A large number and variety of compounds are formed in the process of chlorinating
drinking water. The classes of compounds formed include
trihalomethanes, haloacetic
acids, haloacetonitriles, halophenols, and halopropanones. Many of the compounds have been shown to be toxic and are currently being further evaluated by the U.S. Environmental Protection Agency (EPA). One group of the halopropanones found in chlorinated
drinking water is the dichloropropanones. The toxicological properties of this group have not been well characterized. In addition, a number of investigators have shown that
ketones potentiate the hepatotoxicity of haloalkanes. We conducted a series of studies to explore both the toxicity of the dichloropropanones and their potential interactions with a well-characterized haloalkane,
carbon tetrachloride. A variety of toxicological and biochemical endpoints were used to evaluate the toxicity of the dichloropropanones and their interaction with CCl4, including
cytochrome P-450 concentration,
reduced glutathione levels,
pentane generation, serum
enzyme activities, and histopathology. Administration of
1,1-dichloropropanone (DCP) resulted in elevated serum
enzymes associated with periportal
necrosis.
Glutathione levels were reduced by the administration of 1,1-DCP;
pentane generation was not increased. When 1,1-DCP was given prior to CCl4, the data were consistent with additivity. Administration of 1,3-DCP did not result in elevated serum
enzymes, nor was there histopathologic evidence of
necrosis.
Glutathione levels and
pentane generation in the 1,3-DCP-treated groups were the same as those of controls. Inhibition of the toxicologic effects of CCl4 in a dose-related manner was observed when 1,3-DCP was administered prior to CCl4.