International Programme on Chemical Safety
Poison information Monograph 483
Chemical
Selenium and its compounds
Inorganic; selenium and its compounds.
The main substances of this group are:
Elemental selenium
Selenium salts: selenite and selenate
Selenious acid
Selenic acid
Selenium dioxide
Selenium disulfide
Selenium hexafluoride
Selenium monochloride
Selenium monosulfide
Selenium oxychloride
Selenium tetrachloride
Elemental selenium:
Selenic acid:
Selenious acid:
Selenium dioxide:
Selenium disulfide:
Selenium hexafluoride:
Selenium monochloride:
Selenium monosulfide:
Selenium oxychloride:
Selenium tetrachloride:
The toxicity depends on the chemical form of selenium.
Selenite is more toxic than selenate.
Target organs include: respiratory tract, CNS, cardiovascular system, gastrointestinal tract, skin.
Acute:
Inhalation of hydrogen selenide causes pulmonary oedema. Selenium dusts produce respiratory tract irritation. Exposure to selenium dioxide fumes causes signs and symptoms of metal fume fever.
Ingestion of selenious acid causes corrosive injury to the gastrointestinal tract, stupor, respiratory depression and refractory hypotension and ARDS.
Dermal exposure to selenium dioxide or selenium oxychloride may produce skin burns.
Chronic:
Chronic selenosis is extremely rare but has been reported in an occupational setting. It may be associated with nausea and vomiting, muscle tenderness, tremor, emotional lability, garlicky breath, bitter metallic taste in the mouth, brittle hair and nails, and skin lesions.
Diagnosis of acute poisoning is based on history and the presence of hypotension, loss of consciousness, respiratory depression and a garlicky odour of the breath after exposure to elemental selenium or its compounds.
Diagnosis of chronic poisoning is only confirmed on biological testing.
Eye contact: immediate and copious irrigation with water.
Skin contact: wash contaminated area immediately and copiously with soap or a soft detergent and water. Contaminated clothes should be removed.
Inhalation: remove victim from exposure. Perform respiratory resuscitation as needed. Give supplemental oxygen.
Ingestion: management of acute and chronic intoxication of selenium poisoning is supportive only. Decontamination is not normally indicated (see treatment guide: acid ingestion). There are no antidotes.
Selenium and its compounds have many commercial uses, these include:
Electronics (photoelectric cells, semiconductors, low-voltage rectifiers)
Ceramics, glass (pigments and dyes)
Steel (alloy with copper)
Gun-bluing solutions (selenious acid and copper nitrate and nitric acid)
Rubber vulcanizing
Chemistry (catalyst)
Photocopy (xerographic properties)
Medicine: selenium sulfide is used for the treatment of pityriasis versicolor and palmar plantar mycosis as a 2.5% lotion and dandruff and seborrhoeic dermatitis of the scalp.
For the general population, the primary pathway of exposure to selenium is food (meats, fish, poultry, grains, cereal products), water (selenate) and air (combustion of fossil fuels and coal) but such exposures do not result in poisoning (Barceloux, 1999).
Serious toxicity most commonly occurs following ingestion of gun-bluing solutions.
Occupational exposure can occur in all stages of mining and production of selenium containing compounds.
This is the usual and most dangerous route of entry of selenium compounds in occupational exposure to fumes, dusts or gas.
Selenium compounds may be absorbed through intact skin (e.g. selenium sulfide in shampoos).
No data available.
No data available.
No data available.
The toxicity depends on the chemical form of selenium. Human toxicity from environmental exposure to elemental selenium and selenium salts is rare. Exposure to selenious acid or to selenium dioxide can cause serious toxicity (Barceloux, 1999).
Selenium facilitates the lowering of tissue peroxide levels in the body by destroying hydrogen peroxide through the action of the selenium-containing enzyme, glutathione peroxidase. Animal studies suggest that the cytotoxicity of selenium results from the pro-oxidant catalytic activity of the selenide anions, which produce super oxide anions, hydrogen peroxide and other reactive metabolites. Methylating reactions in plants and animals along with antioxidant defenses counteract the toxicity of selenium species (Barceloux, 1999).
Organic selenium compounds (dimethylselenide, trimethylselenonium ion, selenoethers, selenobetaine) and selenate are much less toxic in animal studies compared with selenite (Barceloux, 1999).
Ingestion of 22 mg sodium selenate/kg caused serious toxicity (Civil & Mc Donald, 1978); ingestion of 1-5 mg sodium selenite/kg caused toxicity which resolved in 24 hours (Barceloux, 1999).
A 30-60 ml ingestion of gun blue (2 % selenious acid) resulted in death (Pentel et al., 1985).
A 10 g oral dose of selenium dioxide resulted in death (Koppel et al., 1986).
A 15 ml ingestion of gun blue (2 % selenious acid) by a two-year-old resulted in death (Nantel et al., 1985).
It is estimated that doses > 900 µg Se/day are necessary to cause selenium toxicity (Yang & Zhou, 1994)
Alkali disease in cattle and horses results from the ingestion of grain and forage containing 5-50 ppm Se.
A subacute form of the disease (blind staggers) occurred in livestock feeding on plants that contained up to 10 000 ppm Se. (Barceloux, 1999)
No data available.
OSHA permissible exposure limit:
Selenium compounds (as Se): 0.2 mg/m3
Selenium hexafluoride: 0.05 ppm (USA)
NIOSH immediately dangerous to life or health level (IDHL)
Selenium compounds: 100 mg/m3
Selenium hexafluoride: 5 ppm
ACGIH Threshold Limit Value (TLV-TWA)
Selenium and compounds as Se: 0.2 mg/m3
Selenium hexafluoride as Se: 0.05 ppm
WHO standard for drinking water: 10 µg Se/L
EPA water quality criterion for chronic exposure to selenium: 5 µg Se/L.
ADI (EPA): 213 µg Se/d
Based on studies on chronic selenosis in China, a maximum safe dietary intake of 400 µg Se was recommended (Yang & Zhou, 1994).
Several studies suggest that selenium is anti-mutagenic and anti-carcinogenic (Bronzetti & Della Croce, 1993).
Human epidemiological and demographic studies do not suggest that selenium is carcinogenic and neither the IARC nor the US NTP lists selenium and its salts as suspected carcinogens (Barceloux, 1999).
However the US NTP (1994) lists selenium sulfide as a suspected carcinogen based on animal studies.
Although selenium is a demonstrated teratogen in birds, there is no evidence for a teratogenic effect in mammals (Barceloux, 1999).
No data available.
Various substances (e.g. arsenic, cysteine, heavy metals, sulfate and vitamins C and E) can alter the toxicity of selenium (Wilber, 1980; Fan et al., 1988).
"Basic analyses"
"Dedicated analyses"
"Optional analyses"
"Basic analyses"
"Dedicated analyses"
"Optional analyses"
"Basic analyses"
"Dedicated analyses"
"Optional analyses"
The usual urine selenium is < 0.03 mg Se/L in normal individuals without occupational exposure (Robberecht & Deelsta, 1984).
Usually no symptoms are associated with urine levels < 0.1 mg Se/L.
Urine concentrations > 0.4 - 0.7 mg Se/L indicates excessive recent exposure.
Blood selenium levels are usually < 0.2 mg/L. The concentration in the erythrocyte is greater than the concentration in plasma and the ratio of plasma Se to erythrocyte Se decreases as the whole blood concentration increases. Plasma concentrations reflect changes in the intake of selenium more rapidly than concentrations of selenium in erythrocytes where proteins firmly bind selenium. Consequently whole blood and selenium content in the erythrocytes are better indicators of long-term exposure to selenium (Yang & Zhou, 1994; Barceloux, 1999)
Barceloux DG (1999) Selenium. Clin Toxicol, 37: 145-172
Robberecht Hj & Deelsta HAP (1984) Selenium in human urine: concentration levels and medical implications. Clin Chim Acta, 136: 107-120
Yang G & Zhou R (1994) Further observations on the human maximum safe dietary selenium intake in a seleniferous area in China. J Trace Elem Electrolytes Health Dis, 8: 159-165
Ingestion of selenious acid causes clinical features of corrosive injury to the gastrointestinal tract, stupor, respiratory depression, hypotension and death. A garlic odour on the breath is characteristic of selenium poisoning (Carter, 1966).
Acute inhalation of high concentrations of hydrogen selenide produces intense upper respiratory tract irritation and metallic taste in the mouth followed by bronchopneumonia and pulmonary oedema.
Inhalation of selenium dusts or fumes is associated with respiratory tract irritation manifested by cough, nasal discharge, epistaxis, loss of smell and headache. Inhalation of selenium dioxide may cause signs and symptoms of metal fume fever (Barceloux, 1999).
Dermal exposure to selenium dioxide or selenium oxychloride is associated with dermatitis and skin burns.
Eyes contact with selenious oxide may produce severe blepharoconjunctivitis.
No data available.
No data available.
Chronic selenosis is a rare entity but has been reported following ingestion of selenium-rich foods. It manifests as morphological changes of the fingernails, alopecia, skin lesions, tooth decay and neurological disorders (Yang et al.,1983).
Chronic inhalation of hydrogen selenide is associated with chronic diarrhea, abdominal pain, garlicky breath, a bitter metallic taste in the mouth and nail changes (Alderman & Bergin, 1986).
No data available.
No data available.
No data available.
No data available.
Acute ingestion of selenious acid is almost invariably fatal. Coma, respiratory depression, hypotension and death can occur several hours after ingestion (Barceloux, 1999).
Severe/refractory hypotension may develop after selenious acid ingestion, secondary to decreased cardiac contractility and low peripheral vascular resistance.
Inhalation of selenium dusts results in respiratory tract irritation. Inhalation of high concentrations of hydrogen selenide may cause bronchopneumonia and pulmonary oedema.
Fatigue, irritability, tremor, hyperreflexia, coma have been described (Barceloux, 1999).
Neurological abnormalities including peripheral anesthesia, acroparesthesia, and pain in the extremities have been reported (Yang et al., 1993).
No data available.
Muscle tenderness has been described.
When ingested, selenium sulfide causes nausea, vomiting, metallic taste in the mouth and garlicky smell on the breath.
No data available.
No data available.
No data available.
No data available.
Selenium oxychloride causes vesicles (Pillière, 1992).
Selenium dioxide is more than a primary irritant, it causes extremely painful burns on the skin which, however, always heal without a scar. Theoretically, the selenium dioxide powder itself does not burn the skin (and if dropped on to the skin should be immediately brushed off dry). However, in practice, in the industrial environment, there is sufficient moisture on the skin from sweating to be taken up by this white solid to form a sticky solution of selenious acid within seconds, or at the most, minutes, of coming into contact with the skin.
After skin exposure to 50 % solution of selenious acid, signs develop within several hours: unremitting intense pain, red and swollen skin, blisters, which may be followed by ulcerations.
Chronic exposure to selenium manifests as brittle nails and hair, pruritic skin rash; longitudinal streaks or transverse lines may appear on the surface of the nail in the form of yellowish-white or red discoloration (Barceloux, 1999).
Nasal discharge, loss of smell, epistaxis have been described after selenium dust exposure (Barceloux, 1999).
Eye contact: immediate and copious irrigation with water.
Skin contact: wash contaminated area immediately and copiously with soap or a soft detergent and water. Contaminated clothes should be removed.
Inhalation: remove victim from exposure. Perform respiratory resuscitation as needed. Give supplemental oxygen.
Ingestion: the management of acute and chronic intoxication of selenium poisoning is supportive only; there are no antidotes. Decontamination attempts are not normally indicated (refer treatment guide: acid ingestion).
Management hypotension and acute pulmonary edema as necessary.
Eye contact: immediate and copious irrigation with water.
Skin contact: wash contaminated area immediately and copiously with soap and water; 10 % sodium thiosulfate solutions may be of benefit in cases of exposure to selenium dioxide (Pillière, 1992). Contaminated clothes should be removed.
Gastrointestinal decontamination is not normally indicated.
There are no methods to increase selenium elimination.
There are no antidotes
There are no antidotes
A young woman exposed repeatedly to hydrogen selenide gas developed gastrointestinal complaints, dental caries, conjunctivitis, nail deformities, and garlic smelling breath (Alderman & Bergin, 1986).
A 15 ml ingestion of gun blue (2% selenious acid) by a 2 year old and 30 to 60 ml ingestion by an adult resulted in death (Nantel et al., 1985; Pentel et al., 1985).
Alderman LC & Bergin JJ (1986) Hydrogen selenide poisoning: an illustrative case with review. Arch Environ Health, 41: 354-358
Barceloux DG (1999) Selenium. Clin Toxicol, 37: 145-172
Bronzetti G & Della Croce C (1993) Selenium: its important roles in life and contrasting aspects. J Environ Pathol Toxicol Oncol, 12: 59-71
Carter RF (1966) Acute selenium poisoning. Med J Aust, 1: 525-528
Civil IDS & Mc Donald MJA (1978) Acute selenium poisoning. Case report. NZ Med J, 87: 354-356
Fan AM, Book SA, Neutra RR, Epstein DM (1988) Selenium and human health implications in California's San Joaquin Valley. J Toxicol Environ Health, 23: 539-559
Koppel C, Baudisch H, Beyer KH, Kloppel I, Schneider V (1986) Fatal poisoning with selenium dioxide. Clin Toxicol, 24: 21-35
Nantel AJ, Brown M, Dery P, Lefebvre L (1985) Acute poisoning by selenious acid. Vet Hum Toxicol, 27: 531-533
NIOSH/OSHA Pocket Guide to Chemical Hazards Editors (2000): National Institute for Occupational Safety and Health (NIOSH) and Occupational Safety and Health Administration (OSHA).
National Toxicology Program (1994). Seventh annual report on carcinogens summary 1994. Washington DC: US Department of Health and Human Services, Public Health Service
Pentel P, Fletcher D, Jentzen J (1985) Fatal acute selenium toxicity. J Forensic Sci, 30: 556-562
Pillière F (1992) Indium et sélénium. Editions techniques. Encycl Med Chir (Paris, France) Toxicologie-Pathologie professionnelle, 16-002-1-10, 4p
Robberecht Hj & Deelsta HAP (1984) Selenium in human urine: concentration levels and medical implications. Clin Chim Acta, 136: 107-120
WHO (1984) Environmental Health Criteria. Selenium. N° 58. Geneva
Wilber CG (1980) Toxicology of selenium: a review. Clin Toxicol, 17: 171-230
Yang G, Wang S, Zhou R, Sun S (1983) Endemic selenium intoxication of humans in China. Am J Clin Nutr, 37: 872-881
Yang G & Zhou R (1994) Further observations on the human maximum safe dietary selenium intake in a seleniferous area in China. J Trace Elem Electrolytes Health Dis, 8: 159-165
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Authors: |
Dr E.A. Scarlato |
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Date: |
28 June 1990 |
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Updated: |
M-O Rambourg Schepens, March 2001 |
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Peer review: |
L. Lefevre, L. Murray, A. Nantel, |
See Also:
Toxicological Abbreviations
Selenium (EHC 58, 1986)
Selenium (ICSC)