Toxicity Profiles
Condensed Toxicity Summary for BENZ[A]ANTHRACENE
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.
September 1992
Prepared by: Andrew Francis, Chemical Hazard Evaluation Group, Biomedical Environmental Information Analysis Section, Health and Safety 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.
Benz[a]anthracene, along with a number of other polycyclic aromatic hydrocarbons, are natural products produced by the incomplete combustion of organic material. The arrangement of the aromatic rings in the benz[a]anthracene molecule gives it a "bay region" often correlated with carcinogenic properties. In general, the bay-region polycyclic aromatic hydrocarbons and some of their metabolites are known to react with cellular macromolecules, including DNA, which may account for both their toxicity and carcinogenicity. The inducible mixed-function oxidase enzymes oxidize benz[a]anthracene to form metabolites with increased water solubility that can be efficiently excreted in the urine. A minor product of this oxidation, a bay-region diol epoxide, reacts readily with DNA and has been shown to be highly carcinogenic (U.S. EPA, 1980; 1984; Jerina, et al., 1977).
The toxic effects of benz[a]anthracene and similar polycyclic aromatic hydrocarbons are primarily directed toward tissues that contain proliferating cells. Animal studies indicate that exposure to bay-region polycyclic aromatic hydrocarbons can damage the hematopoietic system leading to progressive anemia as well as agranulocytosis (Robinson, et al., 1975; Cawein and Sydnor, 1968). The lymphoid system can also be affected resulting in lymphopenia. Toxic effects have been observed in the rapidly dividing cells of the intestinal epithelium, spermatogonia and resting spermatocytes in the testis and primary oocytes of the ovary (Philips et al., 1973; Mackinzie and Angevine, 1981; Kraup, 1970; Ford and Huggins, 1963; Mattison and Thorgeirsson, 1977; U.S. EPA, 1980; 1984). Most of these effects have occurred following both oral and parenteral exposure. Epithelial proliferation and cell hyperplasia in the respiratory tract have been reported following subchronic inhalation exposure (Reznik-Schuller and Mohr, 1974; Saffiotti et al., 1968). However, because of the lack of quantitative data, neither a reference dose nor a reference concentration have been derived (U.S. EPA, 1991).
The primary concern with benz[a]anthracene exposure is its potential carcinogenicity. There is
no unequivocal, direct evidence of the carcinogenicity of the compound to humans, however,
benz[a]anthracene and other known carcinogenic polycyclic aromatic hydrocarbons are components
of coal tar, soot, coke oven emissions and tobacco smoke. There is adequate evidence of its
carcinogenic properties in animals. Oral exposures of mice to benz[a]anthracene have resulted in
hepatomas, pulmonary adenomas and forestomach papillomas (Klein, 1963; Bock and King, 1959; U.S.
EPA, 1991). The EPA weight-of-evidence classification is: B2, probable human carcinogen, for both
oral and inhalation exposure based on adequate animal evidence and no human evidence (U.S. EPA,
1991). A slope factor has not been derived specifically for benz[a]anthracene by the EPA (U.S. EPA,
1991). However, an oral slope factor of 7.3 (mg/kg/day)-1 has been calculated for benzo[a]pyrene
based on the incidence of stomach tumors in mice treated with benzo[a]pyrene (Neal and Rigdon,
1967; U.S. EPA, 1980; 1984; 1992a). A drinking water unit risk of 2.1E-4 (g/L)-1 has also been
calculated for benzo[a]pyrene (U.S. EPA, 1992a). An inhalation slope factor of 6.1 (mg/kg/day)-1
(U.S. EPA, 1992b) was calculated for benzo[a]pyrene based on the incidence of respiratory tumors in
golden hamsters treated with benzo[a]pyrene (Thyssen et al., 1981; U.S. EPA, 1980; 1984). An
inhalation unit risk of 1.7E-3 (g/m3)-1 has also been calculated for benzo[a]pyrene (U.S. EPA,
1992b).
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