Abstract

Some operating rooms are equipped with ultraviolet (u.v.)-radiating germicidal lamps which can decompose halocarbons. One such agent is the widely used anesthetic, halothane. To study the toxicity of u.v. decomposed halothane, mice were exposed to anesthetic concentrations (1.3%) of non- and u.v.-irradiated halothane in oxygen for 90 min. Halothane sleeping times increased from 14.3 min to 72.5 min. Microsomal mixed function oxidase activity decreased, as shown by prolonged pentobarbital sleeping times 1 day after exposure to halothane and irradiated halothane (54.6 min and 149.1 min, respectively, as compared to a 34.6-min control). Quantitative and qualitative differences were found in the amount of [ 14C] pentobarbital metabolites excreted by u.v.-irradiated halothane exposed mice compared to either oxygen or non-irradiated halothane exposed groups. In addition, serum glutamic-oxalacetic transaminase (SGOT) of irradiated halothane-exposed mice increased to 233% of the control values, and serum glutamic-pyruvic transsminase (SGPT) were 377% of control values. No significant changes in SGOT or SGPT occurred in non-irradiated halothane-exposed mice. Hepatic cytochromes P-450 and b 5 decreased 20% and 13%, respectively, in animals exposed to irradiated halothane, with no significant change in mice exposed to non-irradiated halothane. Microsomal aminopyrine demethylase activity in irradiated halothane-exposed mice also fell to 74% of the control or non-irradiated group values. Decomposition was approximately 10-fold greater for halothane irradiated in oxygen than in nitrogen. Inorganic bromine and fluorine were present, and 9 compounds were recognized by gas-liquid chromatography. Debromination and formation of 2,2,2-trifluoroacetyl chloride on irradiation in air are hypothesized to be responsible for the increased toxicity. Studies are in progress to evaluate the toxicity of lower concentrations for longer periods and to identify further the decomposition products.

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