The Risk Assessment Information System

Toxicity Profiles

Condensed Toxicity Summary for PYRENE

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.

AUGUST 1993

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.

Pyrene, also referred to as benzo(def)phenanthrene and -pyrene, is a polycyclic aromatic hydrocarbon (PAH) that can be derived from coal tar. Currently, there is no commercial production or use of this compound. Pyrene is ubiquitous in the environment as a product of incomplete combustion of fossil fuels and has been identified in surface and drinking water, numerous foods, and in ambient air (U.S. EPA, 1988, 1987; IARC, 1983).

Although a large body of literature exists on the toxicity and carcinogenicity of PAHs, toxicity data for pyrene are limited. No human data were available that addressed the toxicity of pyrene. Subchronic oral exposure to pyrene produced nephropathy, decreased kidney weights, increased liver weights, and slight hematological changes in mice (TRL, 1989) and produced fatty livers in rats (White and White, 1939). A single intraperitoneal injection of pyrene produced swelling and congestion of the liver and increased serum aspartate amino transferase (AST) and bilirubin levels in rats (Yoshikawa et al., 1985). No data were available concerning the toxic effects of inhalation exposure to pyrene or data regarding teratogenicity or other reproductive effects by any route of exposure.

A Reference Dose (RfD) of 3E-1 mg/kg/day for subchronic (U.S. EPA, 1993a) and 3E-2 mg/kg/day for chronic oral exposure (U.S. EPA, 1993b) to pyrene was calculated from a no-observed-adverse-effect level (NOAEL) of 75 mg/kg/day in a 13-week gavage study with mice (TRL, 1989). Data were insufficient to derive an inhalation Reference Concentration (RfC) for pyrene (U.S. EPA, 1993a,b).

No oral or inhalation bioassays were available to assess the carcinogenicity of pyrene. Studies involving other routes of exposure (intratracheal, dermal, and subcutaneous) generally gave negative results. Intratracheal administration of pyrene in combination with Fe2O3 particles did not induce tumors in hamsters (Sellakumar and Shubik, 1974). Skin painting assays evaluating complete carcinogenesis in mice (Van Duuren and Goldschmidt, 1976; Horton and Christian, 1974; Roe and Grant, 1964; Wynder and Hoffman, 1959); or initiating (Roe and Grant, 1964); or promoting capacity (Wood et al., 1980; Scribner, 1973; Salaman and Roe, 1956) have been negative or inconclusive. Mice injected subcutaneously with pyrene did not develop tumors (Shear and Leiter, 1941), but there is evidence that pyrene enhances the tumorigenicity of topically applied benzo[a]pyrene (Slaga et al., 1979; Van Duuren and Goldschmidt, 1976; Goldschmidt et al., 1973).

Based on no human data and inadequate data from animal bioassays, U.S. EPA (1993a,b) has placed pyrene in weight-of-evidence group D, not classifiable as to human carcinogenicity.

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