The Risk Assessment Information System

Toxicity Profiles

Condensed Toxicity Summary for SELENIUM

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.

MARCH 1993

Prepared by: Dennis M. Opresko, Ph.D, Chemical Hazard Evaluation Group, Biomedical Environmental Information Analysis Section, Health and Safety Research Division, Oak Ridge National Laboratory*, 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.

Selenium is an essential trace element important in many biochemical and physiological processes including the biosynthesis of coenzyme Q (a component of mitochondrial electron transport systems), regulation of ion fluxes across membranes, maintenance of the integrity of keratins, stimulation of antibody synthesis, and activation of glutathione peroxidase (an enzyme involved in preventing oxidative damage to cells). Recommended human dietary allowances (average daily intake) for selenium are as follows: infants up to 1 year, 10-15 µg; children 1-10 years, 20-30 µg; adult males 11-51+ years, 40-70 µg; adult females 11-51+ years, 45-55 µg; pregnant or lactating women, 65-75 µg. There appears to be a relatively narrow range between levels of selenium intake resulting in deficiency and those causing toxicity.

Selenium occurs in several valence states: -2 (hydrogen selenide, sodium selenide, dimethyl selenium, trimethyl selenium, and selenoamino acids such as selenomethionine; 0 (elemental selenium); +4 (selenium dioxide, selenious acid, and sodium selenite); and +6 (selenic acid and sodium selenate). Toxicity of selenium varies with valence state and water solubility of the compound in which it occurs. The latter can affect gastrointestinal absorption rates.

Gastrointestinal absorption in animals and humans for various selenium compounds ranges from about 44% to 95% of the ingested dose (Thomson and Stewart, 1974; Bopp et al., 1982; Thomson, 1974). Respiratory tract absorption rates of 97% and 94% for aerosols of selenious acid have been reported for dogs and rats, respectively (Weissman et al., 1983; Medinsky et al., 1981). Selenium is found in all tissues of the body; highest concentrations occur in the kidney, liver, spleen, and pancreas (Schroeder and Mitchener, 1971a; Schroeder and Mitchener, 1972; Jacobs and Forst, 1981a; Julius et al., 1983; Shamberger, 1984; Echevarria et al., 1988). Excretion is primarily via the urine (0-15 g/L); however, excretory products can also be found in the feces, sweat, and in expired air.

In humans, acute oral exposures can result in excessive salivation, garlic odor to the breath, shallow breathing, diarrhea, pulmonary edema, and death (Civil and McDonald, 1978; Carter, 1966; Koppel et al., 1986). Other reported signs and symptoms of acute selenosis include tachycardia, nausea, vomiting, abdominal pain, abnormal liver function, muscle aches and pains, irritability, chills, and tremors. Acute toxic effects observed in animals include pulmonary congestion, hemorrhages and edema, convulsions, altered blood chemistry (increased hemoglobin and hematocrit); liver congestion; and congestion and hemorrhage of the kidneys (Smith et al., 1937; Anderson and Moxon, 1942; Hopper et al., 1985).

General signs and symptoms of chronic selenosis in humans include loss of hair and nails, acropachia (clubbing of the fingers), skin lesions (redness, swelling, blistering, and ulcerations), tooth decay (mottling, erosion and pitting), and nervous system abnormalities attributed to polyneuritis (peripheral anesthesia, acroparaethesia, pain in the extremities, hyperreflexia of the tendon, numbness, convulsions, paralysis, motor disturbances, and hemiplegia). In domesticated animals, subchronic and chronic oral exposures can result in loss of hair, malformed hooves, rough hair coat, and nervous system abnormalities (impaired vision and paralysis). Damage to the liver and kidneys and impaired immune responses have been reported to occur in rodents following subchronic and/or chronic oral exposures (Ganther and Baumann, 1962; Beems and van Beek, 1985; NCI, 1980a; Tinsley et al., 1967; Harr et al., 1967; Schroeder, 1967).

Selenium is teratogenic in birds and possibly also in domesticated animals (pigs, sheep, and cattle), but evidence of teratogenicity in humans and laboratory animals is lacking (ASTDR, 1989). However, adverse reproductive and developmental effects (decreased rates of conception, increased rates of fetal resorption, and reduced fetal body weights) have been reported for domesticated and laboratory animals (Harr and Muth, 1972: Wahlstrom and Olson, 1959; Schroeder and Mitchener, 1971b).

The Reference Dose (RfD) for chronic oral exposures is 0.005 mg/kg/day for both selenium and selenious acid (U.S. EPA, 1992a, 1992b). The subchronic RfDs for these compounds are the same as the chronic RfDs (U.S. EPA, 1992c).

In humans, inhalation of selenium or selenium compounds primarily affects the respiratory system. Dusts of elemental selenium and selenium dioxide can cause irritation of the skin and mucous membranes of the nose and throat, coughing, nosebleed, loss of sense of smell, dyspnea, bronchial spasms, bronchitis, and chemical pneumonia (Clinton, 1947; Hamilton, 1949). Other signs and symptoms following acute inhalation exposures include lacrimation, irritation and redness of the eyes, gastrointestinal distress (nausea and vomiting), depressed blood pressure, elevated pulse rate, headaches, dizziness, and malaise (ATSDR, 1989). In animals, acute inhalation exposures also result in severe respiratory effects including edema, hemorrhage, and interstitial pneumonitis (Hall et al., 1951; Dudley and Miller, 1937) as well as in splenic damage (congestion, fissuring red pulp, and increased polymorphonuclear leukocytes) and liver congestion and mild central atrophy (Hall et al., 1951). Information on toxicity of selenium in humans and animals following chronic inhalation exposures is not available, and subchronic and chronic inhalation Reference Concentrations have not been derived.

Epidemiologic studies in humans havation between chronic oral exposures to selenium and an increased incidence of death due to neoplasms. Some studies have indicated that selenium may have anti-neoplastic properties (see Whanger, 1983; Hocman, 1988). In studies on laboratory animals, selenites or selenates have not been found to be carcinogenic; however, selenium sulfide produced a significant increase in the incidence of hepatocellular carcinomas in male and female rats and in female mice and a significant increase in alveolar/bronchiolar carcinomas and adenomas in female mice following chronic oral exposures (NCI, 1980c). EPA has placed selenium and selenious acid in Group D, not classifiable as to carcinogenicity in humans (U.S. EPA, 1992a and 1992b), while selenium sulfide is placed in Group B2, probable human carcinogen (U.S. EPA, 1992d). Quantitative data are, however, insufficient to derive a slope factor for selenium sulfide. Pertinent data regarding the potential carcinogenicity of selenium by the inhalation route in humans or animals were not located in the available literature.

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Last Updated 2/13/98

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