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: Dennis M. Opresko, Ph.D., Chemical Hazard Evaluation Group in the Biomedical and Environmental Information Analysis Section, Health Sciences Research Division, Oak Ridge National Laboratory*.
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.
Ethylbenzene is a colorless, flammable liquid with a pungent odor (Cavender 1994). The water solubility of ethylbenzene is 0.014 g/100 mL and its vapor pressure is 10 mm Hg at 25C (Budavari et al. 1989). Ethylbenzene is commonly used as a solvent, chemical intermediate in the manufacture of styrene and synthetic rubber and as an additive in some automotive and aviation fuels (Cavender 1994). Occupational exposure to ethylbenzene may occur during production and conversion to polystyrene and during production and use of mixed xylenes (Fishbein 1985). The general public can be exposed to ethylbenzene in ambient air as a result of releases from vehicle exhaust and cigarette smoke (Fishbein 1985).
Ethylbenzene can be absorbed through the lungs, digestive tract, and skin (Fishbein 1985). It also crosses the placenta (Cavender 1994). The liver is the major organ of ethylbenzene metabolism. In humans the major metabolites of ethylbenzene are mandelic acid (64 to 70%) and phenylglyoxylic acid (25%) (Bardodej and Bardodejova 1970, Fishbein 1985, Cavender 1994); however, these compounds are only minor metabolites in laboratory animals (EPA 1995). Excretion occurs primarily in the urine (NTP 1992, Climie et al. 1983).
Ingestion of sublethal amounts of ethylbenzene is likely to cause central nervous system (CNS) depression, oro-pharyngeal and gastric discomfort, and vomiting (HSDB 1995); however, specific experimental data are not available. Animal studies indicate that the primary target organs following chronic oral exposures are likely to be the liver and kidney. The oral RfD for chronic exposures is 0.1 mg/kg/day, based on increased weight and histopathological changes in the liver and kidneys of rats (EPA 1996).
Acute exposures to high atmospheric concentrations of ethylbenzene may cause eye and respiratory tract irritation and CNS effects (e.g., coordination disorders, dizziness, vertigo, narcosis, convulsions, pulmonary irritation, and conjunctivitis) (Ivanov 1962). Concentrations of 1000 ppm (434 mg/m3) can be highly irritating to the eyes of humans (Yant et al. 1930); the threshold for eye irritation has been reported to be 200 ppm (879 mg/m3) (Grabt 1986). No evidence is available to suggest that occupational exposures to ethylbenzene result in chronic toxic effects (Fishbein 1985); however, histopathological changes in the liver and kidney have been observed in experimental animals following prolonged inhalation exposures. Laboratory studies also indicate that exposure to ethylbenzene (4340 mg/m3) during gestation results in adverse developmental effects in rats (skeletal variants) and rabbits (reduced number of live offspring per litter). The no-observed-adverse-effect level (NOAEL) for developmental effects was reported to be 434 mg/m3. The inhalation RfC for chronic exposures is 1 mg/m3, based on developmental effects (EPA 1996).
No epidemiological information is available on the potential carcinogenicity of ethylbenzene in humans following oral or inhalation exposures. A statistically significant increase in total malignant tumors was observed in female rats dosed orally with ethylbenzene (Maltoni et al. 1985); however, because of study limitations, these results cannot be considered conclusive. Although ethylbenzene has been tested by NTP in a two-year rodent bioassay, the results of that study are not yet available (NTP 1995). Ethylbenzene is placed by EPA in Group D, not classifiable as to human carcinogenicity, based on a lack of data in humans and animals (EPA 1996).Retrieve Toxicity Profiles Formal Version
Last Updated 8/29/97