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, Chemical Hazard Evaluation and Communication Group, Biomedical and Environmental Information Analysis Section, Health and Safety Research Division, *.
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.
Anthracene, also referred to as paranaphthalene or green oil, is a polycyclic aromatic hydrocarbon (PAH) derived from coal tar and is primarily used as an intermediate in the production of dyes. It has also been used in the production of smoke screens. Anthracene is ubiquitous in the environment as a product of incomplete combustion of fossil fuels. Although a large body of literature exists on the toxicity and carcinogenicity of a number of PAHs, toxicity data for anthracene are limited.
Evidence indicates that anthracene is absorbed following oral and dermal exposure. Targets for anthracene toxicity are the skin, hematopoietic system, lymphoid system, and gastrointestinal tract. Adverse dermatologic effects have been observed in humans and animals in conjunction with acute and subchronic exposure to anthracene. In humans, anthracene may cause acute dermatitis with symptoms of burning, itching, and edema. Prolonged dermal exposure produces pigmentation, cornification of skin surface layers, and telangiectasis (Volkova, 1983). Anthracene is photosensitizing, potentiating skin damage elicited by exposure to ultraviolet (UV) radiation (U.S. EPA, 1987; Dayhaw-Barker et al., 1985; Forbes et al., 1976). Hematologic toxicity was observed in patients receiving intraperitoneal injections of anthracene-containing chemotherapeutic agents (Falkson et al., 1985) and in rats exposed to anthracene by oral gavage and by inhalation (Volkova, 1983). Mice receiving subcutaneous injections of anthracene exhibited adverse lymphoid effects (Hoch-Ligeti, 1941). Long-term use of anthracene-containing laxatives produced melanosis of the colon and rectum (Badiali et al., 1985). Human exposure to anthracene has also been associated with headache, nausea, loss of appetite, inflammation of the gastrointestinal tract, slow reactions, and weakness (Volkova, 1983).
A Reference Dose (RfD) of 3 mg/kg/day for subchronic oral exposure and 0.3 mg/kg/day for chronic oral exposure to anthracene was calculated from a no-observed-adverse-effect level (NOAEL) of 1000 mg/kg/day derived from a 90-day gavage study with mice (U.S. EPA, 1989). Data were insufficient to derive an inhalation Reference Concentration (RfC) for anthracene (U.S. EPA, 1991a,b).
Carcinogenicity bioassays with anthracene generally gave negative results. Studies involving oral administration (Druckrey and Schmahl, 1955; Schmahl, 1955) or intrapulmonary implantation in rats (Stanton et al., 1972) or implantation into the brain of rabbits (Russell, 1947) provided no evidence of carcinogenicity. Negative results were also obtained when anthracene was tested in mice by skin application (Wynder and Hoffman, 1959; Pollia, 1939; Kennaway, 1924a,b) and in mouse-skin initiation assays (LaVoie et al., 1979; Scribner, 1973). However, skin application of anthracene followed by exposure to UV radiation or visible light induced a high incidence of skin tumors in mice (Heller, 1950).
Based on no human data and inadequate data from animal bioassays, U.S. EPA (1991a,b) has placed anthracene in weight-of-evidence group D, not classifiable as to human carcinogenicity. Retrieve Toxicity Profiles Formal Version
Last Updated 8/29/97