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, 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
Acenaphthene, also known as 1,2-dihydroacenaphthylene or 1,8-ethylenenaphthalene, is a tricyclic aromatic hydrocarbon that occurs in coal tar. It is used as a dye intermediate, in the manufacture of some plastics, and as an insecticide and fungicide (EPA, 1980). Acenaphthene has been detected in cigarette smoke, automobile exhausts, and urban air; in effluents from petrochemical, pesticide, and wood preservative industries (EPA, 1980); and in soils, groundwater, and surface waters at hazardous waste sites (ATSDR, 1990).
No absorption data are available for acenaphthene; however, by analogy to structurally-related polycyclic aromatic hydrocarbons (PAHs), it would be expected to be absorbed from the gastrointestinal tract and lungs (EPA, 1988). The anhydride of naphthalic acid was identified as a urinary metabolite in rats treated orally with acenaphthene (Chang and Young, 1943).
Although a large body of literature exists on the toxicity and carcinogenicity of PAHs, primarily benzo[a]pyrene, toxicity data for acenaphthene are limited. Acenaphthene is irritating to the skin and mucous membranes of humans and animals (Sandmeyer, 1981; Knobloch et al., 1969). Acute toxicity data for animals include oral LD50s of 10 g/kg for rats and 2.1 g/kg for mice (Knobloch et al., 1969) and an intraperitoneal LD50 of 600 mg/kg for rats (Reshetyuk et al., 1970). Oral exposure of rats to daily 2-g doses of acenaphthene for 32 days produced peripheral blood changes, mild liver and kidney damage, and pulmonary effects (Knobloch et al., 1969). Subchronic oral exposure to acenaphthene at doses of > 350 mg/kg for 90 days produced increased liver weights, hepatocellular hypertrophy, and increased cholesterol levels in mice. Reproductive effects included decreased ovary weights at doses of > 350 mg/kg and decreased ovarian and uterine activity as well as smaller and fewer corpora lutea at 700 mg/kg/day (EPA, 1989). Adverse effects on the blood, lungs, and glandular tissues were reported in rats exposed daily to 12 mg/m3 of acenaphthene for 5 months (Reshetyuk et al., 1970).
A reference dose (RfD) of 6E-1 mg/kg/day for subchronic oral exposure (EPA, 1993a) and 6.E-2 mg/kg/day for chronic oral exposure to acenaphthene (EPA, 1993b) was calculated from a no-observed- adverse-effect level (NOAEL) of 175 mg/kg/day from a 90-day gavage study with mice. The critical effect was hepatotoxicity. Data were insufficient to derive an inhalation reference concentration (RfC) for acenaphthene (EPA, 1993a,b).
No oral bioassays were available to assess the carcinogenicity of acenaphthene. A limited inhalation study in which rats were exposed to 12 mg/m3 acenaphthene for 5 months and observed an additional 8 months provided no evidence of carcinogenicity (Reshetyuk et al., 1970). The EPA has not assigned a weight-of-evidence classification for carcinogenicity to acenaphthene (EPA, 1993a,b). Retrieve Toxicity Profiles Formal Version
Last Updated 10/07/97