IRIS Toxicological Review of Quinoline [and IRIS Summary] (External Review Draft)

Quinoline can be derived from petroleum, coal processing, production and use facilities, and shale oil. It is used as an intermediate in the production of various compounds and paints, and as a solvent for resins and terpenes. Acute exposures to quinoline vapors can result in irritation to eyes, nose, and throat , and may cause headaches, dizziness, and nausea in humans (EPA 1985). No noncancer dose-response assessment was performed for either oral or inhalation exposure to quinoline because the database lacked suitable human or animal data. No human epidemiological studies or case reports addressing the potential chronic toxicity or carcinogenicity of quinoline were identified, though enzymes that mediate the metabolic activity of quinoline have been identified in both rats and humans (Reigh et al., 1996). Limited oral carcinogenicity bioassays in various laboratory animals have demonstrated that quinoline exposure can lead to tumor formation relatively quickly (within 12 weeks) in rats and mice. U.S. EPA (1985) classified quinoline as Group C carcinogen (i.e., possible human carcinogen) and concluded that the data sets (rats and mice) were cogent enough to warrant a cancer potency determination under the assumption that quinoline is a human carcinogen. In addition, because quinoline has been shown to increase the incidence of rarely observed vascular tumors of the liver in both sexes of two rodent species, it is considered likely to be carcinogenic in humans in accordance with the proposed EPA carcinogen risk assessment guidelines (U.S. EPA 1996a). The present cancer risk assessment estimates human cancer risk from an oral carcinogenicity bioassay in male rats (Hirao et al. (1976). An oral slope factor of 4.5 (mg/kg/day)-1 for humans was calculated from the animal data.