In animals and humans, inhalation, skin and oral absorption are thought to be 80%, 10% and 100% respectively.
Symptoms of poisoning following the ingestion of chloroform include headache, disturbance of consciousness, convulsions, respiratory paralysis, dizziness, abdominal pain, nausea, vomiting and diarrhoea. Inhalation can cause dizziness and shortness of breath.
In the case of ingestion, vomiting induced by ipecac extract is not recommended. Activated carbon slurry, with or without saline, laxative or sorbitol, may be administered orally. Exposed skin should be repeatedly washed with soap to remove contamination. Exposed eyes should be rinsed at room temperature with plenty of water for at least 15 minutes.
Management includes early decontamination, supportive and symptomatic treatment, with respiratory and cardiac monitoring (respiratory assistance, defibrillation, possible fluid rehydration), avoidance of catecholamine medications, and treatment in the event of liver and/or renal failure (renal dialysis). There is no specific antidote.
Chloroform is used as an industrial solvent and an intermediate in the manufacture of polymeric materials. At present, the main use of chloroform is in the production of refrigerant R-22, which is commonly used in the air conditioning industry. Reports from several laboratories suggest that acute renal toxicity of chloroform is species, strain and sex dependent (Eschenbrenner and Miller 1945; Hill et al., 1975; Larson et al. 1993199 4; Ball et al. 1984; Smith et al. 1983198 4; Torkelson et al. 1976), and male mice are more susceptible to infection than rats, rabbits, or dogs, while female mice are resistant. Tubular swelling, necrosis, and casting, mainly confined to proximal tubules, are the major histomathological changes in the kidney after exposure to chloroform in laboratory animals. Chloroform-induced nephrotoxicity was also associated with elevated blood urea nitrogen concentrations, proteinuria, and glycosuria. In vitro uptake of organic anions and cations by renal cortical sections is also inhibited by in vivo chloroform treatment (Kluwe and Hook 1978). Although human exposure to chloroform is associated with oliguria, proteinuria, increased blood urea nitrogen, and tubular necrosis, the threshold dose for renal toxicity of acute human chloroform is unknown. The localization of proximal tubules in human renal injury suggests a common mechanism for chloroform nephrotoxicity in most mammalian species.
Oxidative and reductive pathways of chloroform metabolism have been described, although there is limited data in vivo. Carbon dioxide is the main metabolite of chlorine gas
