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 Group, Biomedical and Environmental, Information Analysis Section, Health Sciences Research Division, Oak Ridge National Laboratory*, 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.
Phenanthrene is a polycyclic aromatic hydrocarbon (PAH) that can be derived from coal tar. Currently, there is no commercial production or use of this compound (U.S. EPA, 1987). Phenanthrene is ubiquitous in the environment as a product of incomplete combustion of fossil fuels and wood and has been identified in ambient air, surface and drinking water, and in foods (U.S. EPA, 1988; IARC, 1983).
Phenanthrene is absorbed following oral and dermal exposure (Storer et al., 1984; Chang, 1943). Data from structurally related PAHs suggest that phenanthrene would be absorbed from the lungs (U.S. EPA, 1987). Metabolites of phenanthrene identified in in vivo and in vitro studies indicate that metabolism proceeds by epoxidation at the 1-2, 3-4, and 9-10 carbons, with dihydrodiols as the primary metabolites (Nordqvist et al., 1981; Chaturapit and Holder, 1978; Sims, 1970; Boyland and Sims, 1962; Boyland and Wolf, 1950).
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 phenanthrene. Single intraperitoneal injections of phenanthrene produced slight hepatotoxicity in rats (Yoshikawa et al., 1985). Data regarding the subchronic, chronic, developmental, or reproductive toxicity in experimental animals by any route of exposure could not be located in the available literature.
Data were insufficient to derive an oral reference dose (RfD) or inhalation reference concentration (RfC) for phenanthrene (U.S. EPA, 1988). The chemical is not currently listed in IRIS or HEAST (U.S. EPA, 1993a,b).
No inhalation bioassays were available to assess the carcinogenicity of phenanthrene. A single oral dose of phenanthrene did not induce mammary tumors in rats (Huggins and Yang, 1962) and a single subcutaneous injection did not result in treatment-related increases in tumor incidence in mice (Steiner, 1955). Neonate mice administered intraperitoneal or subcutaneous injections of phenanthrene also did not develop tumors (Buening et al., 1979). No skin tumors were reported in two skin painting assays with mice (Roe and Grant, 1964; Kennaway, 1924). Phenanthrene was also tested in several mouse skin initiation-promotion assays. It was active as an initiator in one study (Scribner, 1973), inactive as an initiator in four others (LaVoie et al., 1981; Wood et al., 1979; Roe, 1962; Salaman and Roe, 1956), and inactive as a promoter in one study (Roe and Grant, 1964).
Based on no human data and inadequate data from animal bioassays, U.S. EPA (1993a, 1987) has placed phenanthrene in weight-of-evidence group D, not classifiable as to human carcinogenicity.Retrieve Toxicity Profiles Formal Version
Last Updated 2/13/98