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SELENIUM

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) This management primarily deals with inorganic selenium salts. Selenium dioxide and selenious acid are more toxic and are discussed in a separate document.

Specific Substances

    A) No Synonyms were found in group or single elements
    1.2.1) MOLECULAR FORMULA
    1) Se

Available Forms Sources

    A) FORMS
    1) Selenium is available in commercial grade as powder or lumps, or high purity grades up to 99.999% and in 40 and 200 mesh grades (HSDB , 1998; Lewis, 1993).
    2) The most important toxicological selenium compounds include: selenium dioxide, selenious acid, sodium selenite, sodium selenate, and iron selenide. Elemental selenium has not been found to produce serious intoxication in humans although there have been reports of chronic selenium poisoning in animals following the ingestion of seleniferous plants.
    B) SOURCES
    1) Selenium is a non-metallic element with an atomic number of 34. Although widely distributed in nature, it generally occurs naturally in sulfide ores of heavy metals and as part of the minerals clausthalite, naumannite, and tiemannite but not in a pure elemental form. Selenium is an essential trace nutrient in the diets of animals and humans serving as a catalyst for the enzyme glutathione peroxidase. However, selenium is toxic in larger amounts (ACGIH, 1991; Budavari, 1996).
    C) USES
    1) Selenium is used in the manufacture of colored glass (red, ruby, pink, orange) and in pigments, ceramics, semiconductors, electrodes and other electrical instruments, and photocells. It is used in photography, xerography, and telephotography. It is used as a vulcanizing agent for rubber, an alloy for steel and copper, and as a catalyst (ACGIH, 1991; Sittig, 1991).
    2) NUTRITIONAL/SUPPLEMENT FORMS - Selenium supplements can occur in several different forms. Most supplements come in the form of selenomethionine, an amino acid. Blood selenium levels are usually due to the selenomethionine content of food in most individuals. The L-isomer of selenomethionine is considered the preferred form for supplements intended for human consumption (Schrauzer, 2001).
    a) PRODUCT RECALL - In May 2008, a voluntary recall of an over-the-counter liquid nutritional supplement marketed as Total Body Formula and Total Body Mega Formula (distributed by Total Body Essential Nutrition, Atlanta, GA) was conducted due to extremely elevated levels of selenium, as well as moderately elevated chromium levels. Analysis of the product resulted in a selenium concentration of 800.50 mcg/mL instead of the purported selenium concentration of 7.33 mcg/mL per bottle (Sutter et al, 2008).
    3) MEDICINAL/SHAMPOOS - Selenium sulfide is available as an anti-bacterial, antiseborrhic shampoo (Selsun(R), Excel(R)).
    4) INTENTIONAL MISUSE - Two fatal cases of selenium toxicity have been reported, and were likely due to the use of selenium as a homicidal agent. Both individuals died within 24 hours of apparent exposure (Spiller & Pfiefer, 2007).

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Elemental selenium is low in toxicity. All selenium salts may produce toxicity by ingestion, inhalation, and percutaneous absorption.
    B) WITH POISONING/EXPOSURE
    1) Acute selenium poisoning is potentially lethal due to cardiocirculatory failure and/or pulmonary edema. Garlic-like odor on the breath may be noted in patients with selenium poisoning.
    2) Selenium dioxide and selenious acids and its salts are capable of penetrating the skin and can produce acute poisonings.
    3) Selenium DUST is an eye and respiratory tract irritant, and can cause coughing, sneezing, breathing difficulty, and headache. The FUME is also irritating to the eye, nose and throat, and can cause pulmonary edema, delayed in onset by 1 to 4 hours. INHALATION of selenium fumes caused bronchospasm, chills, fever, headache, and chemical pneumonitis; similar to symptoms associated with metal fume fever. Skin burns can also result from exposure to fumes.
    4) Although no predictive nomogram currently exists, NO serious sequelae is anticipated with a blood selenium level under 1,000 micrograms/liter; levels over 2,000 micrograms/liter indicate potential serious effects.
    0.2.3) VITAL SIGNS
    A) WITH POISONING/EXPOSURE
    1) Fever has been reported following selenium exposure.
    0.2.5) CARDIOVASCULAR
    A) WITH POISONING/EXPOSURE
    1) Hypotension, decreased peripheral pulse, dysrhythmias and cardiac arrest have been observed.
    2) Hypotension and tachycardia are early signs of acute toxicity.
    0.2.6) RESPIRATORY
    A) Acute lung injury and cardiopulmonary arrest are possible.
    0.2.7) NEUROLOGIC
    A) Dizziness, decreased reflexes, CNS depression, and coma have been reported.
    0.2.8) GASTROINTESTINAL
    A) Gastrointestinal effects are generally the first symptoms seen. Acute effects may include: vomiting, hypersalivation, diarrhea, abdominal pain, a burning sensation in the nostrils and/or oral mucosa, chemical burns of the alimentary tract and a garlic-like odor on the breath.
    0.2.9) HEPATIC
    A) Fatty degeneration of the liver and cirrhosis have been reported.
    0.2.10) GENITOURINARY
    A) Mild tubular degeneration has been noted.
    0.2.14) DERMATOLOGIC
    A) Dermatitis and nasal irritation may be present.
    B) WITH POISONING/EXPOSURE
    1) Hair loss and nail changes including onycholysis may occur following chronic exposure or following a significant acute exposure. Skin lesions have also occurred with chronic exposure.

Laboratory Monitoring

    A) Whole blood selenium levels in individuals ranged from 1.33 to 7.5 mcg/mL. Normal levels in the US are 0.1 mcg/mL.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) ACTIVATED CHARCOAL: Administer charcoal as a slurry (240 mL water/30 g charcoal). Usual dose: 25 to 100 g in adults/adolescents, 25 to 50 g in children (1 to 12 years), and 1 g/kg in infants less than 1 year old.
    B) Besides supportive treatment, there is no specific treatment for this rare type of human poisoning.
    C) Ascorbic acid and EDTA are of no or equivocal use, and bromobenzene may be dangerous.
    0.4.3) INHALATION EXPOSURE
    A) INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Range Of Toxicity

    A) The Food and Nutrition Board of the National Research Council have suggested a range of 50 to 200 mcg/day as adequate dietary intake. The upper limit of 200 mcg/day is a conservative one. The reference dose (RfD) for selenium set by EPA is 350 mcg/d for an adult weighing 70 kg. Observation in Japanese fishermen suggests that intakes of selenium from 10 to 200 times normal have not been shown to produce toxic effects.
    B) Ingestion of 31 mg/day for 11 days produced symptoms of toxicity.
    C) Fatalities were reported in adults, one of whom ingested 10 g selenium dioxide (100 mg Se/kg) and the other 20 mL of 42% sodium selenate (5 mg Se/kg).
    D) Chronic selenium toxicity was reported in individuals ingesting 3.2 to 6.7 mg/day.

Clinical Effects

Summary Of Exposure

    A) Elemental selenium is low in toxicity. All selenium salts may produce toxicity by ingestion, inhalation, and percutaneous absorption.
    B) WITH POISONING/EXPOSURE
    1) Acute selenium poisoning is potentially lethal due to cardiocirculatory failure and/or pulmonary edema. Garlic-like odor on the breath may be noted in patients with selenium poisoning.
    2) Selenium dioxide and selenious acids and its salts are capable of penetrating the skin and can produce acute poisonings.
    3) Selenium DUST is an eye and respiratory tract irritant, and can cause coughing, sneezing, breathing difficulty, and headache. The FUME is also irritating to the eye, nose and throat, and can cause pulmonary edema, delayed in onset by 1 to 4 hours. INHALATION of selenium fumes caused bronchospasm, chills, fever, headache, and chemical pneumonitis; similar to symptoms associated with metal fume fever. Skin burns can also result from exposure to fumes.
    4) Although no predictive nomogram currently exists, NO serious sequelae is anticipated with a blood selenium level under 1,000 micrograms/liter; levels over 2,000 micrograms/liter indicate potential serious effects.

Vital Signs

    3.3.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Fever has been reported following selenium exposure.
    3.3.3) TEMPERATURE
    A) WITH POISONING/EXPOSURE
    1) CASE SERIES: Selenium poisoning was identified in 201 cases across 10 states in the Southeastern US following the consumption of a dietary supplement manufactured in September 2007, that was incorrectly formulated and contained 200 times (40800 mcg/30 mL) the labeled concentration (200 mcg/30 mL) of selenium. Of the 201 cases, 43 (21%) developed fever (MacFarquhar et al, 2010). Fever has not been previously reported with exposure, and the authors could not determine if fever was directly related to selenium toxicity.

Heent

    3.4.3) EYES
    A) CONJUNCTIVITIS: Redness and blurring of the eyes have been noted (Alderman & Bergin, 1986).
    B) MYDRIASIS has been observed (Gasmi et al, 1997).
    3.4.5) NOSE
    A) BURNING SENSATION of the nostrils, local irritation and necrosis of the oral mucous membranes, sneezing and nasal congestion have been reported (Alderman & Bergin, 1986; Gasmi et al, 1997).
    3.4.6) THROAT
    A) SORE THROAT: Acute sore throats and coryza-like symptoms with lacrimation and metallic taste, and garlicky breath odor are frequently reported (Motley & Ellis, 1937).

Cardiovascular

    3.5.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Hypotension, decreased peripheral pulse, dysrhythmias and cardiac arrest have been observed.
    2) Hypotension and tachycardia are early signs of acute toxicity.
    3.5.2) CLINICAL EFFECTS
    A) CONDUCTION DISORDER OF THE HEART
    1) ECG effects noted include T wave flattening progressing to T wave inversion and a prolonged QT interval (Spiller & Pfiefer, 2007; Williams & Ansford, 2007; Nuttall, 2006; Civil & McDonald, 1978). There have been reports of transient T wave inversion following an overdose. Animal studies reveal direct cardiac effects. Hypotension and decreased peripheral pulse may occur (Gasmi et al, 1997).
    B) HYPOTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) Fatalities due to acute selenium toxicity are typically preceded by refractory hypotension from peripheral vasodilation and direct myocardial depression (Spiller & Pfiefer, 2007; Nuttall, 2006).
    b) CASE SERIES - Patients with severe toxicity have developed circulatory failure related to decreased cardiac contractility and low peripheral vascular resistance. Milder cases developed some hemodynamic disturbances and ECG changes (Gasmi et al, 1997).
    C) CARDIAC ARREST
    1) A 40-year-old female died from cardiac arrest 8 hours after ingestion of a gun blueing agent containing selenious acid, copper sulfate, and hydrochloric acid; postmortem blood selenium concentration was 2600 mcg/L (Gasmi et al, 1997).

Respiratory

    3.6.1) SUMMARY
    A) Acute lung injury and cardiopulmonary arrest are possible.
    3.6.2) CLINICAL EFFECTS
    A) ACUTE LUNG INJURY
    1) Pulmonary edema has been observed following inhalation and ingestion (Nuttall, 2006; Gasmi et al, 1997). Inhalation of selenium dioxide and selenium oxychloride fumes may result in respiratory irritation. Hydrogen selenide gas has resulted in irritation of the mucous membranes of nose, eyes, and upper respiratory tract (Alderman & Bergin, 1986).
    2) CASE REPORT: A young healthy patient developed severe dyspnea and a pneumomediastinum after acute exposure. Initially the patient had severe coughing and wheezing which progressed to irreversible obstructive lung disease (Schecter et al, 1980).
    3) CASE REPORT: A 52-year-old female developed acute respiratory distress syndrome secondary to pulmonary edema following an intentional ingestion of a gun blueing preparation; serum selenium concentration on day 5 was 2765 micrograms/liter. Death occurred on day 6 from an extensive small bowel infarct presumed secondary to prolonged episodes of hypotension (Gasmi et al, 1997).
    B) METAL FEVER
    1) WITH POISONING/EXPOSURE
    a) CASE SERIES: Workers exposed to an undetermined concentration of selenium oxide developed bronchospasm and dyspnea followed within 12 hours by metal fume fever (chills, fever, headache) and bronchitis, leading to pneumonitis in 5 individuals who received less first aid treatment than the other 32 men involved in the incident. All symptoms resolved within one week (Wilson, 1962).

Neurologic

    3.7.1) SUMMARY
    A) Dizziness, decreased reflexes, CNS depression, and coma have been reported.
    3.7.2) CLINICAL EFFECTS
    A) CENTRAL NERVOUS SYSTEM FINDING
    1) Dizziness, CNS depression, tremors, restlessness, fatigue, sluggish pupillary reflexes, headache, clouding of the sensorium, confusion, brain edema, and coma have all been noted with selenium toxicity (MacFarquhar et al, 2010; Nuttall, 2006; Kise et al, 2004).
    2) CASE SERIES: Selenium poisoning was identified in 201 cases across 10 states in the Southeastern US following the consumption of a dietary supplement manufactured in September 2007, that was incorrectly formulated and contained 200 times (40800 mcg/30 mL) the labeled concentration (200 mcg/30 mL) of selenium. Of the 201 cases, 90 (45%) developed headache, 78 (39%) developed tinging and ataxia was reported in 27 (13%) individuals. A follow-up questionnaire was sent to 150 patients after a median of 106 days from the onset of symptoms, persistent symptoms (90 days or more after cessation of the supplement) included memory loss (n=18/83), fatigue (n=22/63), and mood changes (n=14/81) (MacFarquhar et al, 2010).
    3) CASE REPORT: Coma, asystole and apnea occurred in a 17-year-old male following an ingestion of 10 g of selenium dioxide; death occurred 45 minutes after admission with a postmortem blood selenium concentration of 38,000 micrograms/liter (Koppel et al, 1986).
    4) CASE REPORT: A 48-year-old female developed mildly altered consciousness and hematemesis (vomiting garlicky smelling blood) after ingesting 2000 mg of selenium dioxide (10 times the experimental lethal dose in animals) (Kise et al, 2004).
    B) PARESTHESIA
    1) Chronic ingestion of high selenium-content vegetables has produced paresthesias and hyperreflexia indicating a toxic polyneuritis (Yang et al, 1983).

Gastrointestinal

    3.8.1) SUMMARY
    A) Gastrointestinal effects are generally the first symptoms seen. Acute effects may include: vomiting, hypersalivation, diarrhea, abdominal pain, a burning sensation in the nostrils and/or oral mucosa, chemical burns of the alimentary tract and a garlic-like odor on the breath.
    3.8.2) CLINICAL EFFECTS
    A) NAUSEA AND VOMITING
    1) WITH POISONING/EXPOSURE
    a) Nausea, vomiting, hypersalivation, and abdominal pain are frequently present following acute selenium intoxication (Spiller & Pfiefer, 2007; Williams & Ansford, 2007; Schuh & Jappe, 2007; Nuttall, 2006; Diskin et al, 1979; Lombeck et al, 1987; Gasmi et al, 1997).
    b) CASE REPORT: Abdominal pain, vomiting, and diarrhea were reported in a 56-year-old male who ingested 1.7 g of sodium selenite (Gasmi et al, 1997).
    c) CASE SERIES: Selenium poisoning was identified in 201 cases across 10 states in the Southeastern US following the consumption of a dietary supplement manufactured in September 2007, that was incorrectly formulated and contained 200 times (40800 mcg/30 mL) the labeled concentration (200 mcg/30 mL) of selenium. Of the 201 cases, 115 (57%) patients developed nausea and 52 (26%) developed vomiting. A follow-up questionnaire was sent to 150 patients after a median of 106 days from the onset of symptoms, persistent symptoms (90 days or more after cessation of the supplement) included nausea (n=9/83). (MacFarquhar et al, 2010).
    B) DIARRHEA
    1) WITH POISONING/EXPOSURE
    a) Diarrhea is frequently observed following acute selenium intoxication (Sutter et al, 2008; Spiller & Pfiefer, 2007; Williams & Ansford, 2007; Nuttall, 2006).
    b) CASE REPORTS: Severe diarrhea was reported in two adults following inadvertent acute selenium intoxication. Gastrointestinal symptoms resolved with the discontinuation of selenium (Schuh & Jappe, 2007). Diarrhea was reported in previously healthy children (ages 1, 4, and 8 years) inadvertently exposed to excessive amounts of selenium found in a nutritional supplement. The two oldest children had taken the supplement without adverse events prior to a nationwide recall because of excessive amount of selenium (ie, intended selenium content was 7.33 mcg/mL, while the product contained 800.5 mcg/mL). Symptoms improved after stopping the supplement (Webb & Kerns, 2009). Of note, the youngest child was exposed to excessive amounts of selenium during breastfeeding.
    c) CASE SERIES: Selenium poisoning was identified in 201 cases across 10 states in the Southeastern US following the consumption of a dietary supplement manufactured in September 2007, that was incorrectly formulated and contained 200 times (40800 mcg/30 mL) the labeled concentration (200 mcg/30 mL) of selenium. Of the 201 cases, 156 (78%) of the patients developed diarrhea which was the most common adverse event reported (MacFarquhar et al, 2010).
    C) BREATH SMELLS UNPLEASANT
    1) GARLIC-LIKE BREATH: In the absence of strong garlic-like odor of the breath, the differential diagnosis of selenium poisoning is a difficult one. A garlic odor suggests possible garlic, phosphorous, selenium, tellurium, and arsenic. Fumes of selenium have an unpleasant garlic-like odor.
    2) Garlicky odor of the breath is thought to be due to the exhalation of dimethyl selenide and is reported in most cases (Gasmi et al, 1997). Garlicky odor of the breath has also been reported following the ingestion of selenium dioxide (Kise et al, 2004).
    D) ACUTE HEMORRHAGIC GASTRITIS
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 23-year-old woman inadvertently ingested approximately 100 mL of selenite broth (selenite enrichment culture media) and developed hemorrhagic gastritis and severe acute renal failure. Initially, the patient developed nausea and vomiting along with epigastric tenderness. Selenium level was 1.7 micromol/L (normal: 0.75 to 1.51 micromol/L). Hematemesis developed after 48 hours. A gastro-duodenoscopy (OGD) showed severe hemorrhagic gastritis. The patient was started on a proton pump inhibitor and sucralfate, but had another episode of hematemesis. A repeat OGD study showed large clots on the gastric greater curvature along with diffuse mucosal and submucosal hemorrhages. Following aggressive therapy including multiple blood transfusions, fresh frozen plasma, and platelet concentrates the bleeding stopped and the patient gradually improved. At 6 months there was no evidence of gastric strictures (Kamble et al, 2009).
    E) ACUTE BOWEL INFARCTION
    1) CASE REPORT: A 52-year-old female developed ARDS secondary to pulmonary edema following an intentional ingestion of a gun blueing preparation; serum selenium concentration on day 5 was 2765 micrograms/liter. Death occurred on day 6 from an extensive small bowel infarct presumed secondary to prolonged episodes of hypotension (Gasmi et al, 1997).
    F) CHEMICAL BURN
    1) Selenium ingestions can cause first and/or secondary burns or erosion of the alimentary tract (Gasmi et al, 1997). Mouth blisters were reported in young children inadvertently exposed to chronic excessive amounts of selenium found in a nutritional supplement. Of note, the two older children had tolerated the supplement for the prior 3 years. The product underwent a nationwide recall and was found to contain 800.5 mcg/mL instead of the intended 7.33 mcg/mL of selenium (Webb & Kerns, 2009).
    2) CASE REPORT: A 48-year-old female developed mildly altered consciousness and hematemesis (vomiting garlicky smelling blood) after ingesting 2000 mg of selenium dioxide (10 times the experimental lethal dose in animals). Endoscopy showed mucosal damage (necrotic tissue and deep ulcers) throughout the oral cavity, esophagus, and stomach. Within 3 to 6 hours after ingestion, serum and urinary selenium levels peaked above 2000 mcg/L and above 1000 mcg/L, respectively. Following supportive care and hemodialysis, she was discharged uneventfully on day 16 (Kise et al, 2004).

Hepatic

    3.9.1) SUMMARY
    A) Fatty degeneration of the liver and cirrhosis have been reported.
    3.9.2) CLINICAL EFFECTS
    A) LIVER ENZYMES ABNORMAL
    1) Elevation of liver function tests, especially bilirubin, persisted for 6 days after ingestion of sodium selenate (Civil & McDonald, 1978).
    2) CASE REPORT: A 48-year-old female developed mildly altered consciousness and hematemesis (vomiting garlicky smelling blood) after ingesting 2000 mg of selenium dioxide (10 times the experimental lethal dose in animals). She developed liver dysfunction (SGOT 188 units/L; SGPT 192 units/L, total bilirubin 0.6 g/dL) on the 5th day postingestion. Following supportive care and hemodialysis, she was discharged uneventfully on day 16 (Kise et al, 2004).
    B) STEATOSIS OF LIVER
    1) Fatty degeneration of the liver and cirrhosis has been reported (Carter, 1966).

Genitourinary

    3.10.1) SUMMARY
    A) Mild tubular degeneration has been noted.
    3.10.2) CLINICAL EFFECTS
    A) RENAL TUBULAR DISORDER
    1) Mild tubular degeneration of the kidneys has been noted (Carter, 1966).
    B) ACUTE RENAL FAILURE SYNDROME
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 23-year-old woman inadvertently ingested approximately 100 mL of selenite broth (selenite enrichment culture media) and developed hemorrhagic gastritis and severe acute renal failure. Selenium level was 1.7 micromol/L (normal: 0.75 to 1.51 micromol/L). The patient developed oligo-anuria within 48 hours of admission and serum creatinine (692 micromol/L or 7.82 mg/dL) and BUN (25.8 mmol/L) rose significantly. Hemodialysis was started and renal biopsy showed normal glomeruli with proximal tubular epithelial necrosis. The patient continued to receive dialysis for 4 weeks and was discharged to home at 5 weeks. Renal function was completely normal within 8 weeks (Kamble et al, 2009) .

Dermatologic

    3.14.1) SUMMARY
    A) Dermatitis and nasal irritation may be present.
    B) WITH POISONING/EXPOSURE
    1) Hair loss and nail changes including onycholysis may occur following chronic exposure or following a significant acute exposure. Skin lesions have also occurred with chronic exposure.
    3.14.2) CLINICAL EFFECTS
    A) DERMATITIS
    1) Selenium compounds may cause dermatitis.
    B) SKIN LESION
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT - A woman developed sores on her skin and scalp following inadvertent chronic exposure to excessive amounts of selenium found in a nutritional supplement. Four months after onset of illness the patient's selenium concentration was 233 mcg/L (reference range: 110-160). Symptoms gradually improved approximately one month after stopping the supplement (Webb & Kerns, 2009). The product underwent a nationwide recall and was found to contain 800.5 mcg/mL of selenium instead of the intended 7.33 mcg/mL.
    C) HAIR DISCOLORATION
    1) CASE REPORT/CHRONIC - Red hair and fingernails were noted in a 71-year-old male who worked in a selenium refinery for 50 years (Buell, 1983). Chronic ingestion of vegetable with high-selenium content resulted in loss of hair and nails, skin lesions on the back of hands and feet and outside of the legs (Yang et al, 1983).
    D) ALOPECIA
    1) WITH POISONING/EXPOSURE
    a) Hair loss can be observed following chronic selenium toxicity (Webb & Kerns, 2009; Nuttall, 2006). It has also been reported following a significant acute exposure (Sutter et al, 2008; Schuh & Jappe, 2007).
    b) CASE SERIES: Selenium poisoning was identified in 201 cases across 10 states in the Southeastern US following the consumption of a dietary supplement manufactured in September 2007, that was incorrectly formulated and contained 200 times the labeled concentration of selenium. Of the 201 cases, 140 (70%) of the patients developed hair loss. The proportion of scalp hair lost was a median of 50% (range: 10% to 100%). A follow-up questionnaire was sent to 150 patients after a median of 106 days from the onset of symptoms, with 14 (18%; n=78) patients reporting complete hair loss of the scalp (MacFarquhar et al, 2010).
    c) CASE REPORTS - A 51-year-old man and a 44-year-old woman attended a clinic for 14 days to participate in a fasting regimen which included a very low calorie diet, mineral supplements including selenium powder, and developed severe scalp hair loss. The selenium dosage was determined to be approximately 10 times higher than recommended by the treatment protocol (specific dose not specified). Selenium concentrations were 4.4 mcmol/L for the woman and 4.9 mcmol/L for the man (normal 0.75 to 1.8); all other laboratory studies were normal. Two months after exposure, hair regrowth had begun (Schuh & Jappe, 2007).
    E) ALOPECIA TOTALIS
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT/CHRONIC - Total body hair loss was noted in a 31-year-old male exposed to selenium while working in a factory manufacturing photocopy machine drums (Srivastava et al, 1995).
    b) CASE REPORT - A 55-year-old woman developed progressive hair loss on her scalp, which eventually extended to total body hair loss after taking a liquid nutritional supplement containing selenium for approximately 7 weeks. The supplement was found to contain 800.50 mcg/mL of selenium instead of the purported 7.33 mcg/mL per bottle. Based on a daily supplement of 30 mL/day, the patient's daily dose of selenium was 24,015 mcg (304.14 mcmol), or an estimated 400 times the US recommended daily allowance of 55 mcg (Sutter et al, 2008).
    F) DRUG-INDUCED NAIL ABNORMALITY
    1) WITH POISONING/EXPOSURE
    a) Nail changes are often present with chronic selenium exposure (Nuttall, 2006). It has also been observed following a significant acute exposure (Schuh & Jappe, 2007; Sutter et al, 2008)
    b) CASE SERIES: Selenium poisoning was identified in 201 cases across 10 states in the Southeastern US following the consumption of a dietary supplement manufactured in September 2007, that was incorrectly formulated and contained 200 times (40800 mcg/30 mL) the labeled concentration (200 mcg/30 mL) of selenium. Of the 201 cases, 122 (61%) cases developed nail discoloration or brittleness. A follow-up questionnaire was sent to 150 patients after a median of 106 days from the onset of symptoms, persistent symptoms (90 days or more after cessation of the supplement) included fingernail discoloration or brittleness and nail loss (MacFarquhar et al, 2010).
    c) CASE REPORTS - Two adults developed white-brownish discoloration of their nails following acute selenium intoxication. Selenium concentrations were 4.4 mcmol/L for the woman and 4.9 mcmol/L for the man (normal 0.75 to 1.8); all other laboratory studies were normal. Approximately 4 to 5 weeks after exposure, complete onycholysis of all nails of the hand and feet occurred. Within two months of exposure, selenium concentrations returned to normal and nail regrowth had begun (Schuh & Jappe, 2007).
    G) MEE'S LINE
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A woman developed Mees' lines and other symptoms consistent with selenium toxicity after inadvertent chronic exposure to excessive amounts of selenium found in a nutritional supplement. Four months after onset of illness the patient's selenium concentration was 233 mcg/L (reference range: 110-160). Symptoms gradually improved approximately one month after stopping the supplement (Webb & Kerns, 2009). The product underwent a nationwide recall and was found to contain 800.5 mcg/mL of selenium instead of the intended 7.33 mcg/mL.
    b) CASE REPORT: A 55-year-old woman developed progressive Mees lines and total body hair loss after taking a liquid nutritional supplement for approximately 7 weeks. The nutritional supplement was analyzed and found to contain 800.50 mcg/mL of selenium instead of the purported 7.33 mcg/mL per bottle. Based on a daily supplement of 30 mL/day, the patient's daily dose of selenium was 24,015 mcg (304.14 mcmol), or an estimated 400 times the US recommended daily allowance of 55 mcg (Sutter et al, 2008).

Musculoskeletal

    3.15.2) CLINICAL EFFECTS
    A) MUSCULOSKELETAL FINDING
    1) WITH POISONING/EXPOSURE
    a) Muscle spasm may develop following acute toxicity. Elevations of serum creatine kinase (CK) concentrations may also develop, and usually occurs shortly after exposure and peaks at 4 to 5 days; MB fraction of CK usually remains low (Nuttall, 2006).
    B) JOINT PAIN
    1) WITH POISONING/EXPOSURE
    a) CASE SERIES: Selenium poisoning was identified in 201 cases across 10 states in the Southeastern US following the consumption of a dietary supplement manufactured in September 2007, that was incorrectly formulated and contained 200 times (40800 mcg/30 mL) the labeled concentration (200 mcg/30 mL) of selenium. Of the 201 cases, 135 (67%) developed joint pain. A follow-up questionnaire was sent to 150 patients after a median of 106 days from the onset of symptoms, persistent symptoms (90 days or more after cessation of the supplement) included joint pain (n=17/65), muscles pain/aches (n=17/77) and weakness (n=16/80) (MacFarquhar et al, 2010).

Endocrine

    3.16.2) CLINICAL EFFECTS
    A) HYPOTHYROIDISM
    1) Loren et al (1997) reported a case of altered thyroid function in an elderly male given selenium.

Immunologic

    3.19.2) CLINICAL EFFECTS
    A) HYPERSENSITIVITY REACTION
    1) WITH POISONING/EXPOSURE
    a) Several young children (ages 1, 4 and 8 years) were inadvertently exposed to excessive amounts of selenium following nutritional supplementation and developed intermittent symptoms of hives and bronchospasm. The children improved with no permanent sequelae (Webb & Kerns, 2009). Of note, the youngest child was exposed while being breastfed; the mother had also taken the supplement and developed symptoms of selenium toxicity.

Reproductive

    3.20.2) TERATOGENICITY
    A) HUMANS
    1) There has been no association between selenium levels in the diet and birth defects in Venezuela, a high-selenium area (Jaffe & Velez, 1973). One study concluded that there was a possibly lower neonatal death rate in high-selenium areas (Shamberger, 1971), but a reanalysis of the same data concluded the opposite (Cowgill, 1976).
    B) ANIMAL STUDIES
    1) Excess selenium has also reduced reproduction in farm animals, and caused hoof and eye defects and neonatal deaths (Clayton & Clayton, 1993; Barlow & Sullivan, 1982).
    2) Selenium and its compounds have generally not been teratogenic in laboratory animals, but have been fetotoxic at high doses which were also toxic to the mothers (Clayton & Clayton, 1993) Shepard, 1985; (Yonemoto, 1983). Low levels of selenium in the drinking water produced runts and reduced the number of offspring in mice and rats by the third generation (RTECS , 1997; Clayton & Clayton, 1993; Schroeder & Mitfhener, 1971).
    3.20.3) EFFECTS IN PREGNANCY
    A) PLACENTAL BARRIER
    1) Selenium is transferred freely across the placenta and is found in the human fetus in concentrations proportional to the maternal blood level (Alfthan, 1986; Barlow & Sullivan, 1982).
    2) There are several reports of occupational exposure to selenium associated with reproductive effects. In an accidental exposure in a laboratory, all subsequent pregnancies over the next five years were abnormal: four terminated in miscarriage and one live-born infant had club foot deformity (talipes equinovaris) (Robertson, 1970). However, in this case it is not clear what other chemical exposures may have been present on a chronic basis, and there have been no further reports of abnormal pregnancies associated with selenium exposure since this article was published in 1970.
    3) An unconfirmed association with abortions has been suggested (Barlow & Sullivan, 1982).
    4) Selenium levels in blood cells and plasma decline during pregnancy, with the lowest values found at term (Zachara et al, 1993). While selenium levels in serum are normally reduced during pregnancy, they were significantly lower in a group of 40 women who miscarried during the first trimester than in matched women who did not miscarry. The possible benefit of selenium supplementation during pregnancy has not been proven, however (Barrington et al, 1996).
    5) No correlation has been seen between selenium concentrations during pregnancy and either the length of gestation or birth weight (Bedwal et al, 1993). Higher levels of plasma selenium were found in full-term infants than in premature infants (Mask & Lane, 1993).
    6) In one study, parenteral supplementation with 3 mcg/kg/day was effective in increasing serum levels in preterm infants, but not to levels seen in term breastfed infants (Daniels et al, 1996).
    B) ANIMAL STUDIES
    1) When selenium was given to mice in the drinking water at a level of 25 ppm, litter size was 53.8 percent larger, average litter weight was 5 percent higher, and gestation time was 3.2 days shorter than in controls (Chiachun et al, 1991).
    3.20.4) EFFECTS DURING BREAST-FEEDING
    A) BREAST MILK
    1) Selenium has been found in breast milk in varying amounts with an average of 0.02 ppm. No adverse affects have been reported.
    2) Selenium is transferred to breast milk in a dose-related fashion (Bedwal et al, 1993; Barlow & Sullivan, 1982).
    3) CASE REPORT/EXPOSURE - A one-year-old developed symptoms associated with selenium toxicity (ie, intermittent effects included: diarrhea, hives, bronchospasm and mouth blisters described in the child and other siblings; no further specific information was provided) after being breastfed. The mother developed toxicity after inadvertently being exposed to excessive amounts of selenium found in a nutritional supplement; the product was later recalled. The two other siblings also developed symptoms of selenium toxicity after direct oral intake of the supplement. No permanent sequelae were reported (Webb & Kerns, 2009). The mother's selenium concentration was 233 mcg/L (reference range: 110-160), four months after onset of symptoms.
    4) In one study, parenteral supplementation with 3 mcg/kg/day was effective in increasing serum levels in preterm infants, but not to levels seen in term breastfed infants (Daniels et al, 1996).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS7782-49-2 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
    1) IARC Classification
    a) Listed as: Selenium and selenium compounds
    b) Carcinogen Rating: 3
    1) The agent (mixture or exposure circumstance) is not classifiable as to its carcinogenicity to humans. This category is used most commonly for agents, mixtures and exposure circumstances for which the evidence of carcinogenicity is inadequate in humans and inadequate or limited in experimental animals. Exceptionally, agents (mixtures) for which the evidence of carcinogenicity is inadequate in humans but sufficient in experimental animals may be placed in this category when there is strong evidence that the mechanism of carcinogenicity in experimental animals does not operate in humans. Agents, mixtures and exposure circumstances that do not fall into any other group are also placed in this category.
    3.21.3) HUMAN STUDIES
    A) LACK OF EFFECT
    1) Data on mutagenicity and carcinogenicity are inadequate for evaluation (Barlow & Sullivan, 1982).
    2) In one study exposure to selenium was protective against lung cancer in copper smelter workers (Gerhardsson et al, 1986).
    3) Selenium can reduce the toxicity and carcinogenicity of some metals and organic carcinogens, perhaps by different mechanisms. Its activity against metals is thought to be due to competition for metal-binding proteins, while organic carcinogens may be inactivated by its anti-oxidant activity (Whanger, 1992).
    4) In one occupational study of selenium rectifier workers, there were no excess cancer deaths (Glover, 1970).
    5) Epidemiological studies have indicated a possible INVERSE relationship between chronic selenium exposure and cancer (Clayton & Clayton, 1993) ACGIH, 1992).
    6) Selenium had a protective effect against breast cancer in persons who did not take selenium supplements; serum selenium blood levels in the range of 1 to 1.21 mcmol/L had a significant protective effect (Hardell et al, 1993).
    7) No differences were seen in selenium concentration or glutathione peroxidase activity in the blood of women with breast cancer, in comparison with healthy women (Wasowicz et al, 1993).
    8) There was a significantly lower risk of dying from cancer among persons receiving dietary supplementation of beta carotene, vitamin E, and selenium in Linxian County, China, which has one of the highest rates of esophageal/gastric cancer in the world (Blot et al, 1993).
    9) In a prospective study relating levels of selenium in the toenails with risk of lung cancer, subjects in the highest quartile of selenium status had only half the rate of lung cancer as compared to those in the lowest quartile, but only for those subjects with a low intake of vitamin C or beta-carotene (Vandenbrandt et al, 1993).
    10) Higher levels of serum selenium did not protect against development of colon cancer in a case-control study of 25 cancer patients and 139 adenoma patients, compared with 138 cancer-free controls (Nelson et al, 1995). A study of 1312 dermatologic patients with a history of skin carcinomas given 200 mg of selenium or placebo found mixed cancer-preventative results. Treatment for 2.8 to 4.5 years with follow-up of 2 to 6.4 years revealed that selenium did not significantly affect the incidence of basal cell or squamous cell skin cancer. However, it was associated with a significantly reduced cancer mortality, total cancer incidence, and incidences of lung, colorectal, and prostate cancers (Clark et al, 1996).
    11) There was no correlation between risk for development of squamous cell carcinoma and plasma selenium levels in a nested case-control study (Karagas et al, 1997).
    3.21.4) ANIMAL STUDIES
    A) LACK OF EFFECT
    1) Selenium has not conclusively caused cancer in experimental animal studies (Friberg et al, 1986).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Whole blood selenium levels in individuals ranged from 1.33 to 7.5 mcg/mL. Normal levels in the US are 0.1 mcg/mL.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) A study of 10 individuals demonstrated a linear correlation of whole blood selenium levels with dietary intake. For eight individuals on normal diets, intake ranged from 90 to 168 mcg/day and blood levels from 0.143 to 0.211 mcg/mL. Two individuals received 350 mcg and 600 mcg/day for 18 months; whole blood levels were 0.345 and 0.642 mg/mL, respectively. Average hair levels in the United States are 0 to 0.5 ppm. Over a wide range of selenium intakes, 50 to 70% of the total excreted selenium is present in the urine.
    B) REFERENCE RANGE
    1) In the 3rd National Health and Nutrition Examination Survey (NHANES III), serum selenium concentrations (from 5th to 95 percentile) in 7012 US males 14 years of age and older was 101-151 mcg/L. For females in the same age range it was 98 to 150 mcg/L (Nuttall, 2006).
    4.1.3) URINE
    A) URINARY LEVELS
    1) The most reliable indication for determining urinary selenium content is the 24-hour excretion measurement. Normal values are stated as less than 30 mcg/L. In the intoxicated state or exposure to high environmental selenium, urine can be used to monitor selenium status. In pathological conditions where changed selenium levels in urine are found, a combination of monitoring parameters such as selenium blood level, urinary excretion, and glutathione peroxidase activity in erythrocytes or platelets should be recommended (Robberecht & Deelstra, 1984).
    4.1.4) OTHER
    A) OTHER
    1) HAIR
    a) An increase in selenium content in hair was noted 10 weeks after an ingestion of up to 2.88 g in a 2 year old (Lombeck et al, 1987).
    2) OTHER
    a) NAILS - In a study of 142 subjects living in a high selenium area, selenium levels in toenails correlated well with selenium levels in blood, serum, urine and dietary intake (Longnecker et al, 1991).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) Whole blood selenium levels in individuals ranged from 1.33 to 7.5 mcg/mL. Normal levels in the US are 0.1 mcg/mL.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) EMESIS/NOT RECOMMENDED
    1) EMESIS: Ipecac-induced emesis is not recommended because of the potential for CNS depression.
    B) ACTIVATED CHARCOAL
    1) PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION
    a) Consider prehospital administration of activated charcoal as an aqueous slurry in patients with a potentially toxic ingestion who are awake and able to protect their airway. Activated charcoal is most effective when administered within one hour of ingestion. Administration in the prehospital setting has the potential to significantly decrease the time from toxin ingestion to activated charcoal administration, although it has not been shown to affect outcome (Alaspaa et al, 2005; Thakore & Murphy, 2002; Spiller & Rogers, 2002).
    1) In patients who are at risk for the abrupt onset of seizures or mental status depression, activated charcoal should not be administered in the prehospital setting, due to the risk of aspiration in the event of spontaneous emesis.
    2) The addition of flavoring agents (cola drinks, chocolate milk, cherry syrup) to activated charcoal improves the palatability for children and may facilitate successful administration (Guenther Skokan et al, 2001; Dagnone et al, 2002).
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.2) PREVENTION OF ABSORPTION
    A) ACTIVATED CHARCOAL
    1) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.3) TREATMENT
    A) CHELATION THERAPY
    1) EDTA has been shown to be effective in increasing the survival of animals poisoned with selenium, but only if given within 15 minutes of the ingestion. This agent was ineffective in animals poisoned with large doses of selenium and/or if given longer than 15 minutes after the ingestion and EDTA and its selenium complex are thought to be nephrotoxic.
    B) EXPERIMENTAL THERAPY
    1) ASCORBIC ACID
    a) It has been noted that in animals circulating ascorbic acid levels are lowered in selenium poisoning. In vitro experiments also show that the toxic salts of selenium are reduced to relatively non-toxic elemental selenium by ascorbic acid; however, animal studies using large amounts of ascorbic acid have produced equivocal results.
    2) BROMOBENZENE
    a) Bromobenzene has been proposed as useful in the treatment of selenium poisoning; however, when given orally to rats no significant increase in the urinary output of selenium was noted. Moreover, bromobenzene is an extremely toxic drug with severe reactions in man. Its usefulness in human poisonings obviously requires more evidence before being considered.

Abstracts

Case Reports

    A) ADULT
    1) A 57-year-old female began taking 150 mcg selenium tablets as a dietary supplement along with at least one Vitamin C (1 g tablet) daily. Eleven days later, symptoms of toxicity began to develop. She reported progressive hair and nail loss over a three-week period, periodic episodes of nausea and vomiting, a sour-milk breath odor, and increasing fatigue.
    2) The product was recalled several months later due to superpotency. The woman had already consumed 77 tablets which subsequently were found to contain 31 mg of total selenium per tablet. The estimated cumulative dose of selenium ingested over the 77 days was 2,387 mg. The reported serum selenium level of 0.528 mcg/mL was approximately four times the normal level for the US population.
    3) Her symptoms of toxicity may have been minimized by the concurrent ingestion of large Vitamin C doses. Vitamin C reduces selenite to elemental selenium that is poorly absorbed (MMWR, 1984).

Range Of Toxicity

Summary

    A) The Food and Nutrition Board of the National Research Council have suggested a range of 50 to 200 mcg/day as adequate dietary intake. The upper limit of 200 mcg/day is a conservative one. The reference dose (RfD) for selenium set by EPA is 350 mcg/d for an adult weighing 70 kg. Observation in Japanese fishermen suggests that intakes of selenium from 10 to 200 times normal have not been shown to produce toxic effects.
    B) Ingestion of 31 mg/day for 11 days produced symptoms of toxicity.
    C) Fatalities were reported in adults, one of whom ingested 10 g selenium dioxide (100 mg Se/kg) and the other 20 mL of 42% sodium selenate (5 mg Se/kg).
    D) Chronic selenium toxicity was reported in individuals ingesting 3.2 to 6.7 mg/day.

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) Human data are not readily available to identify the estimated toxic dose of selenium compounds.
    2) In rats, the median lethal dose of selenomethionine (a seleno amino acid) given by intraperitoneal injection was estimated to be 4.25 mg Se/kg body weight, which is comparable to selenite or selenate (Schrauzer, 2000).
    B) CASE REPORTS
    1) CASE SERIES - Although a predictive nomogram does not currently exist, a blood selenium concentration under 1,000 mcg/L would predict NO serious damage or mild toxicity; levels over 2,000 mcg/L are predictive of serious damage (Kise et al, 2004; Gasmi et al, 1997).
    2) A 75-year-old man with prostate cancer had a cardiac arrest, which was unresponsive to resuscitation efforts approximately 6 hours after ingesting 10 g of selenium to treat his cancer. Postmortem blood selenium concentration was 3 mg/L (Williams & Ansford, 2007).
    3) A 17-year-old died after ingesting 10 g selenium dioxide (estimated 100 mg Se/kg) (Nuttall, 2006).
    4) A 22-year-old developed abdominal pain, vomiting, diarrhea, cardiovascular failure and died 15 hours after ingesting 20 mL of 42% sodium selenate (estimated 5 mg Se/kg) (Nuttall, 2006).

Maximum Tolerated Exposure

    A) GENERAL/SUMMARY
    1) The recommended dietary allowance for selenium (Se) is 55 mcg daily. However, the average American adult may ingest approximately 80 to 150 mcg Se/d. The Reference Dose for Se from all nutritional sources for an adult (weighing 70 kg) has been established by the Environmental Protection Agency at 350 mcg/d. This corresponds to 5 mcg Se/kg body weight/day or 5 times the recommended dietary allowance (this would allow for an additional 200 mcg Se/d supplement in adult consuming a normal diet) (Schrauzer, 2001; Schrauzer, 2000).
    2) The insoluble selenium sulfide is less toxic than the highly toxic soluble selenites, selenates, and organic selenium compounds (Henschler & Kirschner, 1969).
    B) CASE REPORTS
    1) NUTRITIONAL SUPPLEMENT/RECALLED
    a) CASE SERIES: Selenium poisoning was identified in 201 cases across 10 states in the Southeastern US following the consumption of a dietary supplement manufactured in September 2007, that was incorrectly formulated and contained 200 times (40800 mcg/30 mL) the labeled concentration (200 mcg/30 mL) of selenium. The estimated selenium dose was 41749 mcg/day (recommended daily dietary allowance is 55 mcg/day). Initial serum selenium concentrations were obtained in 8 individuals at a median of 1 day (range: 0 to 33 days) after supplement cessation with a mean concentration of 761 mcg/L (range: 321 to 1550 mcg/L; 3 individuals were above 1000 mcg/L (normal reference mean: 125 mcg/L)). Symptoms reported frequently included: diarrhea (78%), fatigue (75%), hair loss (72%), joint pain (70%), nail discoloration or brittleness (61%) and nausea (58%). A follow-up questionnaire was sent to 150 patients after a median of 106 days from the onset of symptoms, persistent symptoms (90 days or more after cessation of the supplement) were as follows: nail changes (loss, discoloration) (52%), fatigue (35%), and hair loss (29%) (MacFarquhar et al, 2010).
    b) A 55-year-old woman with persistent diarrhea developed progressive hair loss on her scalp, which eventually extended to total body hair loss after taking a liquid nutritional supplement containing selenium for approximately 7 weeks. Other symptoms included generalized muscle cramps, joint pain, nail changes, fatigue, and difficulty concentrating. The nutritional supplement was analyzed and found to contain 800.50 mcg/mL of selenium instead of the purported 7.33 mcg/mL per bottle. Based on a daily intake of 30 mL/day, the patient's estimated dose of selenium was 24,015 mcg (304.14 mcmol), or an estimated 400 times the US recommended daily allowance of 55 mcg (Sutter et al, 2008).
    2) SELENITE BROTH
    a) A 23-year-old woman inadvertently ingested approximately 100 mL of selenite broth (selenite enrichment culture media, contains 4 g sodium selenite/L) and developed severe hemorrhagic gastritis and acute renal failure. Selenium level was 1.7 micromol/L (normal: 0.75 to 1.51 micromol/L). The patient was managed aggressively with multiple blood transfusions, fresh frozen plasma, and hemodialysis for 4 weeks. She was discharged to home at 5 weeks; no permanent sequelae was observed at 6 months (Kamble et al, 2009).
    3) GENERAL
    a) A 48-year-old female developed mildly altered consciousness and hematemesis (vomiting garlicky smelling blood) after ingesting 2000 mg of selenium dioxide (10 times the experimental lethal dose in animals). Endoscopy showed mucosal damage (necrotic tissue and deep ulcers) throughout the oral cavity, esophagus, and stomach. Within 3 to 6 hours after ingestion, serum and urinary selenium levels peaked above 2000 mcg/L and above 1000 mcg/L, respectively. Following supportive care and hemodialysis, she was discharged uneventfully on day 16 (Kise et al, 2004).
    b) An adult reportedly ingested a 1.7 grams of sodium selenite resulting in abdominal pain, vomiting and diarrhea which resolved over one week (Gasmi et al, 1997).
    c) A 15-year-old girl ingested sodium selenate containing sheep drench, estimated dose was 22.3 mg Se/kg. She developed a garlic odor and diarrhea, ECG revealed T wave inversion and QTc prolongation which reached a maximum at 3 days post ingestion and resolved at 2 weeks (Nuttall, 2006).
    4) CASE SERIES
    a) A report by Yang from the Republic of China described a major outbreak of apparent selenium toxicity. The disease was characterized by the loss of hair and nail and skin lesions on the back of the hands and feet and outer side of the legs. In regions of China with the most intense exposure, the residents had symptoms of a toxic polyneuritis. Individual daily intake in the area ranged from 3.2 milligrams to 6.69 milligrams (average 4.99 milligrams), and whole blood levels of selenium ranged from 1.33 micrograms/milliliter to 7.5 micrograms/milliliter (average 3.2 micrograms/milliliter) (Yang et al, 1983).
    b) No clinical evidence of selenium toxicity was found in a group of 142 subjects half of whom had an average selenium intake of more than 200 micrograms/day (range 68 to 724 micrograms/day) (Longnecker et al, 1991).
    C) CHRONIC THERAPY
    1) No adverse effects were reported in individuals ingesting 750 to 850 mcg daily for prolonged periods. Intakes of this magnitude were the basis for the 'No Adverse Effect Level' (NOAEL). The Lowest Adverse Effect Level (LOAEL) is thought to be between 1540 +/- 653 mcg/day (producing overt signs of toxicity), which is based on an average daily selenium intake (Schrauzer, 2001).

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) ACUTE
    a) CASE SERIES: Although a predictive nomogram does not currently exist, a blood selenium concentration under 1000 mcg/L would predict NO serious damage; levels over 2000 mcg/L are predictive of serious damage (Gasmi et al, 1997).
    2) CHRONIC/SUPPLEMENT RECALL
    a) CASE SERIES: Selenium poisoning was identified in 201 cases across 10 states in the Southeastern US following the consumption of a dietary supplement manufactured in September 2007, that was incorrectly formulated and contained 200 times (40800 mcg/30 mL) the labeled concentration (200 mcg/30 mL) of selenium. The estimated selenium dose was 41749 mcg/day (recommended daily dietary allowance is 55 mcg/day). Initial serum selenium concentrations were obtained in 8 individuals at a median of 1 day (range: 0 to 33 days) after supplement cessation with a mean concentration of 761 mcg/L (range: 321 to 1550 mcg/L; 3 individuals were above 1000 mcg/L (normal reference mean: 125 mcg/L)). A follow-up questionnaire was sent to 150 patients after a median of 106 days from the onset of symptoms, persistent symptoms (90 days or more after cessation of the supplement) were as follows: nail changes (loss, discoloration) (52%), fatigue (35%), and hair loss (29%) (MacFarquhar et al, 2010).
    b) CASE REPORT: A woman developed symptoms consistent with selenium toxicity after inadvertent chronic exposure to excessive amounts of selenium found in a nutritional supplement; the product later underwent a nationwide recall. Four months after the onset of illness, the patient's selenium concentration was 233 mcg/L (reference range: 110 to 160 mcg/L). Symptoms gradually improved approximately one month after stopping the supplement (Webb & Kerns, 2009). The product underwent a nationwide recall and was found to contain 800.5 mcg/mL of selenium instead of the intended 7.33 mcg/mL per bottle.
    c) CASE REPORT: A 55-year-old woman developed a serum selenium concentration of 534 mcg/L (or 6.76 mcmol/L), and a spot urinary selenium concentration of 220 mcg/L (or 2.79 mcmol/L) after taking a nutritional supplement containing selenium for approximately 7 weeks. The supplement was analyzed and found to contain 800.5 mcg/mL of selenium instead of the purported 7.33 mcg/mL per bottle. Based on a daily intake of 30 mL/day, the patient's estimated daily dose was 24,015 mcg (304.14 mcmol), or an estimated 400 times the US recommended daily allowance of 55 mcg. The patient was symptomatic, but recovered (Sutter et al, 2008).
    3) POSTMORTEM
    a) The blood selenium concentration was 3 mg/L postmortem in a 75-year-old man that had ingested 10 g of selenium (Williams & Ansford, 2007).

Workplace Standards

    A) ACGIH TLV Values for CAS7782-49-2 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.
    a) Adopted Value
    1) Selenium and compounds, as Se
    a) TLV:
    1) TLV-TWA: 0.2 mg/m(3)
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: Not Listed
    2) Codes: Not Listed
    3) Definitions: Not Listed
    c) TLV Basis - Critical Effect(s): Eye and URT irr
    d) Molecular Weight: 78.96
    1) For gases and vapors, to convert the TLV from ppm to mg/m(3):
    a) [(TLV in ppm)(gram molecular weight of substance)]/24.45
    2) For gases and vapors, to convert the TLV from mg/m(3) to ppm:
    a) [(TLV in mg/m(3))(24.45)]/gram molecular weight of substance
    e) Additional information:
    b) Adopted Value
    1) Selenium and compounds, as Se
    a) TLV:
    1) TLV-TWA: 0.2 mg/m(3)
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: Not Listed
    2) Codes: Not Listed
    3) Definitions: Not Listed
    c) TLV Basis - Critical Effect(s): Eye and URT irr
    d) Molecular Weight: 78.96
    1) For gases and vapors, to convert the TLV from ppm to mg/m(3):
    a) [(TLV in ppm)(gram molecular weight of substance)]/24.45
    2) For gases and vapors, to convert the TLV from mg/m(3) to ppm:
    a) [(TLV in mg/m(3))(24.45)]/gram molecular weight of substance
    e) Additional information:

    B) NIOSH REL and IDLH Values for CAS7782-49-2 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Selenium and compounds (as Se)
    2) REL:
    a) TWA: 0.2 mg/m(3)
    b) STEL:
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s): [*Note: The REL and PEL also applies to other selenium compounds (as Se) except Selenium hexafluoride.]
    3) IDLH:
    a) IDLH: 1 mg Se/m3
    b) Note(s): Not Listed

    C) Carcinogenicity Ratings for CAS7782-49-2 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Selenium and compounds, as Se
    2) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Selenium and compounds, as Se
    3) EPA (U.S. Environmental Protection Agency, 2011): D ; Listed as: Selenium and Compounds
    a) D : Not classifiable as to human carcinogenicity.
    4) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): 3 ; Listed as: Selenium and selenium compounds
    a) 3 : The agent (mixture or exposure circumstance) is not classifiable as to its carcinogenicity to humans. This category is used most commonly for agents, mixtures and exposure circumstances for which the evidence of carcinogenicity is inadequate in humans and inadequate or limited in experimental animals. Exceptionally, agents (mixtures) for which the evidence of carcinogenicity is inadequate in humans but sufficient in experimental animals may be placed in this category when there is strong evidence that the mechanism of carcinogenicity in experimental animals does not operate in humans. Agents, mixtures and exposure circumstances that do not fall into any other group are also placed in this category.
    5) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Selenium and compounds (as Se)
    6) MAK (DFG, 2002): Category 3B ; Listed as: Selenium and its inorganic compounds
    a) Category 3B : Substances for which in vitro or animal studies have yielded evidence of carcinogenic effects that is not sufficient for classification of the substance in one of the other categories. Further studies are required before a final decision can be made. A MAK value can be established provided no genotoxic effects have been detected. (Footnote: In the past, when a substance was classified as Category 3 it was given a MAK value provided that it had no detectable genotoxic effects. When all such substances have been examined for whether or not they may be classified in Category 4, this sentence may be omitted.)
    7) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS7782-49-2 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Selenium compounds (as Se)
    2) Table Z-1 for Selenium compounds (as Se):
    a) 8-hour TWA:
    1) ppm:
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3: 0.2
    a) Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.
    3) Ceiling Value:
    4) Skin Designation: No
    5) Notation(s): Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: ITI, 1995 Lewis, 1996
    1) LD50- (ORAL)RAT:
    a) 6700 mg/kg

Pharmacology Toxicology

Pharmacologic Mechanism

    A) In animals a deficiency state has been identified for selenium. There has not been a similar deficiency state identified in humans. However, some investigators feel that selenium is an essential element important in proper muscle development. Recent data on the distribution of selenium in human organs and tissues has shown a wide variation in levels in patients who were industrially exposed to selenium with no apparent symptoms of intoxication. The urinary levels found ranged from 10 to 150 mcg of selenium/liter. Other reports of chronic exposure to vegetables containing high concentrations of selenium resulted in a number of dermatological and central nervous system problems (Yang et al, 1983).
    B) It is similar to arsenic in that it inactivates the sulfhydryl groups of enzymes. A marked decrease in the amount of ascorbic acid, vitamin K and glutathione were noted in acute poisoning. In the absence of strong garlic- like odor of the breath, the differential diagnosis of selenium poisoning is a difficult one. A garlic odor indicates possibly garlic, phosphorous, selenium, tellurium and arsenic.

Physicochemical

Physical Characteristics

    A) Selenium exists in various forms. Amorphous forms, derived from rapid cooling of molten selenium, are vitreous solids and may be black to dark red-brown to bluish-black. The red or crystalline form consists of transparent, dark red monoclinic crystals. The most stable form is the gray or metallic which consists of gray to black shiny, hexagonal crystals. It also may be a brownish-red liquid (Budavari, 1996).

Molecular Weight

    A) 78.96

Animal Toxicology

Clinical Effects

    11.1.1) AVIAN/BIRD
    A) Wild aquatic birds may ingest a high amount of selenium via bioaccumulation in the food chain from irrigation drainage evaporation ponds. Ohlendorf et al (1988) reported high levels of tissue selenium, 94 and 97 ppm in liver and kidneys (dry weight), respectively, in coots and grebes collected from evaporation ponds. Adult birds were emaciated, had extensive chronic hepatic lesions, and excess fluid and fibrin in the peritoneal cavity. Glycogen, non-protein bound sulfhydral and glutathione peroxidase activity were elevated in liver; protein, total sulfhydral and protein-bound sulfhydral concentrations were lowered. Congenital malformations in eggs with developing embryos collected from this area included anophthalmia, microphthalmia, abnormal beaks, micromelia, ectodactyly and hydrocephaly.
    B) Selenium fed to young chicks produced a reduction in weight gain, 61 and 32%, when 15 mg/kg selenium in diet was given as sodium selenite or selenomethionine, respectively. Supplementation of these diets with various types of arsenicals, cysteine, or a combination of arsenic and cysteine had an ameliorating effect on such toxicity (Lowry & Baker, 1989).
    11.1.2) BOVINE/CATTLE
    A) Prenatal exposure and postnatal through milk results in joint, hoof, and eye abnormalities and a high postnatal mortality (Barlow & Sullivan, 1982).
    B) It is likely that heifers given selenium supplementation and monensin may develop signs of selenium intoxication, eg, acute cariomyopathy (Barlow et al, 1990).
    C) Injectable selenium compounds as oil emulsions are used to combat selenium deficiency in cattle (Krieger et al, 1986). If not appropriately mixed by shaking before use, the aqueous layer in these injectable mixtures may contain high levels of selenium (nearly 80 times than the nominal level in the emulsion) and induce acute toxicosis.
    11.1.3) CANINE/DOG
    A) A case of acute selenium poisoning in a 3-year-old female Chihuahua was reported after injecting 1.5 mL of vitamin E preparation (containing selenium) intramuscularly (Janke, 1989). The pulmonary lesions included congested capillaries in alveolar septae and abundant proteinaceous fluid in alveolar lumina. Other tissues also showed congestion. The liver and kidney of this dog showed greater thatn 12 mcg/g (wet weight) of selenium. The aqueous phase of injectable vitamin preparation had 5.3 mg/mL of selenium and was perhaps inadvertantly injected resulting in the toxicosis.
    11.1.4) CAPRINE/GOAT
    A) Nubian goats were treated by single or repeated daily oral doses of sodium selenite ranging from 0.25 to 160 mg/kg body weight (Ahmed et al, 1988). The selenite at higher doses produced restlessness, frothing of the mouth, dyspnea, diarrhea, paresis of hind limbs, recumbency, and death. Hemoconcentration was evident by increases in Hb, PCV, and RBC. Goats given repeated doses of 5 mg/kg/day of sodium selenite exhibited macrocytic hypochronic anemia and leukopenia before death. Serum GOT, gamma-GT, urea and inorganic phosphate increased, whereas total protein and calcium decreased.
    11.1.5) EQUINE/HORSE
    A) Similar congenital defects seen in calves were observed in foals (Barlow & Sullivan, 1982).
    11.1.6) FELINE/CAT
    A) A pregnant cat was given 0.5 mg/kg/day; a dead kitten was born with tissue Se levels of 19 to 458 mcg/100 g (Barlow & Sullivan, 1982).
    11.1.9) OVINE/SHEEP
    A) Pregnant ewe fed 0.024 ppm diet or injected with 6 mg Se x 10 days before slaughter showed similar maternal and fetal tissue levels (Barlow & Sullivan, 1982).
    B) Acute selenium toxicosis was evaluated in 20 sheep given 0.4 to 1 mg selenium as sodium selenite IM (Blodgett & Bevill, 1987). LD50 was 0.7 mg/kg (+/-0.35) over a 192 hour observation period. Clinical signs included listlessness, drooped ears, and labored respiration, progressing to depression and prostration. Dyspnea, teeth grinding, and anorexia were also observed. Gross pathologic lesions in sheep receiving more than 0.6 mg Se/kg included purple mottled lungs with edema, hyperemia, petechial to diffuse hemorrhages, and straw-colored thoracic fluid with fibrin clots. Highest tissue concentration of selenium was found in liver, followed (in declining order) by kidney and heart.
    C) ACCIDENTAL POISONING BY INJECTION -
    1) 102 tegs received 0.72 mg/kg of selenium and all died. Rams who were injected with 0.38 mg/kg survived, nine of 30 ewes who received 50 mg/kg died, and all 9 lambs receiving 0.45 mg/kg died (Kyle & Allen, 1990).
    2) Symptoms included congested, edematous lungs, watery exudate in the peritoneum, pleura and pericardium, necrosis of the injection site, and copius froth in tracheae and bronchi (Kyle & Allen, 1990).
    11.1.10) PORCINE/SWINE
    A) Animals intoxicated with selenium may experience skeletal muscular degeneration, pancreatic acinar degeneration, and neuronal degeneration (Van Vleet et al, 1974; Herigstad et al, 1973). Intoxications may occur from ingesting selenium concentrating plants such as astragalus species (Baker et al, 1989).
    B) Suckling and weaned piglets exposed to selenium contaminated feed developed acute paralysis (van der Molen et al, 1988). Lesions indicative of selenium poisoning were observed in the central nervous system. Very high levels of selenium were detected in one batch of feed because of an inadvertent human error. Liver, kidney, spleen and blood from effected animal showed elevated selenium concentrations.
    11.1.12) RODENT
    A) Sprague-Dawley rat pups injected with a single subcutaneous injection of 30 mcmol selenium as sodium selenite/kg body weight developed cataract in 20 days (Watanabe & Shearer, 1989). The selenite cataract was accompanied with increased in alpha, beta, and gamma-crystallins in aqueous and vitreous humor.
    11.1.13) OTHER
    A) OTHER
    1) Acute selenium toxicosis was diagnosed in three California sea lions based on clinical signs, pathologic findings, and tissue levels of selenium (Edward et al, 1989). Postmortem findings included hemorrhage into trachea and main airways, bronchi were filled with large blood clots. Abdominal cavity had light-yellow fluid. There was evidence of blood in the stomach and intestines. Liver and kidneys had high selenium levels, 34 to 76 and 7 to 33 mcg/g wet weight, respectively.

Range Of Toxicity

    11.3.2) MINIMAL TOXIC DOSE
    A) GOAT
    1) Daily oral doses of 0.25, 0.5, or 1 mg sodium selenite/kg body weight in goats were nontoxic when given up to 225 days (Ahmed et al, 1988). Doses between 5 and 40 mg/kg killed goats between 2 and 31 days, whereas 80 mg/kg or higher were toxic within a day or less after a single dose.
    B) SHEEP
    1) 102 tegs received 0.72 mg/kg of selenium and all died. Rams who were injected with 0.38 mg/kg survived, nine of 30 ewes who received 50 mg/kg died, and all 9 lambs receiving 0.45 mg/kg died (Kyle & Allen, 1990).

Kinetics

    11.5.1) ABSORPTION
    A) LACK OF INFORMATION
    1) There was no specific information on absorption at the time of this review.
    11.5.2) DISTRIBUTION
    A) SPECIFIC TOXIN
    1) Placental transfer of selenium has been confirmed in mice and rats (Barlow & Sullivan, 1982). Transfer across the placenta is substantial within the first hour of administration but full equilibration may take up to 48 hours.

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