Toxicity Profiles
Condensed Toxicity Summary for ANTIMONY
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.
DECEMBER 1992
Prepared by Robert A. Young, Ph.D., D.A.B.T., Chemical Hazard Evaluation and Communication Group, Biomedical and 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.
Antimony (Sb) is a naturally occurring metal that is used in various manufacturing processes. It exists in valence states of 3 and 5 (Budavari, 1989; ATSDR, 1990). Antimony is a common urban air pollutant (Beliles, 1979). Exposure to antimony may be via inhalation, oral and dermal routes (ATSDR, 1990).
Antimony is sparingly absorbed following ingestion or inhalation (Felicetti et al., 1974a; Gerber et al., 1982; ATSDR, 1990). Both gastrointestinal and pulmonary absorption are a function of compound solubility. Antimony is transported in the blood, its distribution varying among species and dependent on its valence state (Felicetti et al., 1974b). Antimony is not metabolized but may bind to macromolecules and react covalently with sulfhydryl and phosphate groups (ATSDR, 1990). Excretion of antimony is primarily via the urine and feces, and is also dependent upon valence state (Cooper et al., 1968; Ludersdorf et al., 1987; ATSDR, 1990).
Acute oral exposure of humans and animals to high doses of antimony or antimony-containing compounds (antimonials) may cause gastrointestinal disorders (vomiting, diarrhea), respiratory difficulties, and death at extremely high doses (Bradley and Frederick, 1941; Beliles, 1979; ATSDR, 1990). Subchronic and chronic oral exposure may affect hematologic parameters (ATSDR, 1990). Long-term exposure to high doses of antimony or antimonials has been shown to adversely affect longevity in animals (Schroeder et al., 1970). Limited data suggest that prenatal and postnatal exposure of rats to antimony interferes with vasomotor responses (Marmo et al., 1987; Rossi et al., 1987).
Acute inhalation exposure of humans may cause gastrointestinal disorders (probably due to ingestion of airborne antimony) (ATSDR, 1990). Exposure of animals to high concentrations of antimony and antimonials (especially stibine gas) may result in pulmonary edema and death (Price et al., 1979). Long-term occupational exposure of humans has resulted in electrocardiac disorders, respiratory disorders, and possibly increased mortality (Renes, 1953; Breiger et al., 1954). Antimony levels for these occupational exposure evaluations ranged from 2.2 to 11.98 mg Sb/m3. Based on limited data, occupational exposure of women to metallic antimony and several antimonials has reportedly caused alterations in the menstrual cycle and an increased incidence of spontaneous abortions (Belyaeva, 1967). Reproductive dysfunction has been demonstrated in rats exposed to antimony trioxide (Belyaeva, 1967).
No data were available indicating that dermal exposure of humans to antimony or its compounds results in adverse effects. However dermal application of high doses of antimony oxide (1,584 mg Sb/kg) resulted in the death of rabbits within one day (IBTL, 1972). Eye irritation due to exposure to stibine gas and several antimony oxides has been reported for humans (Stevenson, 1965; Potkonjak and Pavlovich, 1983).
The U. S. EPA (U.S. EPA, 1991, 1992) has calculated subchronic and chronic oral reference doses (RfDs) of 4E-4 mg/kg/day based on decreased longevity and alteration of blood chemistry in rats chronically exposed to potassium antimony tartrate in the drinking water (5 ppm equivalent to 0.35 mg Sb/kg/day). An uncertainty factor of 1,000 was applied: 10 for extrapolation from a lowest-observed-adverse-effect-level (LOAEL) to a no-observed-adverse-effect-level (NOAEL), 10 for extrapolation from animal data, and 10 for protection of sensitive populations.
The primary target organ for acute oral exposure to antimony appears to be the gastrointestinal tract (irritation, diarrhea, vomiting) and targets for long-term exposure are the blood (hematological disorders) and liver (mild hepatotoxicity) (ATSDR, 1990). Inhalation exposure to antimony affects the respiratory tract (pneumoconiosis, restrictive airway disorders), with secondary targets being the cardiovascular system (altered blood pressure and electrocardiograms) and kidneys (histological changes) (Renes, 1953; Breiger et al., 1954). Only limited evidence exists for reproductive disorders due to antimony exposure (Belyaeva, 1967).
Although some data indicate that long-term exposure of rats to antimony trioxide and
trisulfide increased the incidence of lung tumors (Wong et al., 1979; Watt, 1980; Groth et al.,
1986; Bio/dynamics, 1989), the U.S. EPA has not evaluated antimony or antimonials for
carcinogenicity and a Weight-of-Evidence classification is currently unavailable.
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