T. Miyazaki

Detection of methamphetamine and amphetamine in a skeletonized body buried for 5 years

A 28-year-old male methamphetamine abuser, who had been buried for 5 years after being killed by strangulation, was found skeletonized. Methamphetamine and amphetamine in the significantly denatured fatty material of the bone marrow were analyzed by gas chromatography and gas chromatography-mass spectrometry. The confirmation of the chemicals was carried out by chemical ionization (CI) mass chromatography, CI mass spectrometry and CI mass fragmentography. The concentrations of methamphetamine and amphetamine determined by CI mass fragmentography were 1.0 mumol/100 g and 0.1 mumol/100 g, respectively. The method used would seem to be very useful for determination of methamphetamine and amphetamine in marked putrefied biological materials.

Fatal and non-fatal methomyl intoxication in an attempted double suicide.

A 79-year-old man and his 73-year-old wife attempted double suicide by ingesting methomyl powder. The woman died 19 h after ingestion in spite of intensive care. At autopsy a large number of miliary hemorrhages were found in both thalami of the brain. Her husband, however, recovered after 10 days of treatment. Methomyl (CAS No. 16752-77-5, Lannate) in the biological materials was analyzed by gas chromatography-mass spectrometry. The methomyl concentration was 44 micrograms/g in the wifes serum sample collected 1 h after ingestion, and 0.2 microgram/g in the blood sample collected at autopsy. The methomyl concentration in the husbands blood sample collected 28 h after ingestion was from 0.01 to 0.1 microgram/g. It is suggested that prompt and adequate intensive care including a direct hemoperfusion is necessary to effect the recovery of patients with lethal blood levels of methomyl. The miliary hemorrhages found in the thalami of the brain are suspected to have been caused by asphyxia induced by methomyl intoxication.

Traumatic rupture of intracranial vertebral artery due to hyperextension of the head: Reports on three cases

In three cases of fatal basal subarachnoid hemorrhage due to rupture of the normal intracranial vertebral artery, the ruptures appeared to have been caused by overstretching of the vertebral artery from traumatic hyperextension of the head. In the first case, that of a 31-year-old male pedestrian who, while intoxicated, had been hit from behind by a car, symmetrically located bilateral complete and incomplete tearing of the vertebral arteries was found. In both of the other two cases, involving women aged 37 and 51 found dead after receiving fist blows to the face while intoxicated, complete rupture of the vertebral artery was found. The blood alcohol concentrations of the three cases ranged from 1.6 to 1.7 mg/g at autopsy.

Cyanide distribution in five fatal cyanide poisonings and the effect of storage conditions on cyanide concentration in tissue.

The cyanide distribution in five fatal cyanide poisonings was analyzed by the pyridine-pyrazolone method using a Conway diffusion cell. In order to study the effect of storage conditions on cyanide concentration in tissue samples, the cyanide concentrations were first measured immediately after collection of the samples at autopsy, then measured again after storage in a refrigerator (4 degrees C) or in a freezer (-20 degrees C) for periods ranging from 1 day to 3 weeks. Concentrations in all but three of the blood samples stored at 4 degrees C or -20 degrees C increased, with concentration ratios based on measurement made before and after storage ranging from 0.71 to 1.46. The concentrations in the liver, kidney, and brain samples either increased or decreased, with ratios of from 0.2 to 8.8. The concentrations in the stomach contents samples decreased rapidly at 4 degrees C, but hardly changed at all at -20 degrees C.

Detection of S-methylfenitrothion, aminofenitrothion, aminofenitroxon and acetylaminofenitroxon in the urine of a fenitrothion intoxication case☆

A 23-year-old male attempted suicide by ingesting approximately 50 ml of 5% fenitrothion emulsion, and vomited soon afterwards. He was admitted to a hospital about 3 h after ingestion. He recovered and was discharged from hospital 3 days after admission. The serum cholinesterase activity (normal range: 175-440 I.U.) was only 29 at 3 h, 32 at 1 day, 59 at 2 days and 75 at 3 days after ingestion. Fenitrothion and its metabolites in the body fluids were extracted by an Extrelut column extraction method, detected by a gas chromatograph equipped with either a hydrogen flame ionization detector or a flame photometric detector, and confirmed by a gas chromatograph-mass spectrometer. Fenitrothion concentration in the blood was 169.5 ng/g at 3 h after ingestion. The half life of blood fenitrothion concentration was found to be about 4.5 h. Fenitrothion metabolites, 3-methyl-4-nitrophenol, aminofenitrothion, aminofenitroxon, acetylaminofenitroxon and S-methylfenitrothion, were detected in the urine samples. All of them except S-methylfenitrothion were detected in the urine samples collected up to 62 h after ingestion. It would appear therefore that fenitrothion poisoning can be determined by detection and analysis of the metabolites in urine even if fenitrothion has not been detected in the blood.

Gas chromatographic determination of cresols in the biological fluids of a non-fatal case of cresol intoxication

A simple and rapid method for analysis of free and conjugated cresols in biological fluids was developed. Prior to and following freeing of the conjugated cresols by acid hydrolysis in a sealed ampoule, free cresols were extracted by Extrelut column extraction, determined by gas chromatography, and confirmed by gas chromatography-mass spectrometry. In a non-fatal case of cresol intoxication a 46-year-old male had ingested about 100 ml of a saponated cresol soap solution. The concentrations of xylenol (2,4- and/or 2,5-dimethylphenol) and p- and m-cresol in the serum sample collected on admission were 15.8 micrograms/g, 43.3 micrograms/g and 73.8 micrograms/g, respectively. The total cresol concentration of 117 micrograms/g in the serum is within the range of fatal concentrations, and it is suspected therefore that the patients recovery was due to adequate therapy alone.

Determination of dimethoate in blood and hemoperfusion cartridge following ingestion of formothion: A case study

A 57-year-old male who had ingested not more than 22 g of formothion was semicomatose on admission to hospital, approximately 1.5 h after ingestion. Dimethoate, a hydrolyzed formothion, was found in blood samples collected from the patient and in the charcoal column in the direct hemoperfusion cartridge which was used 6 to 7.5 h after ingestion. It was extracted and purified by Extrelut column extraction. A gas chromatograph, equipped with a flame photometric detector and a gas chromatograph-mass spectrometer, were used to detect and confirm the presence of dimethoate. The blood dimethoate concentrations which were taken approximately 1.5 and 6 h after ingestion were 21.4 and 12.7 micrograms/g, respectively. A blood dimethoate concentration of 21.4 micrograms/g would appear to indicate a high level of formothion intoxication. The total amount of dimethoate found in the charcoal column used was 15 mg.

Analysis of inflammable substances to determine whether death has occurred before or after burning

SummaryIn two murder cases involving burning, both victims had been set on fire in the open air after being drenched with kerosene. In the first case, carbon monoxide hemoglobin (COHb) saturation was found to be 2.1% in the left heart blood and 0.8% in the right heart blood, a ratio of 2.6 for left to right heart blood. Paraffin hydrocarbons were also detected in the left heart blood. It was determined that the victim had been set on fire before death and that burning had been the cause of death. In the second case, the COHb saturation was 0.21% in the left heart blood and 0.24% in the right heart blood, giving a left-to-right ratio of 0.9. Paraffin hydrocarbons were detected in the hair sample, but not in the left heart blood. It was determined that the victim had been set on fire after death, and the cause of death was suspected to be asphyxia due to compression of the neck.ZusammenfassungBei zwei Mordfällen wurden die Opfer im Freien verbrannt, nachdem sie mit Benzin übergossen wurden waren. Im ersten Fall wurde eine CO-Hemoglobin-Konzentration von 2,1% im Blut des linken und von 0,8% im Blut des rechten Herzens nachgewiesen, woraus sich ein Verhältnis von 2,6 errechnet. Paraffinartige Kohlenwasserstoffe wurden im Blut aus dem linken Herzen nachgewiesen. Es wurde daraus geschlossen, daß des Opfer vor Eintritt des Todes Feuer ausgesetzt war und daß Verbrennung als Todesursache anzusehen ist. Im zweiten Fall lag die CO-Hämoglo-bin-Konzentration im linken Herzblut bei 0,21% and im rechten Herzblut bei 0,24%, woraus sich ein Verhältnis von 0,9 (links zu rechts) errechnete. Paraffinartige Kohlenwasserstoffe wurden in Haarproben, jedoch nicht im linken Herzblut bestimmt. In diesem Fall wurde das Opfer offensichtlich nach Eintritt des Todes infolge von Ersticken verbrannt.

Determination of disulfoton and its metabolites in the body fluids of a Di-Syston® intoxication case

Disulfoton and its metabolites, two sulfoxides and two sulfones, in the body fluids of a patient who had ingested Di-Syston were analyzed by FPD-GC and GC/MS. After the chemicals in the extract (Fraction 1) obtained by Extrelut column extraction were analyzed, disulfoton and sulfoxides in Fraction 1 were oxidized into sulfones. The sulfones in the extract (Fraction 2) obtained by Extrelut column extraction were analyzed and the estimated concentrations of metabolite were calculated. The concentrations of disulfoton and the sum of the metabolites in the blood collected on admission were 0.093 nmol/g (25.4 ng/g) and 4.92 nmol/g (corresponding to 1.35 micrograms/g of disulfoton), respectively. These concentrations appear to indicate a severe level of disulfoton intoxication.

Production of carbon monoxide in cadavers.

Carbon monoxide (CO), total hemoglobin (Hb) and carboxyhemoglobin (HbCO) in the blood and reddish discolored body cavity fluids of cadavers which had not been exposed to fire and CO were analyzed. In 13 cadavers found on land, the maximum saturation of HbCO in the blood was 3.6%, and was 10.1% in the body cavity fluids. There was only one case in which the HbCO saturations in the body cavity fluids were more than 10%. In seven drowned bodies found in fresh water, the highest HbCO saturation in the blood was 6.1%, and was 44.1% in the body cavity fluids. There were three cases in which the HbCO saturations in the body cavity fluids were more than 10%. In 12 drowned bodies found in sea water, the HbCO saturations in the blood were not more than 6.2%, and the maximum saturation of HbCO in the body cavity fluids was 83.7%. There were eight cases in which the HbCO saturations in the body cavity fluids were more than 10%. The results seem to indicate that the interpretation of HbCO saturation in the blood would not be affected significantly by the postmortem formation of CO, and that body cavity fluids should not be used for CO determination.