Selenium exists in four natural oxidation states (+6, +4, 0, and -2) and is found in several compounds capable of causing human poisoning, yet it is an essential trace element in the human diet. Physical properties and toxic air concentrations of common selenium compounds can be found in Table IV-3. Fatal acute selenium poisoning occurs most commonly from ingestion of selenious acid in gun bluing (coating) solutions. Other acute poisonings occur through the use of (often improperly formulated) dietary supplements as well as via exposure to industrial compounds. Illness caused by chronic exposure to selenium is uncommon but is seen in regions with high selenium content in food. Industries using selenium compounds include ceramics, electronics, glass, rubber, and metallurgy. Selenium is produced largely as a byproduct of copper refining.

Animal studies implicate mechanisms involving the formation of superoxide and hydroxyl anions as well as hydrogen peroxide. A garlic breath odor observed in various selenium poisonings is due to in vivo formation of dimethyl selenium.

1. Ingestion
   1. Acute overdose. Rapidly fatal overdoses have occurred from ingestion of gun bluing solutions containing 2-9% selenious acid and 2-4% copper. Ingestion of 15 mL of gun bluing solution containing 4% selenious acid was fatal. The oral mean lethal dose (MLD) of selenite salts in the dog is about 4 mg/kg. Ingestion of 1-5 mg/kg sodium selenite in five adults caused moderate reversible toxicity. Survival after ingestion of 2,000 mg of selenium dioxide has been reported.
   2. Chronic ingestion. Selenium is a component of more than 2 dozen essential proteins. The Food and Nutrition Board, Institute of Medicine recommended daily allowance (RDA) is 55 mcg. The Environmental Protection Agency (EPA) drinking water maximum contaminant level (MCL) is 0.05 mg/L (50 ppb). The EPA minimal risk level for selenium is 5 mcg/kg/d. Chronic ingestion of 850 mcg/d has been associated with toxicity.
2. Inhalation. Recommended workplace exposure limits and acute exposure guideline levels (AEGLs) for selenium compounds are listed in Table IV-3.

1. Acute ingestion of selenious acid causes upper GI corrosive injury, vomiting and diarrhea, hypersalivation, and a garlic odor on the breath. Patients may subsequently develop a rapid deterioration of mental status and restlessness progressing to coma, hypotension from myocardial depression and decreased vascular resistance, respiratory insufficiency, and death. Suicidal ingestion of an unknown amount of selenium dioxide has been fatal. Ingestions of sodium selenate have produced gastroenteritis with garlic breath and T-wave inversion on the ECG. Five patients who ingested large amounts of sodium selenite developed vomiting, diarrhea, chills, and tremor but survived.
2. Chronic ingestion of elemental selenium, sodium selenite, sodium selenate, or selenium dioxide may cause pallor, stomach disorders, nervousness, metallic taste, and garlic breath. Chronic use of elemental selenium may cause selenosis, which also includes skin changes, brittle hair, alopecia, dystrophic nail findings, and alterations in memory.
3. Acute inhalation of hydrogen selenide produces dyspnea, abdominal cramps, and diarrhea. Inhalation of selenium hexafluoride produces severe corrosive injury and systemic toxicity from acids of selenium plus fluoride ion toxicity. Selenium salt inhalation causes dyspnea and skin and mucous membrane irritation.

Is difficult without a history of exposure. Acute severe gastroenteritis with garlic breath odor and hypotension may suggest selenious acid poisoning, but these findings are not specific.

1. Specific levels are not generally available. Various selenium compounds differ in toxic potential, yet selenium is usually determined as total selenium concentration. Selenium can be measured in the blood, hair, and urine. Following absorption, selenium slowly migrates into red blood cells, resulting in an elevated whole blood to plasma ratio. Plasma concentrations are preferred for assessing acute exposure; whole blood is preferred for chronic exposures.
   1. On a normal diet, whole-blood selenium levels range from 0.1 to 0.2 mg/L. One patient with chronic intoxication after ingestion of 31 mg/d had a whole-blood selenium level of 0.53 mg/L.
   2. Average hair levels are up to 0.5 ppm. The relationship between hair and tissue concentrations is not well understood. The utility of hair testing is complicated by the widespread use of selenium disulfide in shampoos.
   3. Both whole-blood and urinary concentrations reflect dietary intake. Overexposure should be considered when blood selenium levels exceed 0.4 mg/L or urinary excretion exceeds 600-1,000 mcg/d.
2. Other useful laboratory studies include electrolytes, glucose, BUN, creatinine, liver aminotransferases, and ECG. After inhalation exposure, obtain blood gases or oximetry and chest radiograph.

1. Emergency and supportive measures
   1. Maintain an open airway and assist ventilation if necessary. Administer supplemental oxygen.
   2. Treat coma, convulsions, bronchospasm, hypotension, and pulmonary edema if they occur. Because hypotension is often multifactorial, evaluate and optimize volume status, peripheral vascular resistance, and myocardial contractility.
   3. Observe for at least 6 hours after exposure.
   4. After ingestion of selenious acid, consider endoscopy to rule out esophageal or gastric corrosive injury.
2. Specific drugs and antidotes. There is no specific antidote. The value of suggested therapies such as chelation, vitamin C, and N-acetylcysteine is not established.
3. Decontamination
   1. Inhalation. Immediately remove the victim from exposure and give supplemental oxygen if available.
   2. Skin and eyes. Remove contaminated clothing and wash exposed skin with soap and copious water. Irrigate exposed eyes with copious tepid water or saline.
   3. Ingestion. GI decontamination is of uncertain benefit. Careful gastric aspiration (using a soft nasogastric tube) followed by activated charcoal may be of value for ingestions of selenious acid seen within 1 hour.
4. Enhanced elimination. There is no known role for any enhanced removal procedure.