NOTE: Although the toxicity values presented in these toxicity profiles were correct at the time they were produced, these values are subject to change. Users should always refer to the Toxicity Value Database for the current toxicity values.
Prepared by Rosmarie A. Faust, Ph.D., Chemical Hazard Evaluation and Communication Program, Biomedical and Environmental Information Analysis Section, Health Sciences Research Division, *, Oak Ridge, Tennessee.
Prepared for OAK RIDGE RESERVATION ENVIRONMENTAL RESTORATION PROGRAM.
*Managed by Martin Marietta Energy Systems, Inc., for the U.S. Department of Energy under contract No. DE-AC05-84OR21400.
Fluoranthene is a polycyclic aromatic hydrocarbon (PAH) that can be derived from coal tar. Occurring ubiquitously in products of incomplete combustion of fossil fuels, fluoranthene has been identified in ambient air, surface, drinking, and waste water, and in char-broiled foods. Currently, there is no commercial production or use of this compound (IARC, 1983).
Fluoranthene can be absorbed through the skin following dermal exposure (Storer et al., 1984) and, by analogy to structurally-related PAHs, would be expected to be absorbed from the gastrointestinal tract and lungs (U.S. EPA, 1988). An in vitro study identified 2-methylfluoranthene and 3-methylfluoranthene and their dihydrodiols as metabolites of fluoranthene (La Voie et al., 1982).
Although a large body of literature exists on the toxicity and carcinogenicity of PAHs, primarily benzo[a]pyrene, toxicity data for phenanthrene are very limited. No human data were available that addressed the toxicity of fluoranthene. Acute toxicity data for animals include an oral LD50 of 2000 mg/kg for rats; a dermal LD50 of 3180 mg/kg for rabbits (Smyth et al., 1962); and an intravenous LD50 of 100 mg/kg for mice (RTECS, 1993). Subchronic oral exposure to fluoranthene at doses of greater than or equal to 250 mg/kg produced nephropathy, increased liver weights, and increased liver enzyme levels in rats (U.S. EPA, 1988). A single intraperitoneal injection of fluoranthene to pregnant rats caused an increased rate of embryo resorptions (Irvin and Martin, 1987). Fluoranthene was photosensitizing, enhancing erythema elicited by ultraviolet radiation in guinea pig skin (Kochevar et al., 1982) and was irritating to the eyes of rabbits (Grant, 1986).
A Reference Dose (RfD) of 4.00E-01 mg/kg/day for subchronic oral exposure and 4.00E-02 mg/kg/day for chronic oral exposure to fluoranthene was calculated from a no-observed-adverse-effect level (NOAEL) of 125 mg/kg/day and a lowest-observed-adverse-effect level (LOAEL) of 250 mg/kg/day derived from a 13-week gavage study with mice (U.S. EPA, 1993a,b). The critical effects were nephropathy, increased liver weights, and changes in clinical and hematological parameters. Data were insufficient to derive an inhalation Reference Concentration (RfC) for fluoranthene (U.S. EPA, 1993a,b).
No oral or inhalation bioassays were available to assess the carcinogenicity of fluoranthene. Bioassays by other exposure routes generally gave negative results. Studies involving topical application to the skin of mice (Horton and Christian, 1974; Hoffmann, 1972; Wynder and Hoffmann, 1959; Suntzeff et al., 1957) and subcutaneous injection in mice (Shear, 1938) provided no evidence of carcinogenicity. Fluoranthene was also inactive in mouse skin initiation and promotion assays (Van Duuren and Goldschmidt, 1976; Hoffmann, et al., 1972). However, fluoranthene has been shown to be active as a cocarcinogen when applied with benzo[a]pyrene to mice by skin application (Van Duuren and Goldschmidt, 1976) and was active as a complete carcinogen in a short-term lung tumor assay with newborn mice (Busby et al., 1984).
Based on no human data and inadequate data from animal bioassays, U.S. EPA (1993a,b) has placed fluoranthene in weight-of-evidence group D, not classifiable as to human carcinogenicity. Retrieve Toxicity Profiles Formal Version
Last Updated 10/31/97