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: H. T. Borges, Ph.D., MT(ASCP), D.A.B.T., Chemical Hazard Evaluation Group, 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.
This report is an update of the Toxicity Summary for Chrysene (CAS Registry No. 218-01-9). The original summary for this chemical was submitted in November 1991. The update was performed by incorporating any new human health toxicity data published since the original submittal of the report. Pertinent pharmacokinetic, toxicologic, carcinogenic, and epidemiologic data were obtained through on-line searches of the TOXLINE database from 1991 through 1994. In addition, any changes to EPA-approved toxicity values (reference doses, reference concentrations, or cancer slope factors) from the Integrated Risk Information System (IRIS) (current as of December 1994) and/or the Health Effects Assessment Summary Tables, Annual FY-94 and July Supplement No. 1, for this chemical were incorporated in this update.
Chrysene, a polycyclic aromatic hydrocarbon, is a ubiquitous environmental contaminant formed primarily by the incomplete combustion of organic compounds. Although present in coal and oil, the presence of chrysene in the environment is the result of anthropogenic activities such as coal combustion and gasification; gasoline exhaust; diesel and aircraft exhaust; and emissions from coke ovens, wood burning stoves, and waste incineration (IARC, 1983; ATSDR, 1990). Chrysene is not produced or used commercially, and its use is limited strictly to research applications.
Little information on the absorption, distribution, metabolism and excretion of chrysene in humans is available. Animal studies have shown that approximately 75% of the administered chrysene may be absorbed by oral, dermal, or inhalation routes (Grimmer et al., 1988; Modica et al., 1983; Chang, 1943). Following its absorption, chrysene is preferentially distributed to highly lipophilic regions of the body, most notably adipose and mammary tissue (Bartosek et al., 1984; Modica et al., 1983). Phase I metabolism of chrysene, whether in the lung, skin, or liver, is mediated by the mixed function oxidases. The metabolism results in the formation of 1,2-, 3,4-, and 5,6-dihydrodiols as well as the formation of 1-, 3-, and 4-phenol metabolites (Sims, 1970; Nordquist et al., 1981; Jacob et al., 1982, 1987). Additional Phase I metabolism of chrysene 1,2-dihydrodiol forms chrysene 1,2-dihydrodiol-3,4-epoxide and 9-hydroxychrysene 1,2-diol-3,4-oxide. These metabolites were shown to have mutagenic and alkylating activity (Hodgson et al., 1983; Wood et al., 1977; Wood et al., 1979). Phase II metabolism of chrysene results in the formation of glucuronide and sulfate ester conjugates; however, glutathione conjugates of diol- and triol-epoxides are also formed (Sims and Grover, 1974, 1981; Hodgson et al., 1986; Robertson and Jernström, 1986). Hepatobiliary secretion with elimination in the feces is the predominant route of excretion (Schlede et al., 1970; Grimmer et al., 1988).
Human or animal systemic, developmental, and reproductive health effects following exposure to chrysene were not identified. Because of the lack of systemic toxicity data, the reference dose (RfD) and the reference concentration (RfC) for chrysene have not been derived (EPA, 1994a, b). Target organs have not been described, although chrysene may induce immunosuppression similar to certain other PAHs. Oral and inhalation carcinogenic bioassays were not identified. In mouse skin painting studies, chrysene was an initiator of papillomas and carcinomas. In addition, intraperitoneal injections of chrysene have induced liver adenomas and carcinomas in male CD-1 and BLU/Ha Swiss mice. Although oral and inhalation slope factors have not been derived, EPA (1994a,b) has classified chrysene in weight-of-evidence Group B2, probable human carcinogen, based on the induction of liver tumors and skin papillomas and carcinomas following treatment and the mutagenicity and chromosomal abnormalities induced in in vitro tests. Retrieve Toxicity Profiles Formal Version
Last Updated 8/29/97