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, Chemical Hazard Evaluation and Communication Group, Biomedical and Environmental Information Analysis Section, Health and Safety Research Division, *.
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.
Anthracene, also referred to as paranaphthalene or green oil, is a polycyclic aromatic hydrocarbon (PAH) derived from coal tar and is primarily used as an intermediate in the production of dyes. It has also been used in the production of smoke screens. Anthracene is ubiquitous in the environment as a product of incomplete combustion of fossil fuels. Although a large body of literature exists on the toxicity and carcinogenicity of a number of PAHs, toxicity data for anthracene are limited.
Evidence indicates that anthracene is absorbed following oral and dermal exposure. Targets for anthracene toxicity are the skin, hematopoietic system, lymphoid system, and gastrointestinal tract. Adverse dermatologic effects have been observed in humans and animals in conjunction with acute and subchronic exposure to anthracene. In humans, anthracene may cause acute dermatitis with symptoms of burning, itching, and edema. Prolonged dermal exposure produces pigmentation, cornification of skin surface layers, and telangiectasis (Volkova, 1983). Anthracene is photosensitizing, potentiating skin damage elicited by exposure to ultraviolet (UV) radiation (U.S. EPA, 1987; Dayhaw-Barker et al., 1985; Forbes et al., 1976). Hematologic toxicity was observed in patients receiving intraperitoneal injections of anthracene-containing chemotherapeutic agents (Falkson et al., 1985) and in rats exposed to anthracene by oral gavage and by inhalation (Volkova, 1983). Mice receiving subcutaneous injections of anthracene exhibited adverse lymphoid effects (Hoch-Ligeti, 1941). Long-term use of anthracene-containing laxatives produced melanosis of the colon and rectum (Badiali et al., 1985). Human exposure to anthracene has also been associated with headache, nausea, loss of appetite, inflammation of the gastrointestinal tract, slow reactions, and weakness (Volkova, 1983).
A Reference Dose (RfD) of 3 mg/kg/day for subchronic oral exposure and 0.3 mg/kg/day for chronic oral exposure to anthracene was calculated from a no-observed-adverse-effect level (NOAEL) of 1000 mg/kg/day derived from a 90-day gavage study with mice (U.S. EPA, 1989). Data were insufficient to derive an inhalation Reference Concentration (RfC) for anthracene (U.S. EPA, 1991a,b).
Carcinogenicity bioassays with anthracene generally gave negative results. Studies involving oral administration (Druckrey and Schmahl, 1955; Schmahl, 1955) or intrapulmonary implantation in rats (Stanton et al., 1972) or implantation into the brain of rabbits (Russell, 1947) provided no evidence of carcinogenicity. Negative results were also obtained when anthracene was tested in mice by skin application (Wynder and Hoffman, 1959; Pollia, 1939; Kennaway, 1924a,b) and in mouse-skin initiation assays (LaVoie et al., 1979; Scribner, 1973). However, skin application of anthracene followed by exposure to UV radiation or visible light induced a high incidence of skin tumors in mice (Heller, 1950).
Based on no human data and inadequate data from animal bioassays, U.S. EPA (1991a,b) has placed anthracene in weight-of-evidence group D, not classifiable as to human carcinogenicity.
Anthracene (CAS No. 120-12-7), also referred to as paranaphthalene or green oil, is the simplest tricyclic aromatic hydrocarbon and has a chemical formula of C14H10 and molecular weight of 178. Having a melting point of 216C and a boiling point of 340C, anthracene is a colorless crystalline compound with violet fluorescence. It is soluble in a variety of organic solvents, including ethanol, methanol, benzene, toluene, and carbon disulfide, but is almost insoluble in water (Budavari et al., 1989; U.S. EPA, 1987). It is susceptible to oxidation by ozone, peroxides, and other oxidants (U.S. EPA, 1987). Anthracene is derived from coal tar and is primarily used as an intermediate in the production of dyes. It has also been used in the production of smoke screens, scintillation counter crystals, and organic semiconductor research (Hawley, 1987; IARC, 1983). Anthracene is ubiquitous in the environment as a product of incomplete combustion of fossil fuels. It has been identified in surface and drinking water, ambient air, exhaust emissions from internal combustion engines, smoke of cigarettes and cigars, and in smoked foods and edible aquatic organisms. Anthracene is one of a number of polycyclic aromatic hydrocarbons (PAHs) on EPA's priority pollutant list (ATSDR, 1990; U.S. EPA, 1987). Although a large body of literature exists on the toxicity and carcinogenicity of other PAHs, toxicity data for anthracene are limited.
Indirect evidence suggests that anthracene is absorbed following oral exposure. Rats ingesting diets containing 0.2-1.0% anthracene or receiving 200 mg anthracene by gavage eliminated 43-84% of the dose in feces within 2-3 days (Chang, 1943). The efficiency of intestinal absorption of anthracene in the rat appears to be influenced by the presence of bile in the intestine. When the bile was diverted from the intestine by bile duct cannulation, the absorption of anthracene was only 70.8% of that observed in the presence of normal amounts of bile (Rahman et al., 1986). In general, oral absorption of PAHs is enhanced when the compounds are solubilized in a vehicle that is readily absorbed, such as certain oils (ATSDR, 1990).
The presence of anthracene in the blood of humans following dermal application of 2% crude coal tar on two consecutive days provided evidence of percutaneous absorption of anthracene (Storer et al., 1984). Yang et al. (1986) estimated that 52% of a single application of 9.3 µg/cm2 anthracene to the shaved backs of rats was absorbed in six days. The permeation of anthracene decreased significantly over time. Diffusion through the stratum corneum depended on the amount of anthracene on the skin's surface.
Anthracene was detected in the blood of humans following topical applications of 2% crude coal tar on two consecutive days (Storer et al., 1984). Anthracene concentrations in human liver and fat samples obtained at autopsy ranged from 110 to 240 ppt and from 25 to 575 ppt, respectively (Obana et al., 1981). Although anthracene readily penetrates the skin, very little is distributed to tissues. Only 1.3% of a dermally applied dose of anthracene (9.3 µg/cm2) was detected in tissues (unspecified) of rats six days after administration (Yang et al., 1986).
Following a single intratracheal instillation of 14C-anthracene, 99.7% and 0.3% of the administered radioactivity was cleared from the lungs, with half-times of 0.1 hour and 25.6 hours, respectively (Bond et al., 1985). Studies with mice subcutaneously injected with anthracene during gestation indicate that anthracene can pass through placental membranes (U.S. EPA, 1990).
Metabolites resulting from epoxidation at the 1,2-bond of anthracene have been identified in the urine of rats and rabbits fed diets containing anthracene (Sims, 1964; Boyland and Burrows, 1935; Boyland and Levi, 1935) and in in vitro studies that incubated anthracene with rat liver microsomes (Akhtar et al., 1979). The major metabolic product is the 1,2-dihydrodiol of anthracene and its sulfate and glucuronide conjugates. Metabolites resulting from oxidation at the 9- and 10-positions of anthracene such as 9,10-dihydrodiol and 2,9,10-trihydroxyanthracene were identified in rat urine (Sims, 1964) but not in in vitro studies using hepatic microsomes (Akhtar et al., 1979), suggesting possible extrahepatic origin.
No studies were located regarding the excretion of anthracene in humans. Orally administered anthracene appears to be eliminated by rats primarily (53-84%) in the feces (Chang, 1943). Metabolites of orally administered anthracene have been detected in the urine of rats (Sims, 1964). Six days after dermal application of 9.3 µg/cm2 of anthracene, rats eliminated 29% and 22% of the applied dose in urine and feces, respectively (Yang et al., 1986).
Information on the acute oral toxicity of anthracene in humans was unavailable.
Nagornyi (1969) reported that single oral doses of 1.47 or 2.44 g/kg of commercial anthracene or 17 g/kg of pure anthracene were not lethal to mice. Observed toxic effects included fatigue, asthenia, hyperemia of the kidney, liver, heart, and lungs, lipid changes of the liver, and leukocytosis. Orally administered anthracene (50 mg/mL corn oil by gavage) followed by ultraviolet (UV) radiation of the skin for 1 hour produced keratitis of the exposed skin in mice. This effect was less pronounced in mice exposed only to UV light and was not evident in vehicle controls (Dayhaw-Barker et al., 1985).
Information on the subchronic oral toxicity of anthracene in humans was unavailable.
Crl:CD-1 mice were treated by gavage once daily for 90 days with 0, 250, 500, or 1000 mg anthracene/kg/day (U.S. EPA, 1989). There were no compound-related effects on survival, clinical signs, body weight, food consumption, ophthalmology, clinical chemistry, organ weights, gross pathology, or histopathology.
Repeated intragastric exposure of rats to anthracene (dose and duration not specified) gave rise to a decrease in hemoglobin, reticulocytosis, leukopenia, and an increase in residual blood nitrogen (Volkova, 1983). Intragastric administration of 100 mg anthracene/kg/day for 4 days induced increased carboxylesterase activity in the gastrointestinal mucosa (Nousiainen et al., 1984) and a slight increase in liver cytosolic aldehyde dehydrogenase activity of rats (Torronen et al., 1981). Anthracene did not stimulate liver regeneration (an indicator of the ability to induce a proliferative process) in partially hepatectomized rats fed diets containing 514 mg/kg/day for 10 days (Gershbein, 1975).
Patients who periodically consumed anthracene-containing laxatives over a 30-year period had an increased incidence (73.4%) of melanosis (unusual deposit of black pigments) of the colon and rectum compared with individuals who did not use such laxatives (26.6%) (Badiali et al., 1985).
In a chronic bioassay, Schmahl (1955) exposed BDI and BDIII rats to diets containing anthracene at an estimated daily dose of 5-15 mg/rat. The experiment was terminated when a total dose of 4.5 g/rat was achieved or on the 550th day of the experiment. No treatment-related effects on lifespan or gross and histological appearance of tissues were observed.
Information on the oral developmental and reproductive toxicity of anthracene in humans or animals was unavailable.
Information on the acute and subchronic inhalation toxicity of anthracene in humans or animals was unavailable.
Information on the chronic inhalation toxicity of anthracene in humans was unavailable.
Chronic inhalation of an aerosol containing 0.05 or 0.01 mg/L anthracene (duration not specified) was associated with reduced body weight gain, decreased hemoglobin levels, reticulocytosis, leukopenia, and an increase in residual blood nitrogen in rats (Volkova, 1983).
Information on the inhalation developmental and reproductive toxicity in humans or animals was unavailable.
Available data are insufficient to calculate an RfC.
Topically applied anthracene increases the sensitivity of human skin to ultraviolet light (U.S. EPA, 1987). Anthracene can cause acute dermatitis with symptoms of burning, itching, and edema which, are more pronounced in bare skin regions. Other symptoms are irritation of the upper airways, lacrimation, photophobia, edema of the eye lids, and conjunctival hyperemia. The acute symptoms disappear within several days after cessation of contact (Volkova, 1983).
The intraperitoneal LD50 for the mouse is > 430 mg/kg (Salamone, 1981). Acute (96-hour) dermal application of anthracene to the backs of hairless mice, followed by ultraviolet radiation (UV) exposure for 40 minutes, resulted in enhanced dermal inflammation compared to mice exposed exclusively to UV. However, this effect was reversed within 48 hours (Forbes et al., 1976).
Hematopoietic toxicity was observed in patients with primary liver or metastatic breast cancer who had been treated intermittently for 9 weeks by intravenous injection with mitoxantrone or bisantrene, both anthracene-containing chemotherapeutic agents (Falkson et al., 1985). The primary effects were myelosuppression, characterized by leukopenia and thrombocytopenia. However, the amount of anthracene in the drugs and presence of other components were not identified.
Prolonged dermal exposure to anthracene produced pigmentation of bare skin regions, cornification of skin surface layers, and telangiectasis. The photosensitizing effect of industrial anthracene is more pronounced than that of pure anthracene due to the presence of other heavy hydrocarbons, such as acridine, carbazole, and phenanthrene. Other effects that could not be attributed to a specific route of exposure included headache, nausea, loss of appetite, inflammation of the gastrointestinal tract, slow reactions, and weakness (Volkova, 1983).
In a study by Gerarde (1960), 9/10 mice survived seven daily intraperitoneal injections of anthracene at doses of 500 mg/kg/day. Daily intraperitoneal injections of 160 µmol/kg anthracene for 14 days did not significantly affect the immune response in B6C3F1 mice (White et al., 1985).
Lymphoid effects including treatment-related increases in reticulum cells, accumulation of iron, decreased lymphoid cells, and dilated lymph sinuses were seen in albino mice receiving weekly subcutaneous injections of a 0.05% colloidal solution of anthracene in gelatin for 40 weeks (Hoch-Ligeti, 1941).
Daily applications of 40% anthracene in vaseline to the skin of guinea pigs caused reddening of the skin, whereas applications of industrial grade anthracene (containing 20% anthracene) gave rise to swelling and soreness (Volkova, 1983).
Information on the chronic toxicity of anthracene by other routes of exposure in humans or animals is unavailable.
Information on the developmental and reproductive toxicity of anthracene in humans by other routes of exposure is unavailable.
Shabad et al. (1972) administered anthracene (total dose 8 mg/mouse) as a daily subcutaneous injection or as a single dose during the last week of gestation to dams of three strains of mice. Fetuses were removed and kidney cells established in culture. The fetal cells exhibited enhanced plating efficiency as well as some hyperplastic changes by comparison with fetal cells obtained from untreated animals.
Information on other target organs following oral exposure to anthracene toxicity was not available.
Information on other target organs following inhalation exposure to anthracene was not available.
Information concerning target organs following other routes of exposure to anthracene was not available.
Information on the carcinogenicity of anthracene in humans was unavailable.
Administration of diets that supplied a total dose of 4.5 g anthracene/rat over 78 weeks produced tumors in 2/28 BDI or BDIII rats. One liver sarcoma was observed after 18 months and one uterine adenocarcinoma after 25 months (Druckrey and Schmahl, 1955; Schmahl, 1955). A control group was not used and the tumors were not ascribed to treatment.
Information on the carcinogenicity of anthracene in humans or animals was unavailable.
Three cases of epithelioma of the hand, cheek, and wrist, respectively, were reported in men handling 40% crude anthracene (composition not characterized). Two of the workers had been exposed to crude anthracene for 30 and 32 years, respectively. Workers in the same factory who had contact only with purified anthracene did not develop tumors or other skin lesions (Kennaway, 1924a,b).
No lung tumors were observed in female Osborne-Mendel rats one year after receiving single lung implants of 0.5 mg anthracene dissolved in a 1:1 mixture of beeswax and tricaprylin (Stanton et al., 1972). Implants of pellets containing 4-20 mg anthracene into the cerebrum, cerebellum, or eye of rabbits did not induce gliomas. However, nonspecific granulomatous reactions were seen in all rabbits. The animals died or were killed between 20 and 54 months after implantation (Russell, 1947).
Several tests for complete carcinogenicity and skin tumor initiating activity do not provide evidence of carcinogenicity for anthracene, but contradictory results were obtained when the chemical was applied to the skin with exposure to UV radiation. Swiss mice receiving topical applications of 10% anthracene in acetone to their backs 3 times/week for life did not develop skin tumors after 20 months (Wynder and Hoffman, 1959). No skin tumors were reported in mice given skin applications of 40% anthracene in lanolin or of anthracene in benzene or sesame oil (dose and number of applications not specified) (Pollia, 1939; Kennaway, 1924a,b).
Skin application of 10% anthracene followed by either UV radiation alone or with exposure to visible light induced a high incidence of skin tumors in white mice 5-8 weeks after the start of treatment. Many of the skin tumors were carcinomas, several of which had metastasized. No skin tumors were seen in control groups (Heller, 1950). By contrast, the incidence of skin tumors was not significantly increased in a study by Forbes et al (1976) in which hairless mice received daily topical applications of 4 µg anthracene, followed by UV radiation for 2 hours, for 38 weeks.
LaVoie et al. (1979) evaluated the tumor-initiating ability of anthracene by applying 1 mg of anthracene in acetone to the skin of female CRl:CD/1 mice followed by three weekly applications of 12-o-tetradecanoyl-phorbol-13-acetate (TPA) as a promoting agent for 20 weeks. There was no significant increase in the incidence of skin tumors compared with controls. In another initiation study, a single dermal application of 10 µm anthracene in benzene was administered to female CD-1 mice; this treatment was followed by twice-weekly applications of TPA for 35 weeks. By week 20, 2/28 mice developed skin tumors; this increased to 4/28 by week 35. One control mouse developed a skin tumor at week 25 (Scribner, 1973).
Dermal application of 200 µg (0.05 mg/cm2) anthracene to the backs of mice did not induce melanocyte activation (Iwata et al., 1981).
Although several noncarcinogenic PAHs have been shown to reduce the ability of benzo(a)pyrene to produce injection site sarcomas, anthracene exhibited no such inhibitory effects (Falk and Kotin, 1964).
Classification D -- Not classifiable as to human carcinogenicity (U.S. EPA, 1991a,b)
Basis -- Based on no human data and on inadequate data from animal bioassays.
None were calculated.
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