An unusual trichloroethanol fatality attributed to sniffing trichloroethylene.

We report the death of a 28-year-old man due to sniffing a contact cement containing trichloroethylene. Initial testing revealed the presence of 80 mg/L trichloroethanol in cardiac blood, and the death was ruled as being due to trichloroethanol toxicity resulting from chloral hydrate ingestion. However, further investigation of the case revealed that the trichloroethanol resulted from trichloroethylene abuse. Subsequent targeted analysis for trichloroethylene, four months after the death, confirmed its presence in cardiac blood (1.1 mg/L), bile (4.5 mg/L), and liver (2.5 mg/kg). Trichloroethanol was initially detected during routine drug screening that employed gas chromatography (GC) using an HP-5 column with electron capture detection and subsequently quantitated by GC using the same column as for the initial screen, but with flame-ionization detection (FID); ethchlorvynol was the internal standard. Trichloroethylene was quantitated by headspace GC with a Restek Rtx-BAC1 column and FID; 1,1,1-trichloroethane was the internal standard.

Fatal intoxications with chloral hydrate.

An alcoholic man, treated with chloral hydrate (CH) syrup to which he was dependent, was discovered comatose and in respiratory arrest. Death occurred on the ninth day of hospitalization following cerebral oedema. A woman, alcohol addicted, depressed, and epileptic was admitted in the Intensive Care Unit with heart and respiratory failure following CH absorption. She died three days later after a deep coma. In these two cases, CH intoxication was confirmed by toxicological analysis: CH and its major metabolite, trichloroethanol (TCE), were identified and determined in serum and urine using headspace-capillary gas chromatography-mass spectrometry. The concentrations measured were compared with those found in previously published fatalities. The analytical method used can be proposed for both clinical and forensic cases.

Acute ethylene chlorohydrin poisoning: experience of a poison control center.

BACKGROUND: Ethylene chlorohydrin (CAS 107-07-3), a chemical once used in hastening grape vine sprouting in Taiwan, has caused severe toxicity upon acute exposure. Although such use of ethylene chlorohydrin is now prohibited in Taiwan, poisoning still occurs following its illegal use. Since data concerning human ethylene chlorohydrin poisoning remain rare, we report our experience in treating acute ethylene chlorohydrin-poisoned patients. METHODS: A retrospective analysis was conducted to evaluate patients with ethylene chlorohydrin poisoning reported to Taiwan Poison Control Center during 1985-1998. RESULTS: Seventeen patients with ethylene chlorohydrin poisoning were identified. There were 11 male and 6 female patients, ranging in age from 2 to 70 years (median 53 years). The intent of exposure was suicide in 5, accident in 9, and occupational exposure in 3 patients. Oral ingestion was the most common route of exposure (14 patients). Seven out of the 17 patients died within 24 hours due to metabolic acidosis and respiratory failure. Ethanol therapy, used in 2 patients, had no apparent benefit. Moderate or mild poisoning was characterized by gastrointestinal effects only and an uneventful recovery. CONCLUSIONS: Ethylene chlorohydrin can result in severe metabolic acidosis, respiratory failure, coma, and death after acute exposure.

Concentrations of trichloroethylene and its metabolites in blood and urine after acute poisoning by ingestion.

A 58-year-old man fell into a trichloroethylene reservoir bath head first, during a maintenance degreasing bath and accidentally ingested the solvent. Although he showed deep coma, chemical burns and pneumonia on admission, these symptoms gradually subsided. The concentrations of trichloroethylene (TRI) and its metabolites, trichloroethanol (TCE) and trichloroacetic acid (TCA) in blood and urine were measured during hospitalization. Eight hours after the accident, the concentrations of TRI and its metabolites in serum were 31.4 micrograms/ml TRI, 16.5 micrograms/ml TCE and 79.5 micrograms/ml TCA. The serum TRI concentration decreased to 4.3 micrograms/ml on the following day. Elimination of TCE and TCA from serum occurred biphasically, the estimated half-lives of each metabolites being about 52.6 and 50.4 h in an initial fast phase and 268.3 and 277.2 h in a subsequent slow phase, respectively. Urinary TRI excretion persisted for the first 2 days. The urinary TCE and TCA excretions were longer than that of TRI with a biphasic decrease and the total amount of TCE excreted during the first 2 days was about two times that of TCA. The half-life of urinary TCE excretion (t1/2 25.7 h) was shorter than that of TCA (t1/2 52.1 h) in the fast phase but did no difference during the slow phase, with each half-time being about 166.3 h. The kinetics of TRI metabolites in blood and urine in this case were in slight agreement with the results following inhalation exposure previously reported in the literature.

[Induction of sister chromatide exchange by trichloroethylene and its metabolites (author's transl)]. / Induction d'échanges entre les chromatides soeurs (SCE) par le trichloréthylène et ses métabolites.

The mutagenecity of trichloroethylene and its metabolites (trichloroethanol and chloral hydrate) have been tested by using the method of sister chromatide exchanges (SCE). We have found the increasing SCE in workers chronically exposed to trichloroethylene. The increasing of SCE was also observed when the human lymphocytes were exposed to trichloroethanol and chloral hydrate in vitro in certain concentrations. The all results of tests groups are compared with those of the control groups and the difference is statistically significant.

Acute triclofos poisoning in a preterm infant.

A preterm infant with accidental triclofos sodium poisoning is described. He developed deep coma, severe hypothermia, mild by hypotension and lack of the primitive and deep tendon reflexes. During recovery, the primitive reflexes were the last to appear. The natural course of triclofos poisoning, and its influence on the immature central nervous system of the preterm infant are discussed.