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Hazardous Air Pollutants (HAPs)

Other Classes -> Other Inorganic Compounds

Trace element

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phonon wavenumber

4.28 (NIOSH, 2024) - Denser than water; will sink

4.39 g/cu cm (alpha form); 4.809 g/cu cm (gray selenium); 4.28 g/cu cm (vitreous selenium)

Vitreous, Black selenium; dark red-brown to bluish-black solid; density = 4.28; softens at 50 to 60 °C and becomes elastic at 70 °C. Red amorphous form; density = 4.26. When freshly precipitated, reacts with water at 50 °C forming selenious acid and hydrogen. Soluble in carbon disulfide, methylene iodide, benzene or quinoline /amorphous forms/

Relative density (water = 1): 4.8

4.28

4.809 @25 °C

Selenium exists in several allotropic forms. 3 are generally recognized ... Selenium can be prepd with either amorphous or crystalline structure. ... Amorphous is either red, in powder form or black, in vitreous form. Crystalline monoclinic selenium is deep red; crystalline hexagonal form, the most stable variety, is a metallic gray.

Insoluble (NIOSH, 2024)

Insoluble

Soluble in aq potassium cyanide soln, potassium sulfite soln, dilute aqueous caustic alkali soln

Insoluble in water and alcohol

Soluble in concentrated nitric acid.

Soluble in carbon disulfide, 2 mg/100 mL at room temperature; soluble in ether

1265 °F at 760 mmHg (NIOSH, 2024)

1265 °F

685 °C

685 °C

1265 °F

685 °C @760 [mm Hg]

Danger

H301: Toxic if swallowed [Danger Acute toxicity, oral]

P260, P261, P264, P270, P271, P273, P301+P316, P304+P340, P316, P319, P321, P330, P403+P233, P405, and P501 (click each P-code to see the statement)

Danger

H301+H331 (27.4%): Toxic if swallowed or if inhaled [Danger Acute toxicity, oral; acute toxicity, inhalation]

P260, P261, P264, P270, P271, P273, P301+P316, P304+P340, P316, P319, P321, P330, P403+P233, P405, and P501 (click each P-code to see the statement)

Chemical: Selenium

Regulation (EC) No 1935/2004 (amended)

Selenium is listed on the EPA's Chemical Data Reporting (CDR) system. Manufacturers and importers of Selenium are required to report information about their production and use of this chemical to the EPA under the Toxic Substances Control Act (TSCA). (40 eCFR Part 711)

Status: Active Update: 04-10-2021 https://echa.europa.eu/registration-dossier/-/registered-dossier/15204

Selenium: Does not have an individual approval but may be used under an appropriate group standard

The New Jersey Worker and Community Right to Know Act requires public and private employers to provide information about hazardous substances at their workplaces. (N.J.S.A. 34:5A-1 et. seq.)

Excerpt from ERG Guide 151 [Substances - Toxic (Non-Combustible)]:

Not combustible. Gives off irritating or toxic fumes (or gases) in a fire. Risk of fire and explosion on contact with oxidants.

Selenium is a naturally occurring mineral element that is distributed widely in nature in most rocks and soils. In its pure form, it exists as metallic gray to black hexagonal crystals, but in nature it is usually combined with sulfide or with silver, copper, lead, and nickel minerals. Most processed selenium is used in the electronics industry, but it is also used: as a nutritional supplement; in the glass industry; as a component of pigments in plastics, paints, enamels, inks, and rubber; in the preparation of pharmaceuticals; as a nutritional feed additive for poultry and livestock; in pesticide formulations; in rubber production; as an ingredient in antidandruff shampoos; and as a constituent of fungicides. Radioactive selenium is used in diagnostic medicine.

Selenium is a naturally occurring substance that is toxic at high concentrations but is also a nutritionally essential element. Hydrogen selenide is the most acutely toxic selenium compound. Acute (short-term) exposure to elemental selenium, hydrogen selenide, and selenium dioxide by inhalation results primarily in respiratory effects, such as irritation of the mucous membranes, pulmonary edema, severe bronchitis, and bronchial pneumonia. Epidemiological studies of humans chronically (long-term) exposed to high levels of selenium in food and water have reported discoloration of the skin, pathological deformation and loss of nails, loss of hair, excessive tooth decay and discoloration, lack of mental alertness, and listlessness. Epidemiological studies have reported an inverse association between selenium levels in the blood and cancer occurrence and animal studies have reported that selenium supplementation, as sodium selenate, sodium selenite, and organic forms of selenium, results in a reduced incidence of several tumor types. The only selenium compound that has been shown to be carcinogenic in animals is selenium sulfide, which resulted in an increase in liver tumors from oral exposure. EPA has classified elemental selenium as a Group D, not classifiable as to human carcinogenicity, and selenium sulfide as a Group B2, probable human carcinogen.

Selenosis has been documented in animals and humans living in areas with high selenium contamination of soil and groundwater. In humans, symptoms of this disease include fatigue, dermatitis, gastrointestinal disturbances, garlic odor of the breath and sweat, and increased dental caries. Liver injury is observed in feeding studies of experimental animals. [ACGIH] Burning selenium produces selenium dioxide fume, an irritant inhalant that can induce pulmonary edema at sufficient dose; [Harber, p. 502] In high-dose reproductive studies in animals, selenium causes low birth weight and birth defects. [ATSDR Case Studies #29] Chinese villagers studied in 1983 developed selenosis after using coal ash as a crop fertilizer. They also inhaled smoke from burning coal indoors. In extreme cases with intake averaging 0.09 mg/kg/day, patients developed neurological disease including increased tendon reflexes, convulsions, and paralysis. Similar neurological problems have been observed in animals fed high doses of selenium. A NOAEL of 0.015 mg selenium/kg/day corresponding to a blood level of 0.97 mg/L was calculated. The calculated LOAEL was 0.023 mg selenium/kg/day. The recommended dietary allowance (RDA) for selenium is 0.001 mg/kg/day. Follow-up in 1992 revealed that villagers with hair loss and nail deformities recovered and that average blood levels dropped from 1.346 mg/L to 0.819 mg/L. [ATSDR ToxProfiles] The most common compound reported in cases of selenium poisoning by ingestion is 4% selenious acid in gun bluing (coating) solutions. As little as 15 ml can be fatal. Patients have corrosive gastroenteritis with vomiting, diarrhea, and garlic odor. Other compounds reported in poisoning cases by ingestion are selenium dioxide, sodium selenate, and sodium selenite. [Olson, p. 416-418] See Hydrogen selenide.

DHHS/ATSDR; Toxicological Profile for Selenium (1989) ATSDR/TP-89/21

WHO; Environmental Health Criteria 58: Selenium (1987). EHC are designed for scientists and administrators responsible for the establishment of safety standards and regulations and provide basic scientific risk evaluations of a wide range of chemicals and groups of chemicals.[Available from, as of April 1, 2011: http://www.inchem.org/documents/ehc/ehc/ehc58.htm#SectionNumber:7.1]

US Dept of Interior/Fish & Wildlife Service Contaminant Reviews; Selenium Hazards to Fish, Wildlife, and Invertebrates: A Synoptic Review Biol Rept No (85)1.5 (1985)

U.S. Dept Health & Human Services/Agency for Toxic Substances & Disease Registry; Toxicological Profile for Selenium (September 2003). The ATSDR toxicological profile succinctly characterizes the toxicologic and adverse health effects information for a hazardous substance.[Available from, as of March 22, 2011: http://www.atsdr.cdc.gov/substances/indexAZ.asp#S]

WHO; Environmental Health Criteria 58: Selenium (1987). EHC are designed for scientists and administrators responsible for the establishment of safety standards and regulations and provide basic scientific risk evaluations of a wide range of chemicals and groups of chemicals.[Available from, as of April 1, 2011: http://www.inchem.org/documents/ehc/ehc/ehc58.htm#SectionNumber:7.1]

D010; A solid waste containing selenium (such as selenium, elemental) may become characterized as a hazardous waste when subjected to the Toxicity Characteristic Leaching Procedure listed in 40 CFR 261.24, and if so characterized, must be managed as a hazardous waste.

D010; A solid waste containing selenium (such as selenium, elemental) may become characterized as a hazardous waste when subjected to the Toxicity Characteristic Leaching Procedure listed in 40 CFR 261.24, and if so characterized, must be managed as a hazardous waste.

Excerpt from ERG Guide 151 [Substances - Toxic (Non-Combustible)]:

Use foam, powder, carbon dioxide. NO water.

Fresh air, rest. Refer for medical attention.

Rinse and then wash skin with water and soap.

Rinse with plenty of water (remove contact lenses if easily possible).

Rinse mouth. Refer for medical attention .

Excerpt from NIOSH Pocket Guide for Selenium:

(General first aid procedures)

TIH (Toxic Inhalation Hazard) - Term used to describe gases and volatile liquids that are toxic when inhaled. Some are TIH materials themselves, e.g., chlorine, and some release TIH gases when spilled in water, e.g., chlorosilanes. [ERG 2016].

0.02 [mg/m3], as Se, inhalable fraction (metal and inorganic compds)[German Research Foundation (DFG)]

Extinguishant: For selenium, water

If material on fire or involved in fire: Extinguish fire using agent suitable for type of surrounding fire. Material itself does not burn or burns with difficulty. Keep run-off water out of sewers and water sources. /Selenium compound, solid, nos/

Personnel protection: Wear appropriate chemical protective clothing. Wear positive pressure self-contained breathing apparatus when fighting fires involving this material. /Selenium compound, solid, nos/

Usually stored at room temperature. Precautions must be taken to avoid contact with water or prolonged exposure to air and other materials with which it may react. Storage area construction must be such that rain water will not leak in or ground water will not enter. Used drums should be stored in this same dry area to avoid contamination /SRP: of the area/ and to minimize any hazard due to the residues.

SRP: Wastewater from contaminant suppression, cleaning of protective clothing/equipment, or contaminated sites should be contained and evaluated for subject chemical or decomposition product concentrations. Concentrations shall be lower than applicable environmental discharge or disposal criteria. Alternatively, pretreatment and/or discharge to a permitted wastewater treatment facility is acceptable only after review by the governing authority and assurance that "pass through" violations will not occur. Due consideration shall be given to remediation worker exposure (inhalation, dermal and ingestion) as well as fate during treatment, transfer and disposal. If it is not practicable to manage the chemical in this fashion, it must be evaluated in accordance with EPA 40 CFR Part 261, specifically Subpart B, in order to determine the appropriate local, state and federal requirements for disposal.

Persons not wearing protective equipment and clothing should be restricted from areas of spills until cleanup has been completed. /Selenium and its inorganic cmpd/

If selenium or its inorganic compounds are spilled, the following steps should be taken: 1. Ventilate area of spill. 2. Collect spilled material in the most convenient and safe manner and deposit in sealed containers for reclamation or for disposal in a secured sanitary landfill. Liquid containing selenium and its inorganic compounds should be absorbed in vermiculite, dry sand, earth, or a similar material. Waste disposal method: Selenium and its inorganic compounds may be disposed of in sealed containers in a secured sanitary landfill. /Selenium and its inorganic cmpd/

Environmental considersations: Land spill: Cover solids with a plastic sheet to prevent dissolving in rain or fire fighting water. Dike surface flow using soil, sand bags, foamed polyurethane, or foamed concrete. /Selenium compound, solid, nos/

Environmental considerations: Water spill: Use natural barriers or oil spill control booms to limit spill travel. Use natural deep water pockets, excavated lagoons, or sand bag barriers to trap material at bottom. Use mechanical dredges or lifts to remove immobilized masses of pollutants and precipitates. /Selenium compound, solid, nos/

Generators of waste (equal to or greater than 100 kg/mo) containing this contaminant, EPA hazardous waste number D010, must conform with USEPA regulations in storage, transportation, treatment and disposal of waste.

SRP: Wastewater from contaminant suppression, cleaning of protective clothing/equipment, or contaminated sites should be contained and evaluated for subject chemical or decomposition product concentrations. Concentrations shall be lower than applicable environmental discharge or disposal criteria. Alternatively, pretreatment and/or discharge to a permitted wastewater treatment facility is acceptable only after review by the governing authority and assurance that "pass through" violations will not occur. Due consideration shall be given to remediation worker exposure (inhalation, dermal and ingestion) as well as fate during treatment, transfer and disposal. If it is not practicable to manage the chemical in this fashion, it must be evaluated in accordance with EPA 40 CFR Part 261, specifically Subpart B, in order to determine the appropriate local, state and federal requirements for disposal.

Generators of waste (equal to or greater than 100 kg/mo) containing this contaminant, EPA hazardous waste number D010, must conform with USEPA regulations in storage, transportation, treatment and disposal of waste.

... As the price of selenium is very high; recovery of it by processing selenium containing waste is economical. For example, selenium refineries are equipped with wet scrubbers that employ an approx 50% soln of hydrobromic acid containing free bromine. The acid fumes are adsorbed in a lime and soda bed, and the selenium separated from the hydrobromic acid soln by distilliation is recycled. ... If possible, convert selenium compounds to an insoluble form with SO2 before landfill or solidification. Do not use metal and acid to reduce selenium compounds. This will produce toxic gaseous hydrogen selenide.

SRP: Wastewater from contaminant suppression, cleaning of protective clothing/equipment, or contaminated sites should be contained and evaluated for subject chemical or decomposition product concentrations. Concentrations shall be lower than applicable environmental discharge or disposal criteria. Alternatively, pretreatment and/or discharge to a permitted wastewater treatment facility is acceptable only after review by the governing authority and assurance that "pass through" violations will not occur. Due consideration shall be given to remediation worker exposure (inhalation, dermal and ingestion) as well as fate during treatment, transfer and disposal. If it is not practicable to manage the chemical in this fashion, it must be evaluated in accordance with EPA 40 CFR Part 261, specifically Subpart B, in order to determine the appropriate local, state and federal requirements for disposal.

Depending upon the industrial source, selenium occurs in either the particulate or the soluble form. For the former, physical treatment processes such as sedimentation or filtration are quite effective. Lime precipitation of soluble selenium has been shown to be ineffective. Alum coagulation/coprecipitation is somewhat effective, with removal efficiencies approaching 50% achievable. Iron coagulation/coprecipitation is capable of above 80% selenium removal, with efficiency increasing with decreasing pH. Activated carbon adsorption is not effective, except in one reported instance involving high pH pretreatment. The most efficient process for soluble selenium appears to be anion exchange. Preoxidation of the selenite to selenate is reported to enhance exchange capacity. /Selenium compounds/

Personal protection: particulate filter respirator adapted to the airborne concentration of the substance. Do NOT let this chemical enter the environment. Sweep spilled substance into covered containers. If appropriate, moisten first to prevent dusting. Carefully collect remainder. Then store and dispose of according to local regulations.

Smoking, eating and drinking at the workplace should be prohibited and messrooms and sanitary facilities including showers and locker rooms should be provided at a point distant from exposure areas.

Where there is any possibility of exposure of an employee's body to selenium, selenium oxychloride, sodium selenite, sodium selenate, selenium dioxide, or liquids containing these compounds, facilities for quick drenching of the body should be provided within the immediate work area for emergency use.

Employees should be provided with and required to use impervious clothing, gloves, face shields (eight inch minimum), and other appropriate protective clothing necessary to prevent repeated or prolonged skin contact with selenium, sodium selenite, or sodium selenate.

Non-impervious clothing which becomes contaminated with selenium, sodium selenite, sodium selenate, selenium dioxide or liquids containing these compounds should be removed promptly and not reworn until the contaminant is removed from the clothing.

For more Preventive Measures (Complete) data for SELENIUM, ELEMENTAL (12 total), please visit the HSDB record page.

If the concentration of selenium in the urine of workers on a particular process is above 0.1 mg/L then action should be taken to improve the industrial hygiene of that process. /Selenium compounds/

Samples of lung tissue from deceased copper smelter workers contained a median selenium concentration of 152 ppb; tissue samples from deceased rural and urban human control subjects contained 110 and 136 ppb Se, respectively(1). Selenium was detected in plasma at concentrations of 85.0 ug/L in non-smokers, 87.1 ug/L in ex-smokers, and 85.2 ug/L in smokers(2). The median selenium plasma concentration in three human subjects who never ate fish was 80.2 ug/L; in 32 subjects who ate fish at least twice per week the median plasma selenium level was 94 ug/L(2). The median plasma selenium level in 195 human subjects living in areas receiving acidic precipitation was 85.0 ug/L; median selenium plasma levels in a reference population, 91 subjects, was 89.7 ug/L(2). Selenium was detected in human hair samples from 17 ethnic and territorial groups from the former USSR, at mean concentrations ranging from 0.26 to 1.8 ppm dry weight for males and 0.23 to 2.02 ppm dry weight in females; the highest concentrations occurred in Tuvinians, Mong.-Taiga dist.(3). Selenium content of expressed human breast milk (foremilk) from Belgian mothers decreased with increasing time of lactation and plateaued at a concentration of about 9.4 ng/g(4). Forty-seven samples of human milk collected from five middle-class women from Burundi, Africa, contained selenium at an average concentration of 15.2 ng/mL 2 days after delivery and 5.2 ng/mL 2 weeks after delivery(5). Blood samples from the district of Angmagssalik, East Greenland contained selenium at concentrations ranging from 1.09 to 2.19 umol/L in males and 1.50 to 2.34 umol/L in females(6). Scalp hair from persons from different Mediterranean areas contained selenium at concentrations ranging from 0.30 to 0.74 ug/g; scalp hair samples from controls contained 0.22 to 0.71 ug/g(7). Hair samples collected from a laboratory worker over a period of years contained selenium at concentrations ranging from 0.33 to 0.68 ug/g(7). Selenium concentrations in human placenta obtained after normal births in Genova, Italy ranged from 0.38 to 1.03 ug/g dry weight, average 0.77 ug/g dry weight(8). Median selenium concentrations in lung tissue of Swedish workers, employed in refining and smelting, were 0.13 ug/g; lung tissue from controls contained a median selenium concentration of 0.11 ug/g(9).

Mean selenium concentrations in urine of healthy persons from the USA ranged from 7 to 76 ug/L; mean selenium levels in urine samples of burn patients were 16 ug over 24 hours and alcoholic subjects were 30 ug over 24 hours(1). Mean selenium concentrations in human nails from Japan, India, U.S.A., Canada, and Poland were 1.6, 0.79, 0.32, 0.45, and 1.0 ppm, respectively(2). Mean selenium concentrations in human hair collected from Canada, U.S.A., Poland, Japan, and India were 16.4, 21.7, 0.35, 3.90, and 10.8 ppm, respectively(3). Selenium was identified in 7 of 9 human adipose tissue samples at concentrations ranging from 0.030 to 0.056 ug/g(4). Mean selenium concentrations of 11.4 and 10.7 ng/mL for colostrum (<5 days postpartum) and transitional (6-15 days postpartum) milk, and 8.4 and 5.3 ng/mL for mature milk at one month and up to 2 months, respectively, were detected in Spanish human milk samples collected from April 1996 to September 1997 in Valencia and Castellon provinces(5). Selenium was detected in human serum samples from 27 non-fish-eating volunteers in Sweden, at concentrations ranging from 53 to 103 ug/L, with a median of 76 ug/L(6).

The concentrations of selenium in 210 samples of blood from people in 16 cities of the United States ranged from 0.10 to 0.34 and averaged 0.206 ppm. There was some tendency for the blood values for selenium to be higher in geographic areas where the concentrations of selenium are higher in the soil and in plants. However, the variation in the selenium content of blood was much less pronounced than the variation in selenium in locally produced foods ... . The concentration in normal plasma does not exceed 0.15 ppm ... . /Selenium/

In normal persons without unusual exposure, the concentration of selenium in the liver ranges from 0.55 to 1.34 ppm; in the heart it ranges from 0.14 to 0.67 ppm ... . The concentration in normal urine is 0.01 -0.16 ppm ... .

Normal values in selected human organs taken at autopsy from individuals with no record of exposure to excess selenium in the diet or otherwise (N = 11): blood 0.05 - 0.28 ppm; liver 0.005 - 0.40 ppm; spleen 0.10 - 0.45 ppm (sic); kidneys 0.21 - 1.00 ppm.

Four groups of 20 female OSU-Brown rats were fed 150 mg N-2-fluorenyl-acetamide per kg of diet plus 2.5, 0.5, 0.1 or 0 mg selenium per kg of diet. Incidences of mammary adenocarcinomas and/or hepatic carcinomas at 200 days were 0/20, 2/20, and 12/20, respectively.

Interaction has been studied in the rat. Selenite increased the whole-body retention of bismuth, but reduced the level in the kidneys. A redistribution of bismuth form a low-molecular-weight protein (molecular weight 7000) (metallothionein-like protein) to proteins of higher molecular weight was seen in the kidneys. Similar interaction has also been reported for inorganic mercury and cadmium. /Selenite/

Arsenic, whether in organic or inorganic form...counteracts toxicity of selenium to animals. This action is not due to interference by arsenic with absorption of selenium but by its capacity to maintain the succinic hydrogenase of the liver which is lowered by selenium. ...

The protective effect of arsenic (5 mg/kg sodium arsenite) against selenosis produced by feeding seleniferous grain (15 mg/kg) was discovered ... . Arsenite can increase the biliary and the fecal excretion of selenium up to 10 fold and because of effective inhibition of methylation, exhalation of methylated selenium compounds is reduced. Arsenic and selenium are excreted as a glutathione complex in the bile. ... /Selenium/

For more Interactions (Complete) data for SELENIUM COMPOUNDS (23 total), please visit the HSDB record page.

Cardiovascular (Heart and Blood Vessels), Dermal (Skin), Gastrointestinal (Stomach and Intestines, part of the digestive system), Hepatic (Liver), Neurological (Nervous System), Renal (Urinary System or Kidneys), Respiratory (From the Nose to the Lungs)

Dermal

Eyes, skin, respiratory system, liver, kidneys, blood, spleen

Chronic oral exposure to high concentrations of selenium compounds can produce a disease called selenosis. The major signs of selenosis are hair loss, nail brittleness, and neurological abnormalities (such as numbness and other odd sensations in the extremities). Animal studies have shown that selenium may also affect sperm production and the female reproductive cycle. (L619)

LC50 Tanytarsus dissimilis (Chironomid) 42,400 ppb/96 hr /Selenium salts/

LC50 Apeltes quadracus (Fourspine sickleback) 17,350 ppb/96 hr /Selenium salts/

LC50 Lagodon rhomboides (Pinfish) 4400 ppb/96 hr /Selenium salts/

LC50 Melanogrammus aeglefinus (Haddock, larvae) 600 ppb/96 hr /Selenium salts/

For more Ecotoxicity Values (Complete) data for SELENIUM COMPOUNDS (34 total), please visit the HSDB record page.

AQUATIC FATE: In aqueous solution, selenium forms oxyanions and exhibits anionic chemistry(1). Volatilization of the ionic forms of selenium is not expected to be an important fate process(SRC). Speciation of selenium is determined by the pH and redox potential of the solution; elemental selenium is favored by low pH and reducing conditions(1). At pHs <7 and under mildly reducing conditions, selenites are reduced to elemental selenium(1). Reducing conditions in surface sediments of ponded laboratory sediment columns promoted reduction of soluble Se(VI) to soluble Se(IV) to insoluble Se(0), allowing a net accumulation of insoluble elemental selenium(2). In sediments, reduced and tightly bound selenium will remain relatively immobile unless the sediments are chemically or biologically oxidized(3).

ATMOSPHERIC FATE: Hydrogen selenide released to the air is unstable and will be oxidized to elemental selenium and water. Selenium dioxide released to the air from the combustion of fossil fuels is expected to be reduced to elemental selenium by sulfur dioxide formed during the combustion(1).

TERRESTRIAL FATE: The behavior of selenium in soils is affected by redox conditions, pH, hydrous oxide content, clay content, organic materials and the presence of competing anions(1). Heavy metal selenides, which are insoluble, predominate in acidic soils and soils with high amounts of organic matter; selenium in this form is immobile(2). Sodium and potassium selenites dominate in neutral, well-drained mineral soils(2). Selenite (Se(IV)) is soluble, but can strongly adsorb to soil minerals and organic material(3). Iron and manganese oxides sorb Se(IV), with iron oxides sorbing more than manganese(4). In alkaline, well-oxidized soil environments, selenates, Se(VI) predominate; selenates are very mobile because of their high water solubility and low tendency to adsorb onto soil particles(2). No sorption of sodium selenate was observed in 10 of 11 soils; a log Kd value of 0.958 was determined in Kula soil (pH 5.9, 6.62% TOC, 73.7% sand, 25.4% silt, 0.9% clay)(5). Se(IV) adsorption was observed to decrease with increasing pH from 4 to 9 and Se(VI) adsorption was minimal under most pH conditions(4). In soils, elemental selenium and inorganic selenium compounds can be methylated by microorganisms and subsequently volatilize to the atmosphere(1,2); dimethylselenide and dimethyl diselenide are the principal products(2).

AQUATIC FATE: In aqueous solution, selenium forms oxyanions and exhibits anionic chemistry(1). Volatilization of the ionic forms of selenium is not expected to be an important fate process(SRC). Speciation of selenium is determined by the pH and redox potential of the solution; elemental selenium is favored by low pH and reducing conditions(1). Selenates are stable under alkaline oxidizing conditions(1). Selenious acid species occur under the intermediate to slightly oxidizing conditions encountered in aerobic water(1). Over the pH range of 3 to 9, the biselenite species predominates; at pHs >9, selenite is the major species(1). At pHs <7 and under mildly reducing conditions, selenites are reduced to elemental selenium(1). Reducing conditions in surface sediments of ponded laboratory sediment columns promoted reduction of soluble Se(VI) to soluble Se(IV) to insoluble Se(0), allowing a net accumulation of insoluble elemental selenium(2). In sediments, reduced and tightly bound selenium will remain relatively immobile unless the sediments are chemically or biologically oxidized(3). Biological methylation of selenium may occur in aquatic environments; inorganic selenium undergoes biological methylation to dimethyl selenide and dimethyl diselenide(1,4). Bioconcentration factors have been measured in a variety of aquatic organisms(SRC). Algae and daphnids concentrated (75)Se more strongly from selenite (BCFs ranged from 220 to 3,600) than selenate (BCFs ranged from 65 to 500)(5). BCF values for (75)Se after 28 days exposure to three selenium species were: 72 in macrophytes, 141 in periphyton, and 351 in zooplankton (as selenate); 363 in macrophytes, 755 in periphyton, and 1,087 in zooplankton (as selenite); and 3,266 in macropytes, 16,836 in periphyton, and 28,870 in zooplankton (as Se-methionine)(6).

ATMOSPHERIC FATE: Most selenium compounds are expected to exist solely in the particulate phase in the ambient atmosphere(1). Particulate-phase selenium may be removed from the air by wet or dry deposition(SRC). Volatile selenium compounds, selenium dioxide, hydrogen selenide, dimethyl selenide, and dimethyl diselenide, are expected to exist in the gaseous state in the atmosphere(1,2). Hydrogen selenide released to the air is unstable and will be oxidized to elemental selenium and water(2). Selenium dioxide released to the air from the combustion of fossil fuels is expected to be reduced to elemental selenium by sulfur dioxide formed during the combustion(2).

Selenium (Se) is an essential trace element ... In foods, Se is predominantly present as selenomethionine, which is an important source of dietary Se in humans, and also as a chemical form that is commonly used for Se supplements in clinical trials.

Mean selenium concentrations in food ranged from 0.001 to 0.048 mg/100 g(1).

Selenium has been detected in the following commonly consumed infant foods collected between 1982 and 1984, mean concentration (mg/100 g): dry infant mixed cereal prepared with whole milk, 0.002; beef infant food, 0.005; pork infant food, 0.011; chicken/turkey infant food, 0.013; chicken/turkey and vegetables infant food, 0.006; beef and vegetables infant food, 0.003; ham and vegetables infant food, 0.003; chicken and noodles infant food, 0.002; tomatoes, beef, and macaroni infant food, 0.002; carrots infant food, 0.001; and applesauce/applesauce with other fruit infant food, 0.001(1). Average concentration of selenium in the US infant diet by food group in Fiscal Year 1979 (81/82), ppm: whole milk, 0.004 (0.009); other dairy and dairy substitutes, 0.002 (0.015); meat, fish and poultry, 0.107 (0.112); grain and cereal products, 0.156 (0.192), potatoes, 0.002 (0.002); vegetables, 0.004 (0.007); oils and fats, 0.012 (0.005); sugar and adjuncts, 0.011; and beverages, 0.002(2,3). Average concentration of selenium in the US toddler diet by food group in Fiscal Year 1979 (81/82), ppm: whole milk, 0.004 (0.009); other dairy and dairy substitutes, 0.018 (0.022); meat, fish and poultry, 0.160 (0.208); grain and cereal products, 0.158 (0.189); potatoes, 0.002 (0.003); vegetables, 0.007 (0.003); fruit and fruit juices, 0.011; oils and fats, 0.013 (0.036); sugar and adjuncts, 0.008 (0.005); and beverages, 0.003(2,3).

Selenium was detected in Brazil nuts collected from two regions in Brazil, Acre-Rondonia and Manaus-Belem, at average concentrations of 3.06 and 36.0 ppm, respectively(1). Concentrations of selenium in wheat flour from markets in different areas of Pakistan range from 0.13 to 0.24 ppm, mean 0.19 ppm(2). Selenium has been detected in different wheat products including wheat grain 0.129 ppm, wheat flour 0.127 ppm, Maida 0.122 ppm, and semolina 0.11 ppm(2). Selenium was detected in 15 edible mushroom species sampled from 1993-1999 around the central part of the Mexican Volcanic Belt in Mexico, at average, median, and geometric mean concentrations of 2.06, 1.44 and 1.59 mg/kg dry weight, respectively(3). Fifteen edible seaweed samples (six from British Columbia, seven from Japan, one from Norway, and one undisclosed) were analyzed and found to contain selenium at concentrations ranging from at or below the detection limit (0.1 ug/g) to 6.2 ug/g dry weight(4).

Neurotoxin - Other CNS neurotoxin

Selenium supplementation has a very low adverse effect profile. Most adverse reactions center on selenium sulfide. The more common adverse effects include redness, burning, itching, stinging, scalp sores, increased oiliness, nail hyperpigmentation, and skin irritation, creating contact dermatitis. Less common effects associated specifically with selenium sulfide shampoo include scalp hyperpigmentation, scalp discoloration, and alopecia. A rare non-dermatologic effect includes nausea due to the odor of the medication. There are no reported severe reactions to using this drug.

The substance can be absorbed into the body by inhalation and by ingestion.

inhalation, ingestion, skin and/or eye contact

Oral(L619) ; inhalation (L619) ; dermal (L619).

ENVIRONMENTAL: Selenium content of processed cow milk from Belgium was 8.7 ng/mL in whole milk, 9.5 ng/mL in full cream milk, 8.4 ng/mL in semi-skimmed milk, and 8.8 ng/mL skimmed milk(1). Selenium was detected in goat and cow milk from Burundi, Africa: goat colostrum at mean concentrations of 135.1 ng/mL on day 1 and 65.4 ng/L on day 2, mature goat milk at 23.1 ng/mL, cow colostrum (day 2) at 63.3 ng/mL, mature cow milk, 25.9 ng/mL and processed cow milk at 12.3 ng/mL(2).

ENVIRONMENTAL: Selenium content of expressed human breast milk (foremilk) from Belgian mothers decreased with increasing time of lactation and plateaued at a concentration level of about 9.4 ng/g(1). Forty-seven samples of human milk collected from five middle-class women from Burundi, Africa, contained selenium at an average concentration of 15.2 ng/mL 2 days after delivery and 5.2 ng/mL 2 weeks after delivery(2). Mean (range) selenium concentrations of 11.4 (6.7-20.3) and 10.7 (5.5-21.0) ng/mL for colostrum and transitional milk, and 8.4 (4.3-12.6) and 5.2 (3.0-8.7) ng/mL for mature milk at one month and up to 2 months, respectively, were detected in Spanish human milk samples collected from April 1996 to September 1997 in Valencia and Castellon provinces(3). Selenium contents of infant formulas ranged (mean concentration) from 2.7 to 9.6 (4.5) and 1.8 to 7.5 ng/mL for soy and milk-based formulas, respectively(3).

Selenium is an essential trace element and has been shown to be a natural component in the enzyme glutathione peroxidase and other proteins. Most selenium compounds are water-soluble and can efficiently be taken up in the intestine. Soluble as well as non-soluble compounds can be taken up by the lungs. When given in excess, selenium compounds are rapidly distributed to major organs of the body. ... Identified metabolites are trimethylselenide in urine and dimethylselenide in breath. ... in man ... toxic effects have been reported at 1 mg/dl. ... Toxic effects have been seen at blood levels ranging from 0.179 ug/ml-7.5 ug/ml. In most parts of the world normal urine levels do not exceed 0.03 ug/ml. Occupationally exposed workers usually excrete less than 0.1 ug/ml. The LD50 ranges between 1.5 and 6 mg/kg for many selenium compounds and animal species. The CNS seems to be the target organ ... but the liver, heart, and lungs may also be affected. A few cases of selenium poisoning in humans have been described ... either after consumption of selenium or after exposure via inhalation. Gastrointestinal and neurological symptoms predominated. Chronic poisoning due to long term exposure has been reported in livestock and humans from geographical areas where soil contains high levels of selenium. In rodent liver cirrhosis is a common effect while typical effects in domestic animals are: emaciation, deformation of hooves, loss of hair, and joint erosions. In humans consuming 5 mg selenium per day, hair and nail problems are very common. Skin lesions and depigmentation are also common signs of intoxication. In more severe cases neurological and gastrointestinal symptoms predominate. ... Several selenium compounds have been tested for possible carcinogenic potential. Selenium sulfide has been shown to induce liver cancer in two species while no convincing evidence of carcinogenicity has been presented for other selenium compounds. ... Some selenium compounds may induce DNA damage and some previous reports indicate a teratogenic potential ... . Selenium may prevent or alleviate toxic effects of arsenic, cadmium, mercury, platinum, and silver. Conversely, some of these metals protect against selenium toxicity.

Selenium is an essential trace element and has been shown to be a natural component in the enzyme glutathione peroxidase and other proteins. Most selenium compounds are water-soluble and can efficiently be taken up in the intestine. Soluble as well as non-soluble compounds can be taken up by the lungs. When given in excess, selenium compounds are rapidly distributed to major organs of the body. ... Identified metabolites are trimethylselenide in urine and dimethylselenide in breath. ... in man ... toxic effects have been reported at 1 mg/dl. ... Toxic effects have been seen at blood levels ranging from 0.179 ug/ml-7.5 ug/ml. In most parts of the world normal urine levels do not exceed 0.03 ug/ml. Occupationally exposed workers usually excrete less than 0.1 ug/ml. The LD50 ranges between 1.5 and 6 mg/kg for many selenium compounds and animal species. The CNS seems to be the target organ ... but the liver, heart, and lungs may also be affected. A few cases of selenium poisoning in humans have been described ... either after consumption of selenium or after exposure via inhalation. Gastrointestinal and neurological symptoms predominated. Chronic poisoning due to long term exposure has been reported in livestock and humans from geographical areas where soil contains high levels of selenium. In rodent liver cirrhosis is a common effect while typical effects in domestic animals are: emaciation, deformation of hooves, loss of hair, and joint erosions. In humans consuming 5 mg selenium per day, hair and nail problems are very common. Skin lesions and depigmentation are also common signs of intoxication. In more severe cases neurological and gastrointestinal symptoms predominate. ... Several selenium compounds have been tested for possible carcinogenic potential. Selenium sulfide has been shown to induce liver cancer in two species while no convincing evidence of carcinogenicity has been presented for other selenium compounds. ... Some selenium compounds may induce DNA damage and some previous reports indicate a teratogenic potential ... . Selenium may prevent or alleviate toxic effects of arsenic, cadmium, mercury, platinum, and silver. Conversely, some of these metals protect against selenium toxicity.

Selenium is considered a relatively non-toxic supplement. However, extremely high selenium intake can result in diarrhea, fatigue, hair loss, joint pain, nail discoloration or brittleness, and nausea. Due to selenium supplementation toxicity being extremely rare, there is no current treatment for selenium overdose. If selenium toxicity is suspected, it is best to stop using the supplement.

Selenium readily substitutes for sulfur in biomolecules and in many biochemical reactions, especially when the concentration of selenium is high and the concentration of sulfur is low. Inactivation of the sulfhydryl enzymes necessary for oxidative reactions in cellular respiration, through effects on mitochondrial and microsomal electron transport, might contribute to acute selenium toxicity. Selenomethionine (a common organic selenium compound) also appears to randomly substitute for methionine in protein synthesis. This substitution may affect the structure and functionability of the protein, for example, by altering disulfide bridges. Inorganic forms of selenium appear to react with tissue thiols by redox catalysis, resulting in formation of reactive oxygen species and causing damage by oxidative stress. (L619)

D010; A solid waste containing selenium (such as selenium, elemental) may become characterized as a hazardous waste when subjected to the Toxicity Characteristic Leaching Procedure listed in 40 CFR 261.24, and if so characterized, must be managed as a hazardous waste.

D010; A solid waste containing selenium (such as selenium, elemental) may become characterized as a hazardous waste when subjected to the Toxicity Characteristic Leaching Procedure listed in 40 CFR 261.24, and if so characterized, must be managed as a hazardous waste.

Listed as a hazardous air pollutant (HAP) generally known or suspected to cause serious health problems. The Clean Air Act, as amended in 1990, directs EPA to set standards requiring major sources to sharply reduce routine emissions of toxic pollutants. EPA is required to establish and phase in specific performance based standards for all air emission sources that emit one or more of the listed pollutants. Selenium is included on this list.

Listed as a hazardous air pollutant (HAP) generally known or suspected to cause serious health problems. The Clean Air Act, as amended in 1990, directs EPA to set standards requiring major sources to sharply reduce routine emissions of toxic pollutants. EPA is required to establish and phase in specific performance based standards for all air emission sources that emit one or more of the listed pollutants. Selenium cmpds are included on this list.

Persons in charge of vessels or facilities are required to notify the National Response Center (NRC) immediately, when there is a release of this designated hazardous substance, in an amount equal to or greater than its reportable quantity of 100 lb or 45.4 kg. The toll free number of the NRC is (800) 424-8802. The rule for determining when notification is required is stated in 40 CFR 302.4 (section IV.D.3.b). [No reporting of releases of this hazardous substance is required if the diameter of the pieces of the solid metal released is larger than 100 micrometers (0.004 inches).]

Reportable Quantities for Radionuclides [Table#4955]

Toxic pollutant designated pursuant to section 307(a)(1) of the Federal Water Pollution Control Act and is subject to effluent limitations. /Selenium and compounds/

Toxic pollutant designated pursuant to section 307(a)(1) of the Federal Water Pollution Control Act and is subject to effluent limitations. /Selenium and compounds/

(AZ) ARIZONA 10 ug/L /Selenium/

(NY) NEW YORK 10 ug/L /Selenium/

(AZ) ARIZONA 10 ug/L /Selenium/

(NY) NEW YORK 10 ug/L /Selenium/

(AZ) ARIZONA 45 ug/L /Selenium/

(CT) CONNECTICUT 10 ug/L /Selenium/

(ME) MAINE 35 ug/L /Selenium/

(MN) MINNESOTA 30 ug/L /Selenium/

(AZ) ARIZONA 45 ug/L /Selenium/

(CT) CONNECTICUT 10 ug/L /Selenium/

Maximum contaminant levels for inorganic contaminants: 0.05 mg/L /Selenium/

Maximum contaminant levels for inorganic contaminants: 0.05 mg/L /Selenium/

Maximum contaminant level goals for inorganic contaminants: 0.05 mg/L /Selenium/

Maximum contaminant level goals for inorganic contaminants: 0.05 mg/L /Selenium/

D - Dermatologicals

QD - Dermatologicals

It is an essential micronutrient for mammals and other animals but is toxic in large amounts. Selenium protects intracellular structures against oxidative damage. It is an essential component of glutathione peroxidase.

Deficiency diseases have been described in many farm animals and laboratory animals and include dysfunction of several organs and growth retardation. Reproductive failures are seen in rodents, dogs, pigs, monkeys, cows, and ewes. Myopathies are also seen in a number of species, especially in ruminants. Pigs are often affected by cardiomyopathy. Liver necrosis, hemolysis, kidney degeneration, exudative diathesis, and pancreatic fibrosis are other important signs of deficiency, the latter two especially in poultry. /Selenium/

Selenium deficiency in otherwise well-nourished individuals is not likely to cause overt symptoms. However, selenium deficiency may lead to biochemical changes that can predispose a person to illness associated with other stresses, such as: (1) Keshan disease, a cardiomyopathy found only in selenium-deficient children that appears to be triggered by an additional stress, possibly an infection or chemical exposure, and (2) Kashin-Beck disease, an endemic disease of cartilage that occurs in preadolescence or adolescence, /and/ has been reported in some of the low-selenium areas of Asia, although the pathogenesis remains uncertain. /Selenium/

DIETARY REFERENCE INTAKES FOR SELENIUM BY LIFE STAGE GROUPS (EAR = Estimated Average Requirement. RDA - Recommended Dietary Allowance. AI = Adequate Intake. UL = Tolerable Upper Intake Level) /Selenium/

For more Bionecessity (Complete) data for SELENIUM COMPOUNDS (32 total), please visit the HSDB record page.

Selenium is first metabolized to selenophosphate and selenocysteine. Selenium incorporation is genetically encoded through the RNA sequence UGA. This sequence is recognized by RNA ste loop structures called selenocysteine inserting sequences (SECIS). These structures require the binding of SECIS binding proteins (SBP-2) to recognize selenocystiene. The specialized tRNA is first bound to a serine residue which is then enzymatically processed to a selylcysteyl-tRNA by selenocystiene sythase using selenophosphate as a selenium donor. Other unidentified proteins are required as part of the binding of this tRNA to the ribosome. Selenoproteins appear to be necessary for life as mice with the specialized tRNA gene knocked out exhibited early embryonic lethality. The most important selenoproteins seem to be the glutathione peroxidases and thioredoxin reductases which are part of the body's defenses againts reactive oxygen species (ROS). The importance of selenium in these anti-oxidant proteins has been implicated in the reduction of atherosclerosis by preventing the oxidation of low density lipoprotein. Selenium supplementation is also being investigated in the prevention of cancer and has been suggested to be beneficial to immune function.

Converging data from epidemiological, ecological, and clinical studies have shown that selenium (Se) can decrease the risk for some types of human cancers. Induction of apoptosis is considered an important cellular event that can account for the cancer preventive effects of Se. Prior to occurrence of apoptosis, Se compounds alter the expression and/or activities of signaling molecules, mitochondria-associated factors, transcriptional factors, tumor suppressor genes, and cellular reduced glutathione. Mechanistic studies have demonstrated that the methylselenol metabolite pool has many desirable attributes of chemoprevention, whereas the hydrogen selenide pool with excess of selenoprotein synthesis can lead to DNA single-strand breaks. To elucidate the effects of Se on cytotoxic events, it should be remembered that the chemical forms and the dose of Se, and the experimental system used, are determinants of its biological activities. This mini-review focuses on elucidation of the molecular mechanisms of cancer prevention by Se with the apoptotic approach. /Selenium/

Selenium status can also influence thyroid hormone function via the deiodinase enzymes. Selenium is a critical component of the deiodinase enzymes, including iodothyronine 5'-deiodinases, which convert the prohormone thyroxine (T4) to the active circulating form, triiodothyronine (T3). Selenium is also a component of GPX, the main enzyme responsible for protecting thyroid cells against oxidative damage. GPX is involved in the detoxification of hydrogen peroxide, which is produced in the thyroid during the conversion of T4 to T3. /Selenium/

Selenium readily substitutes for sulfur in biomolecules and in many biochemical reactions, especially when the concentration of selenium is high and the concentration of sulfur is low in the organism. Inactivation of the sulfhydryl enzymes necessary for oxidative reactions in cellular respiration, through effects on mitochondrial and microsomal electron transport, might contribute to acute selenium toxicity. Selenium may have a role in hepatic heme metabolism that is related to GPX or lipid peroxidation. Selenocysteine is specifically found in some proteins (e.g., glutathione peroxidase); selenomethionine appears to randomly substitute for methionine in protein synthesis. This appears to be an additional mechanism for intermediate- or chronic-duration toxicity. Skin, hair, and nail damage are significant indicators of chronic selenium overexposure. The mechanism causing these integumentary effects is unclear, but could be related to the high selenium concentrations in these tissues as a consequence of the substitution of selenium for sulfur in certain amino acids, including the disulfide bridges that provide tertiary structure and function to proteins. For example, substitution of selenium for sulfur in keratin results in weakened physical protein structure and failure of keratinized tissues such as hair and hoof. The nails and hair are considered to be routes for excretion of excess selenium. /Selenium/

Considerable evidence is available supporting oxidative stress as the key biochemical lesion of selenium intoxication. Inorganic forms of selenium appear to react with tissue thiols by redox catalysis resulting in formation of reactive oxygen species (superoxide anion (O2 -)). For example, selenite is a prooxidant catalyst that reacts with GSH endogenously in cells or extracellularly causes toxicity by the formation of superoxide and elemental selenium. Selenocystamine (a diselenide) catalyzes the formation of superoxide under aerobic conditions in the presence of thiol; this reaction could play a role in the toxicity of diselenides and alkylselenols. Selenium can have inhibitory effects on thiol proteins by modification via (1) formation of S-Se-S (selenotrisulfides) and S-Se (selenylsulfide) bonds, (2) catalysis of S-S (disulfide bonds) with no incorporation of selenium in the protein, and (3) formation of Se-Se diselenides. Proteins that contain regulatory cysteines can similarly form selenium adducts with toxicity resulting from inactivation of essential thiol groups. /Selenium/

Epidemiologic and experimental evidences indicate that selenium, an essential trace element, can reduce the risk of a variety of cancers. Protection against certain types of cancers, particularly colorectal cancers, is closely associated with pathways involving cyclooxygenase-2 (COX-2). /It was/ found that AMP-activated protein kinase (AMPK), which functions as a cellular energy sensor, mediates critical anticancer effects of selenium via a COX-2/prostaglandin E(2) signaling pathway. Selenium activated AMPK in tumor xenografts as well as in colon cancer cell lines, and this activation seemed to be essential to the decrease in COX-2 expressions. Transduction with dominant-negative AMPK into colon cancer cells or application of cox-2(-/-)-negative cells supported the evidence that AMPK is an upstream signal of COX-2 and inhibits cell proliferation. In HT-29 colon cancer cells, carcinogenic agent 12-O-tetradecanoylphorbol-13-acetate (TPA) activated extracellular signal-regulated kinase (ERK) that led to COX-2 expression and selenium blocked the TPA-induced ERK and COX-2 activation via AMPK. The role of a reactive oxygen species as an AMPK activation signal in selenium-treated cells /was also demonstrated/.

Half life was observed to increase with chronic dosing time. For day 1-2 half life was 1.7 days. For day 2-3 half life was 3 days. For day 3-14 half life was 11.1 days.

Whole body: 140 days; [TDR, p. 1075]

The distribution and retention of inhaled selenious acid and selenium metal aerosols which were similar in size and chemical form to selenium aerosols that may be produced during fossil fuel combustion /was studied/. Beagle dogs were given 10 to 61 ug Se/kg of body weight by inhalation. ... Approximately 50% of the deposited Se was eliminated with a biological half life of 1.2 days. ... The long-term component of the whole-body retention function for both inhaled aerosols had a half-life of about 34 days and accounted for about 20% of the initial Se dose.

Several studies indicate at least biphasic elimination of whole-body selenium in rats. The amount excreted during this initial phase has been shown to be dose dependent. A second phase, which does not seem to be influenced by selenium dose, has a half time of approximately 30-70 days in most species. /Selenium/

In studies on humans, three phases of elimination can usually be identified after selenite admin. The half-time of the first phase is about 1 day, the second 8-20 days, and the third 65-116 days. In some studies, the half time of the terminal phase for selenium elimination was longer when selenomethionine was used instead of selenite. /Selenite/

The excretion pattern of a single exposure to selenite appears to have at least two phases: a rapid initial phase with as much as 15 to 40 percent of the absorbed dose excreted in the urine the first week. There is expotential excretion of the remainder of the dose with a half life of 103 days. /Selenite/

Selenium supplements are typically available in the form of sodium selenite which is metabolized to selenide through either glutathione conjugation and subsequent reduction by glutathione reductase enzymes or reduction by thioredoxin reductases. Selenide is further metabolized to selenocystein by cysteine synthases and to selenophosphate by selenophosphate synthases. Selenide is also metabolized progressively to methyl-selenol, dimethyl selenide, then trimethylselenonium. Selenocysteine is degraded to methyl-selenol, pyruvate and ammonia by cysteine beta lyase. Selenocystein reacts with oxygen to form selenocysteine selenoxide which spontaneously degrades to methylselenic acid, pyruvate and ammonia. Methylselenic acid can be converted to methylselenol via conjugation with thiol groups on proteins like glutathione.

Selenium compounds are in part reduced in the body to elemental selenium... Much is metabolized to dimethyl selenide which is excreted by the lungs, imparting a garlic-like odor.

Most dietary selenium is in the form of selenomethionine (the major dietary form of selenium) or selenocysteine, both of which are well absorbed. Other forms of selenium include selenate and selenite, which are not major dietary constituents, but are commonly used in fortified foods and dietary supplements. Two pools of reserve selenium are present in the body. The first is as selenomethionine, which is not known to have a physiological function separate from that of methionine. The second reserve pool is the selenium found in liver glutathione peroxidase. Ingested selenite, selenate, and selenocysteine are all metabolized directly to selenide, the reduced form of selenium. Selenomethionine can also be metabolized to selenide. /Selenium/

In the liver, many selenium compounds are biotransformed to excretable metabolites. Identified metabolites are trimethylselenide in urine and dimethylselenide in breath. /Selenium/

Selenium in the animal body is methylated as an effective detoxication mechanism. ... Selenium in the animal body is in large part attached to protein.

The biological role of selenium in mammals including man is attributed to the presence of selenocysteine at each of four catalytic sites of the enzyme glutathione peroxidase ... . This enzyme uses glutathione to reduce peroxides in cells and, in this way, protects membrane lipids and possibly proteins and nucleic acids from damage by oxidants or free radicals. It may be a functional component of heme oxidase, another enzyme that contains selenium. The requirement for selenium is related to the degree of oxidant activity and the supply of nutrients such as zinc, copper, manganese, iron, and vitamin E, so that increased amounts of these elements increase the need for selenium. Large doses of iron and copper in animals may produce myopathies that resemble effects produced by selenium deficiency per se. /Selenium/

Naturally occurring or synthetic substances that inhibit or retard oxidation reactions. They counteract the damaging effects of oxidation in animal tissues.

A group of chemical elements that are needed in minute quantities for the proper growth, development, and physiology of an organism. (From McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)

Oral bioavailability of 90% when given as L-selenomethionine. Tmax of 9.17h.

Mainly excreted in urine as 1beta-methylseleno-N-acetyl-d-galactosamine and trimethylselenonium. The amount excreted as 1beta-methylseleno-N-acetyl-d-galactosamine plateaus at doses around 2microg after which the amount excreted as trimethylselenonium increases. Some selenium is also excreted in feces when given orally.

Elemental selenium .. is poorly absorbed.

... The distribution and retention of inhaled selenious acid and selenium metal aerosols ... similar in size and chemical form to selenium aerosols that may be produced during fossil fuel combustion /were examined/. Beagle dogs were given 10 to 61 ug Se/kg of body weight by inhalation. Aerosols generated for the inhalation exposures were also collected and instilled into the upper respiratory tracts or stomachs of additional dogs to measure systemic absorption at these sites. Selenium-75, incorporated into the aerosols, was used to determine the Se content in the whole animal, excreta, and individual tissues as a function of time. Virtually all inhaled selenious acid aerosol was rapidly absorbed into the blood from the lungs, gastrointestinal tract, and the nasal membranes. Selenium metal aerosols were less rapidly absorbed. Selenium that was absorbed into the blood was translocated to the liver, kidney, spleen, and heart. Selenium-75 in these organs had a biological half-life of 30 to 40 days. Approximately 50% of the deposited Se was eliminated with a biological half life of 1.2 days. Urine was the major route of excretion, accounting for 70 to 80% of the excreted Se. The long-term component of the whole-body retention function for both inhaled aerosols had a half-life of about 34 days and accounted for about 20% of the initial Se dose. ... Although absorption of selenious acid into blood following inhalation was more rapid than absorption of selenium metal, once absorbed the disposition of both compounds was similar. 6845362

Selenide can be metabolized to a precursor of other reactions or be converted into an excretory metabolite. Selenium is excreted mainly through the urine. The breath may also contain volatile metabolites when large amounts of selenium are being excreted. /Selenide/

At high or toxic dose levels, excretion through expired air becomes important and even predominant. /Selenium/

Selenium is used in the electronics industry; the glass industry; in pigments used in plastics, paints, enamels, inks, and rubber; as a catalyst in the preparation of pharmaceuticals; in antidandruff shampoos (selenium sulfide); and as a constituent of fungicides.

Selenium is an essential trace element in the body. It is present in high concentrations in some soils. In industry, selenium exposure can occur in copper smelting and in the production of pigments, glass, rubber, plastics, pharmaceuticals, and electronic devices. [ACGIH] Used to make photocells, solar cells, photographic exposure meters, and rectifiers; also used as a vulcanizing agent, a glass decolorizer, a photographic toner, and a stainless steel additive; [Rom, p. 1092] Fly ash from burning coal is the major emission source; [ATSDR ToxProfiles]

Steel Producing [Category: Industry]

As ingredient of toning baths in photography; as pigment in mfr of ruby-, pink-, orange-, or red-colored glass; as metallic base in making electrodes for arc lights, electrical instruments and apparatus; as rectifier in radio and television sets; in selenium photocells, in semiconductor fusion mixtures, selenium cells, telephotographic apparatus; as vulcanizing agent in processing of rubber; as catalyst in determination of nitrogen by Kjeldahl method; for dehydrogenation of organic compounds.

In glass manufacturing, selenium is used to decolorize the green tint caused by iron impurities in container glass and other soda-lime silica glass and is used in architectural plate glass to reduce solar heat transmission. ... Selenium is used in catalysts to enhance selective oxidation; in plating solutions, where it improves appearance and durability; in blasting caps and gun bluing; in rubber compounding chemicals; in the electrolytic production of manganese to increase yields; and in brass alloys to improve machinability.

... Dietary supplement for livestock and as a fertilizer additive to enrich selenium-poor soils. It is used as a metallurgical additive to improve machinability of copper, lead, and steel alloys. ...

COMMERCIAL GRADE CONTAINS A MIN OF 99% SELENIUM & MAY CONTAIN MAX 0.2% TELLURIUM, 0.1% IRON, 0.005% LEAD & 0.005% COPPER AS IMPURITIES. ... THE HIGH PURITY GRADE ... IS REPORTED TO CONTAIN A MIN OF 99.99% SELENIUM. IMPURITIES WHICH MAY BE PRESENT @ CONCN NO GREATER THAN 1-2 MG/KG EACH ARE MERCURY, TELLURIUM, IRON, ARSENIC & OTHER NON-FERROUS METALS UNDESIRABLE IN ELECTRONIC & ELECTROSTATIC APPLICATIONS. HIGHER CONCN OF "INERT" CONTAMINANTS SUCH AS SODIUM, MAGNESIUM, CALCIUM, ALUMINUM & SILICON CAN BE TOLERATED. THE ULTRA HIGH PURITY GRADE, PREPARED ONLY ON A LABORATORY SCALE, IS REPORTED TO CONTAIN 0.0001-0.001% IMPURITIES.

Metal, waste and scrap, metric tons: 161 (1986); 162 (1987); 243 (1988); 372 (1989); estimated 260 (1990).

Metal, waste and scrap, metric tons: 175 (1992); 261 (1993); 246 (1994); 269 (1995); and an estimated 270 (1996).

Selenium: Salient Export Statistics for the United States

Metal and dioxide, metric tons: 431 (1986); 445 (1987); 425 (1988); 417 (1989); estimated 400 (1990).

Metal and dioxide, metric tons: 371 (1992); 382 (1993); 411 (1994); 324 (1995); and an estimated 360 (1996).

Selenium: Salient Import Statistics for the United States

2023: 100,000 - <250,000 lb

(1985) 1.95X10+8 g

Refinery: 253 metric tons (1989); estimated 270 metric tons (1990).

Refinery, metric tons: 243 (1992); 283 (1993); 360 (1994); 373 (1995); and an estimated 350 (1996).

Production volume for non-confidential chemicals reported under the 2006 Inventory Update Rule. Chemical: Selenium. Aggregated National Production Volume: 500,000 to <1 million lbs.

END USE: Electronic and photocopier components, 35%; Glass manufacturing, 30%; Chemical and pigments, 25%; and Other, 10% (1985).

Use of selenium and selenium compounds can be divided into the following categories: electronic applications 25%, pigments 10%, glass 40%, metallurgy 10%, agricultural and biological applications 5%, and other uses (additives for rubber vulcanization, oxidation catalysts) 10%.

Estimated consumption of selenium by end use was as follows: electronic and photocopier components, 35%; chemical and pigments, 20%; glass manufacturing, 25%; and other, 20% (1991).

The estimated consumption of selenium by end use was as follows: electronics, 25%; glass manufacturing, 25%; chemicals and pigments, 20%; and other, including agriculture and metallurgy, 20%.

For more Consumption Patterns (Complete) data for SELENIUM, ELEMENTAL (6 total), please visit the HSDB record page.

Use of selenium and selenium compounds can be divided into the following categories: electronic applications 25%, pigments 10%, glass 40%, metallurgy 10%, agricultural and biological applications 5%, and other uses (additives for rubber vulcanization, oxidation catalysts) 10%.

Electrolytic copper refinery slimes are the principal source of selenium and its sister element, tellurium ... Slimes generated by the refining of primary copper, copper produced from ores and concentrates, generally contain from 5-25% selenium and 2-10% tellurium. ... Some of the first processes to recover selenium on a commercial basis were based on roasting of copper slimes with soda ash to convert both selenium and tellurium to the +6 oxidation state. ... Slimes are intensively mixed with sodium carbonate, a binder such as bentonite, and water to form a stiff paste. The paste is extruded or pelletized and allowed to dry. ... Roasting occurs between temperatures of 530-650 °C. ... Conversion of both elements to the hexavalent form is complete. The roasted pellets or extrudes are ground and leached in water. The hexavalent selenium dissolves as sodium selenate, Na2SeO4. Sodium tellurate, being highly insoluble in the now very strongly alkaline solution, remains in the residue. The separation between selenium and tellurium is readily achieved, provided all tellurium is oxidized to the hexavalent state. ... There are two processes commonly employed for reducing selenium from solution. ... In the first process, employed commercially for may years, selenium is leached from the slimes in the form of the hexavalent sodium selenate. It is recovered from solution by crystallization and the crystalline sodium selenate is mixed with charcoal. Under controlled conditions of heating, the Na2SeO4 is reduced to sodium selenide. The sodium selenide cake is leached with water to form a typically liver-red solution of sodium selenide, which is readily oxidized to the elemental form by blowing air through the solution. ... In the second process, reduction of the hexavalent selenium is accomplished using concentrated hydrochloric acid or ferrous iron salts catalyzed by chloride ions as the reductant.

Acid roasting technology relies on differences in the volatility of the tetravalent oxides of selenium and tellurium at roasting temperatures of 500-600 °C to selectively volatilize selenium from slimes. Acid roasting uses sulfuric acid as the oxidant for the conversion of selenium/selenides and tellurium/tellurides to their respective tetravalent oxides. ... Because the oxidation reactions take place well below the temperature at which significant volatilization of elemental selenium occurs, only the readily scrubbable selenium dioxide is present in the vapor phase. Thus, the scrubbing of the off-gases is highly efficient, resulting in virtually complete recovery of the selenium from the gas stream.

Wet chlorination is performed by sparging slimes slurried either in water or hydrochloric acid using chlorine gas, or other oxidants such as sodium chlorate or hydrogen peroxide which liberate chlorine from hydrochloric acid, at about 100 °C. Under these conditions, selenium and selenides rapidly oxidize and dissolve. ... Selenium tetrachloride hydrolyzes to form hydrochloric acid, the degree of hydrolysis depending on the acidity of the solution. ... Selenium and precious metals can be removed selectively from the chlorination liquor by reduction with sulfur dioxide. ... Under proper conditions of precipitation, a selenium/precious metals product substantially free of other impurities can be obtained. Selenium can be recovered in a pure state by vacuum distillation, leaving behind a precious metals residue.

Classically, the purification of elemental selenium from tellurium is achieved by distillation because of the much greater volatility of selenium compared to tellurium. The advantages of distillation, typically at 1.0-0.255 kPa (0.015-0.037 psi) and 300-400 °C, are its simplicity and the absence of emission problems, if performed under vacuum on properly dried, acid-free material. Single-stage distillation can also be carried out at atmospheric pressure at 680_C from cast-iron or iron alloy retorts. In this manner most of the occluded impurities such as sulfur dioxide, water, organic matter, halogens, sulfuric acid, and mercury are expelled to a scrubber, leaving the bulk of the nonvolatile impurities such as tellurium and other metals in the residue. Distillation from a quartz retort upgrades the quality of the selenium. ... A simpler and highly effective purification can be achieved by fluxing molten selenium at about 300 °C in the presence of a eutectic mixture of potassium and sodium nitrates. At 300 °C, selenium does not react significantly with the eutectic nitrate mixture; however, tellurium is oxidized, as are many other impurity metals, and passes into the molten flux layer.

Most binary selenides are formed by heating selenium in the presence of the element, reduction of selenites or selenates with carbon or hydrogen, and double decomposition of heavy-metal salts in aqueous solution or suspension with a soluble selenide salt, eg, Na2Se or (NH4)2Se. /Binary selenides/

Selenium oxyhalides ... are prepared by the addition of a halogen to a dry mixture or a carbon tetrachloride suspension of selenium and selenium dioxide. /Selenium oxyhalides/

Four grades of selenium are available. There is the commercial or refined grade, which contains >99.5 wt% selenium and various impurities, usually <0.2 wt% tellurium, <0.1 wt% iron, <0.005 wt% lead, and <0.005 wt% copper. This grade is sold mainly as 75-mm (200-mesh) powder as well as in smaller quantities of coarser size and as lump. A second, more select pigment grade has a purity of 99.7%. The third grade, high purity selenium, contains 99.999 wt% of selenium, although this figure of purity is obtained by difference and not by a direct determination. This grade is sold usually in shotted form but also in small amounts as a powder. Some users have their own specifications, which reflect a particular application of selenium. ... The fourth grade, called ultrahigh purity selenium, is claimed to contain 99.999-99.9999 wt% selenium.

Available as pellets or powder.

Grades: Commercial (powder or lumps), high-purity up to 99.999%.

Most domestic selenium was produced as commercial-grade metal, averaging a minimum of 99.5% selenium and available in various forms, including shot, lump, or powder, or as pigment-grade powder having a minimum 99.8% selenium content.

Cosmetics product ingredient: Selenium (7782-49-2) and selenium compounds

Information on 1 consumer products that contain Selenium in the following categories is provided: