IPCS INCHEM Home

SELENIUM

1. NAME
   1.1 Substance
   1.2 Group
   1.3 Synonyms
   1.4 Identification numbers
      1.4.1 CAS
      1.4.2 Other numbers
   1.5 Main brand names/main trade names
   1.6 Main manufacturers and/or importers
2. SUMMARY
   2.1 Main risks and target organs
   2.2 Summary of clinical effects
   2.3 Diagnosis
   2.4 First-aid measures and management principles
4. USES/HIGH RISK CIRCUMSTANCES OF POISONING
   4.1 Uses
      4.1.1 Uses
      4.1.2 Description
   4.2 High risk circumstances of poisoning
   4.3 Occupationally exposed populations
5. ROUTES OF EXPOSURE
   5.1 Oral
   5.2 Inhalation
   5.3 Dermal
   5.4 Eye
   5.5 Parenteral
   5.6 Others
7. TOXICOLOGY
   7.1 Mode of action
   7.2 Toxicity
      7.2.1 Human data
         7.2.1.1 Adults
         7.2.1.2 Children
      7.2.2 Relevant animal data
      7.2.3 Relevant in vitro data
      7.2.4 Workplace standards
      7.2.5 Acceptable daily intake (ADI) and other guidelines levels
   7.3 Carcinogenicity
   7.4 Teratogenicity
   7.5 Mutagenicity
   7.6 Interactions
8. TOXICOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS
   8.1 Material sampling plan
      8.1.1 Sampling and specimen collection
         8.1.1.1 Toxicological analyses
         8.1.1.2 Biomedical analyses
         8.1.1.3 Arterial blood gas analysis
         8.1.1.4 Haematological analyses
         8.1.1.5 Other (unspecified) analyses
      8.1.2 Storage of laboratory samples and specimens
         8.1.2.1 Toxicological analyses
         8.1.2.2 Biomedical analyses
         8.1.2.3 Arterial blood analysis
         8.1.2.4 Haematological analyses
         8.1.2.5 Other (unspecified) analyses
      8.1.3 Transport of laboratory samples and specimens
         8.1.3.1 Toxicological analyses
         8.1.3.2 Biomedical analyses
         8.1.3.3 Arterial blood gas analysis
         8.1.3.4 Haematological analyses
         8.1.3.5 Other (unspecified) analyses
   8.2 Toxicological analyses and their interpretation
      8.2.1 Tests on toxic ingredient(s) of material
         8.2.1.1 Simple qualitative test(s)
         8.2.1.2 Advanced qualitative confirmation test(s)
         8.2.1.3 Simple quantitative method(s)
         8.2.1.4 Advanced quantitative method(s)
      8.2.2 Tests for biological specimens
         8.2.2.1 Simple qualitative test(s)
         8.2.2.2 Advanced qualitative confirmation test(s)
         8.2.2.3 Simple quantitative methods(s)
         8.2.2.4 Advanced quantitative method(s)
         8.2.2.5 Other dedicated method(s)
      8.2.3 Interpretation of toxicological analyses
   8.3 Biomedical investigations and their interpretation
      8.3.1 Biochemical analysis
         8.3.1.1 Blood, plasma or serum
         8.3.1.2 Urine
         8.3.1.3 Other fluids
      8.3.2 Arterial blood gas analyses
      8.3.3 Haematological analyses
      8.3.4 Interpretation of biomedical investigations
   8.4 Other biomedical (diagnostic) investigations and their interpretation
   8.5 Overall interpretation of all toxicological analyses and toxicological investigations
   8.6 References
9. CLINICAL EFFECTS
   9.1 Acute poisoning
      9.1.1 Ingestion
      9.1.2 Inhalation
      9.1.3 Skin exposure
      9.1.4 Eye contact
      9.1.5 Parenteral exposure
      9.1.6 Other
   9.2 Chronic poisoning
      9.2.1 Ingestion
      9.2.2 Inhalation
      9.2.3 Skin exposure
      9.2.4 Eye contact
      9.2.5 Parenteral exposure
      9.2.6 Other
   9.3 Course, prognosis, cause of death
   9.4 Systematic description of clinical effects
      9.4.1 Cardiovascular
      9.4.2 Respiratory
      9.4.3 Neurological
         9.4.3.1 CNS
         9.4.3.2 Peripheral nervous system
         9.4.3.3 Autonomic nervous system
         9.4.3.4 Skeletal and smooth muscle
      9.4.4 Gastrointestinal
      9.4.5 Hepatic
      9.4.6 Urinary
         9.4.6.1 Renal
         9.4.6.2 Others
      9.4.7 Endocrine and reproductive systems
      9.4.8 Dermatological
      9.4.9 Eye, ears, nose, throat: local effects
      9.4.10 Hematological
      9.4.11 Immunological
      9.4.12 Metabolic
         9.4.12.1 Acid base disturbances
         9.4.12.2 Fluid and electrolyte disturbances
         9.4.12.3 Others
      9.4.13 Allergic reactions
      9.4.14 Other clinical effects
      9.4.15 Special risks: pregnancy, breast feeding, enzyme deficiencies
   9.5 Others
10. MANAGEMENT
   10.1 General principles
   10.2 Life supportive procedures and symptomatic treatment
   10.3 Decontamination
   10.4 Elimination
   10.5 Antidote treatment
      10.5.1 Adults
      10.5.2 Children
   10.6 Management discussion: alternatives, controversies and research needs
11. ILLUSTRATIVE CASES
   11.1 Case reports from literature
13. REFERENCES

International Programme on Chemical Safety

Poison information Monograph 483

Chemical

1. NAME

1.1 Substance

Selenium and its compounds

1.2 Group

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

1.3 Synonyms

1.4 Identification numbers

1.4.1 CAS

Elemental selenium: 7782-49-2

Selenic acid: 7783-08-6

Selenious acid: 7783-00-8

Selenium dioxide: 7446-08-4

Selenium disulfide: 7488-56-4

Selenium hexafluoride: 7783-79-1

Selenium monochloride: 10025-68-0

Selenium monosulfide: 7446-34-6

Selenium oxychloride: 7791-23-3

Selenium tetrachloride: 10026-03-6

1.4.2 Other numbers

1.5 Main brand names/main trade names

1.6 Main manufacturers and/or importers

2. SUMMARY

2.1 Main risks and target organs

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.

2.2 Summary of clinical effects

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.

2.3 Diagnosis

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.

2.4 First-aid measures and management principles

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.

4. USES/HIGH RISK CIRCUMSTANCES OF POISONING

4.1 Uses

4.1.1 Uses

4.1.2 Description

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.

4.2 High risk circumstances of poisoning

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.

4.3 Occupationally exposed populations

Occupational exposure can occur in all stages of mining and production of selenium containing compounds.

5. ROUTES OF EXPOSURE

5.1 Oral

5.2 Inhalation

This is the usual and most dangerous route of entry of selenium compounds in occupational exposure to fumes, dusts or gas.

5.3 Dermal

Selenium compounds may be absorbed through intact skin (e.g. selenium sulfide in shampoos).

5.4 Eye

No data available.

5.5 Parenteral

No data available.

5.6 Others

No data available.

7. TOXICOLOGY

7.1 Mode of action

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).

7.2 Toxicity

7.2.1 Human data

7.2.1.1 Adults

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).

7.2.1.2 Children

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 g Se/day are necessary to cause selenium toxicity (Yang & Zhou, 1994)

7.2.2 Relevant animal data

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)

7.2.3 Relevant in vitro data

No data available.

7.2.4 Workplace standards

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

7.2.5 Acceptable daily intake (ADI) and other guidelines levels

WHO standard for drinking water: 10 g Se/L

EPA water quality criterion for chronic exposure to selenium: 5 g Se/L.

ADI (EPA): 213 g Se/d

Based on studies on chronic selenosis in China, a maximum safe dietary intake of 400 g Se was recommended (Yang & Zhou, 1994).

7.3 Carcinogenicity

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.

7.4 Teratogenicity

Although selenium is a demonstrated teratogen in birds, there is no evidence for a teratogenic effect in mammals (Barceloux, 1999).

7.5 Mutagenicity

No data available.

7.6 Interactions

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).

8. TOXICOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS

8.1 Material sampling plan

8.1.1 Sampling and specimen collection

8.1.1.1 Toxicological analyses

8.1.1.2 Biomedical analyses

8.1.1.3 Arterial blood gas analysis

8.1.1.4 Haematological analyses

8.1.1.5 Other (unspecified) analyses

8.1.2 Storage of laboratory samples and specimens

8.1.2.1 Toxicological analyses

8.1.2.2 Biomedical analyses

8.1.2.3 Arterial blood analysis

8.1.2.4 Haematological analyses

8.1.2.5 Other (unspecified) analyses

8.1.3 Transport of laboratory samples and specimens

8.1.3.1 Toxicological analyses

8.1.3.2 Biomedical analyses

8.1.3.3 Arterial blood gas analysis

8.1.3.4 Haematological analyses

8.1.3.5 Other (unspecified) analyses

8.2 Toxicological analyses and their interpretation

8.2.1 Tests on toxic ingredient(s) of material

8.2.1.1 Simple qualitative test(s)

8.2.1.2 Advanced qualitative confirmation test(s)

8.2.1.3 Simple quantitative method(s)

8.2.1.4 Advanced quantitative method(s)

8.2.2 Tests for biological specimens

8.2.2.1 Simple qualitative test(s)

8.2.2.2 Advanced qualitative confirmation test(s)

8.2.2.3 Simple quantitative methods(s)

8.2.2.4 Advanced quantitative method(s)

8.2.2.5 Other dedicated method(s)

8.2.3 Interpretation of toxicological analyses

8.3 Biomedical investigations and their interpretation

8.3.1 Biochemical analysis

8.3.1.1 Blood, plasma or serum

"Basic analyses"

"Dedicated analyses"

"Optional analyses"

8.3.1.2 Urine

"Basic analyses"

"Dedicated analyses"

"Optional analyses"

8.3.1.3 Other fluids

8.3.2 Arterial blood gas analyses

8.3.3 Haematological analyses

"Basic analyses"

"Dedicated analyses"

"Optional analyses"

8.3.4 Interpretation of biomedical investigations

8.4 Other biomedical (diagnostic) investigations and their interpretation

8.5 Overall interpretation of all toxicological analyses and toxicological investigations

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)

8.6 References

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

9. CLINICAL EFFECTS

9.1 Acute poisoning

9.1.1 Ingestion

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).

9.1.2 Inhalation

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).

9.1.3 Skin exposure

Dermal exposure to selenium dioxide or selenium oxychloride is associated with dermatitis and skin burns.

9.1.4 Eye contact

Eyes contact with selenious oxide may produce severe blepharoconjunctivitis.

9.1.5 Parenteral exposure

No data available.

9.1.6 Other

No data available.

9.2 Chronic poisoning

9.2.1 Ingestion

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).

9.2.2 Inhalation

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).

9.2.3 Skin exposure

No data available.

9.2.4 Eye contact

No data available.

9.2.5 Parenteral exposure

No data available.

9.2.6 Other

No data available.

9.3 Course, prognosis, cause of death

Acute ingestion of selenious acid is almost invariably fatal. Coma, respiratory depression, hypotension and death can occur several hours after ingestion (Barceloux, 1999).

9.4 Systematic description of clinical effects

9.4.1 Cardiovascular

Severe/refractory hypotension may develop after selenious acid ingestion, secondary to decreased cardiac contractility and low peripheral vascular resistance.

9.4.2 Respiratory

Inhalation of selenium dusts results in respiratory tract irritation. Inhalation of high concentrations of hydrogen selenide may cause bronchopneumonia and pulmonary oedema.

9.4.3 Neurological

9.4.3.1 CNS

Fatigue, irritability, tremor, hyperreflexia, coma have been described (Barceloux, 1999).

9.4.3.2 Peripheral nervous system

Neurological abnormalities including peripheral anesthesia, acroparesthesia, and pain in the extremities have been reported (Yang et al., 1993).

9.4.3.3 Autonomic nervous system

No data available.

9.4.3.4 Skeletal and smooth muscle

Muscle tenderness has been described.

9.4.4 Gastrointestinal

When ingested, selenium sulfide causes nausea, vomiting, metallic taste in the mouth and garlicky smell on the breath.

9.4.5 Hepatic

No data available.

9.4.6 Urinary

9.4.6.1 Renal

No data available.

9.4.6.2 Others

No data available.

9.4.7 Endocrine and reproductive systems

No data available.

9.4.8 Dermatological

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).

9.4.9 Eye, ears, nose, throat: local effects

Nasal discharge, loss of smell, epistaxis have been described after selenium dust exposure (Barceloux, 1999).

9.4.10 Hematological

9.4.11 Immunological

9.4.12 Metabolic

9.4.12.1 Acid base disturbances

9.4.12.2 Fluid and electrolyte disturbances

9.4.12.3 Others

9.4.13 Allergic reactions

9.4.14 Other clinical effects

9.4.15 Special risks: pregnancy, breast feeding, enzyme deficiencies

9.5 Others

10. MANAGEMENT

10.1 General principles

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).

10.2 Life supportive procedures and symptomatic treatment

Management hypotension and acute pulmonary edema as necessary.

10.3 Decontamination

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.

10.4 Elimination

There are no methods to increase selenium elimination.

10.5 Antidote treatment

10.5.1 Adults

There are no antidotes

10.5.2 Children

There are no antidotes

10.6 Management discussion: alternatives, controversies and research needs

11. ILLUSTRATIVE CASES

11.1 Case reports from literature

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).

13. REFERENCES

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

14. AUTHOR(S), REVIEWER(S) DATE
(INCLUDING EACH UP-DATE), COMPLETE ADDRESSES

Authors:

Dr E.A. Scarlato
Dr J. Higa
Sección Toxicología
Hospital de Clínicas
José de San Martín
Buenos Aires
Argentina

Date:

28 June 1990

Updated:

M-O Rambourg Schepens, March 2001

Peer review:

L. Lefevre, L. Murray, A. Nantel,
Edinburgh, September 2001.



    See Also:
       Toxicological Abbreviations
       Selenium (EHC 58, 1986)
       Selenium (ICSC)
.