Chloral hydrate susceptibility factors

The toxieity of triehloroethylene is dependent upon metabolism and induction of cytochrome P450. Triehloroethylene is metabolized through chloral hydrate to compounds including trichloroacetic acid and dichloroacetic acid which alter intercellular communication, induce peroxisome proliferation and may promote tumor production. Significant variability in trichloroethylene metabolism in 23 human haptic microsomal samples was reported by Lipscomb et al. It was also demonstrated that the trichloroethylene metabolism is dependent on enzymatic activities of the cytochrome system, and they conclude that their data indicates that humans are not uniform in their capacity for CPY dependent metabolism of trichloroethylene and increased activity may increase susceptibility to trichloroethylene induced toxicity in humans. These observations are compatible with the variability reaction which is depending on nutritional factors, enzyme induction factors, hormonal factors and interaction with other environmental chemicals, prescription medications and general health conditions, and explains the variable reports as far as trichloroethylene and level of liver toxicity in the various individuals studied. 

Susceptibility factors Age The effects of chloral hydrate have been studied in an observational study in 1903 infants and young children, 568 of whom were no more than 6 months old, by measuring auditory brainstem responses [22 ]. The sedation rate with a single dose of chloral hydrate 40 mg/kg of 8% was 100% in those under 6 months old, but 28% of the older children needed an additional dose. Adverse events included hyperactivity in 152 children (8%), minor respiratory distress in 10 (0.4%), vomiting in 217 (11.4%), apnea in 4 (0.2%), and a rash in 10 (0.4%). 

---