Metabolic interactions

One of the routes of metabolism of methylene chloride is a microsomal oxidation process (involving cytochrome P450). Carbon monoxide is formed by this microsomal oxidation pathway (Gargas et al., 1986) and concurrent exposure to acetone may increase the production of carbon monoxide, by the acetone-induced augmentation of this pathway.

• Aromatic hydrocarbons

Studies in rats have shown that a single oral administration of an aromatic hydrocarbon (benzene, toluene or m-xylene) 16-24 hours before the administration of methylene chloride, increases the peak carboxyhaemoglobin concentration. The half-life of methylene chloride in blood was shorter, indicating that the metabolic degradation of methylene chloride is enhanced by the aromatic hydrocarbons. This effect on the peak carboxyhaemoglobin concentration was dependent on the time interval between aromatic hydrocarbon and methylene chloride treatment, since earlier administration of toluene or m-xylene decreased the carboxyhaemoglobin elevation. Disulfiram treatment blocked carboxyhaemoglobin elevation completely and corresponding increases in the concentration and half-life of methylene chloride were observed (Kim and Kim, 1996).

A study in experimental animals found that a one day exposure to 11,000 ppm methylene chloride and 24,000 ppm ethanol produced a decrease in hepatic triglyceride concentrations, histological changes and carboxyhaemoglobin concentrations relative to the effects of methylene chloride exposure alone. Also, exposure to 560-600 ppm methylene chloride and 22,800-23,900 ppm ethanol decreased carboxyhaemoglobin concentrations compared to methylene chloride alone, which suggests an antagonistic effect. However, exposure to 500 ppm methylene chloride and 26,200 ppm ethanol over five days caused an increase in liver damage, suggesting that ethanol may potentiate the effects of methylene chloride (Balmer et al., 1976).

Smoking increases the blood carboxyhaemoglobin concentration, as does exposure to methylene chloride. Smoking, during and after exposure to methylene chloride, produced an additive increase in carboxyhaemoglobin concentrations (DiVincenzo and Kaplan, 1981a).

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