifylline determination in postmortem specimens.

A 78-year-old woman was found dead in her basement. Qualitative screening of available postmortem specimens detected the presence of diltiazem and pentoxifylline. Quantitations were carried out by gas chromatography using nitrogen-phosphorus detection and confirmed by gas chromatography-mass spectrometry with the following results: blood, 0.59 mg/dL diltiazem and 0.63 mg/dL pentoxifylline; urine, 1.17 mg/dL diltiazem and 0.08 mg/dL pentoxifylline; bile, 0.40 mg/dL diltiazem and 0.22 mg/dL pentoxifylline; gastric contents, 0.28 mg/dL diltiazem and 0.02 mg/dL pentoxifylline. Both drugs were found qualitatively in formaline-fixed tissues.

Unusual death attributed to the combined effects of chloral hydrate, lidocaine, and nitrous oxide.

A case in which the death of a 2-year-old male child was the result of an acute intoxication with chloral hydrate, lidocaine, and nitrous oxide is presented. Trichloroethanol (TCE), the primary metabolite of chloral hydrate, was qualitatively detected by the Fujiwara reaction. Quantitation of TCE was carried out by gas chromatography-mass spectrometry (GC-MS) with the following results: plasma, 79.0 mg/L; urine, 31.0 mg/L; gastric contents, 454.0 mg/L; bile, 111.0 mg/L; vitreous, 40.2 mg/L; cerebrospinal fluid (CSF), 68.3 mg/L; and liver, 164 mg/kg. Lidocaine was quantitated by GC analysis using nitrogen-phosphorus detection with the following results: plasma, 11.9 mg/L; urine, 3.7 mg/L; gastric contents, 15.3 mg/L; bile, 19.0 mg/L; vitreous, 17.8 mg/L; CSF, 9.4 mg/L; and liver, 19.0 mg/kg. Nitrous oxide was quantitated in the blood with a value of 4.4 mL/L.

Generation and fate of enamines in the microsomal metabolism of cyclic tertiary amines.

Microsomal oxidation of 1-benzylpiperidine (1-BP) and its cis-2,6-dimethyl analog was studied to assess the involvement of endocyclic enamines, in equilibrium with the initially formed iminiums, in the metabolic activation of cyclic tertiary amines such as phencyclidine. Since the iminiums can be trapped with cyanide, the selective prevention by cyanide of the metabolic production of 1-benzyl-3-piperidone from 1-BP implicates the iminium in equilibrium with enamine as the source of this metabolite. In cases where iminium-enamine coupling is sterically prevented, the iminium in equilibrium with enamine species can be studied independently and are found to be more potent metabolism-dependent inactivators of cytochrome P-450 than are the corresponding parent amines. Possible mechanisms for biological oxidation of cyclic enamines to reactive intermediates are considered.

Haemoprotein-mediated metabolism of enamines and the possible involvement of one-electron oxidations.

1. Microsomal metabolism of 1-benzylpiperidine (1-BP), its cis-2,6-dimethyl (cis-2,6-DMBP), 4,4-dimethyl (4,4-DMBP), and alpha, alpha-dimethyl (alpha, alpha-DMBP) analogues, and phencyclidine (PCP) has been studied to assess the involvement of P450 oxidation of the enamine tautomers of the initial endocyclic iminium metabolites. 2. The selective prevention by cyanide of the metabolite production of 1-benzyl-3-piperidone but not 1-benzyl-3-piperidinol from 1-BP is consistent with the enamine as the source of the 3-one metabolite. 3. The parent amines and particularly the independently prepared iminium species induced a pattern of metabolism-dependent irreversible inactivation of P450 benz-phetamine demethylase activity, consistent with involvement of enamine C-3 oxidation in the inactivation process. 4. Substrate activity of the endocyclic enamines and alpha-aminoketones (presumably the enol-enamine tautomers) for horseradish peroxidase under conditions where simple aliphatic amines display no activity is consistent with metabolic one-electron oxidations of the enamines.