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SODIUM SELENATE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Sodium selenate is a colorless water-soluble selenium salt.

Specific Substances

    A) No Synonyms were found in group or single elements
    1.2.1) MOLECULAR FORMULA
    1) O4-Se.2Na

Available Forms Sources

    A) FORMS
    1) Sodium selenate is a colorless, rhombic crystalline solid, water-soluble selenium salt.
    2) Little is known about the toxicity of sodium selenate. This review is based on the toxicity of SELENIUM. Effects attributed specifically to sodium selenate are identified.
    3) All selenium salts can produce toxicity by ingestion, inhalation, and percutaneous absorption (Proctor et al, 1988; Ellenhorn & Barceloux, 1988; Clayton & Clayton, 1981; Sax & Lewis, 1989), although specific information on the possible dermal absorption of sodium selenate was not found (EPA, 1985).
    4) Elemental selenium has a relatively low order of toxicity; indeed, selenium is an ESSENTIAL TRACE METAL, and CHRONIC DEFICIENCY can lead to fatal cardiomyopathies (Ellenhorn & Barceloux, 1988; Baselt & Cravey, 1989).
    5) Sodium selenate can release toxic and irritating fumes of selenium and sodium oxide when heated to decomposition (Sax & Lewis, 1989; EPA, 1985).
    B) USES
    1) It is used as a chemical reagent and an insecticide for certain horticultural applications on nonedible plants (Clayton & Clayton, 1981; Budavari, 1989; Sax & Lewis, 1987; Sax & Lewis, 1989; EPA, 1985).

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 has a relatively low order of toxicity; selenium is an ESSENTIAL TRACE METAL, and CHRONIC DEFICIENCY can lead to fatal cardiomyopathies. Industrial workers exposed for up to 26 years had a normal death pattern. All selenium salts can produce toxicity by ingestion, inhalation, and percutaneous absorption, although specific information on the possible dermal absorption of sodium selenate was not found.
    B) Chronic selenium poisoning resembles chronic arsenic poisoning. Nausea, vomiting, white streaks of the nails, pallor, upper respiratory irritation, paronychiae, hair loss, skin rashes, irritability, fatigue, hyperreflexia, EKG changes, a garlic odor on the breath, and a metallic taste in the mouth may be noted with chronic selenium exposure.
    1) Screening laboratory values such as complete blood counts and liver and renal function tests are usually within normal limits. Liver and renal lesions have been seen in experimental animals.
    C) Acute poisonings with selenium metal and its salts are rare. SELENITE toxicity may include facial flushing, a lightheaded sensation, and muscle tenderness and tremors.
    1) Inhalation of selenium dusts may cause headache, cough, nasal discharge, upper respiratory tract irritation, epistaxis, and olfactory fatigue. Transient dyspnea has been seen.
    2) Severe eye irritation may be seen with selenium dust exposure.
    D) While chronic occupational selenium exposure has not been reported to result in disabling disease, paralysis and hemiplegia were noted in an endemic outbreak of dietary hyperselenosis in China.
    E) Acute ingestion of 2000 mg of sodium selenate by an adolescent caused a garlic odor of the breath, diarrhea, EKG changes indicating possible anterolateral myocardial damage, elevated liver function tests, muscle aches and pains, and irritability.
    F) Anemia and marked hepatic necrosis, hemorrhage, and cirrhosis were found in experimental animals fed 5 to 15 ppm of selenium chronically in the diet. These effects have not been reported in exposed humans.
    G) Sodium selenate releases toxic and irritating fumes of selenium and sodium oxide when heated to decomposition.
    0.2.4) HEENT
    A) Redness of the eyes and blurred vision have been noted. Severe eye irritation may be seen with selenium dust exposure. Inhalation of selenium dusts can cause nasal discharge, upper respiratory tract irritation, epistaxis, and olfactory fatigue.
    B) A burning sensation of the nostrils and local irritation have been noted, as well as sneezing and nasal congestion. Acute sore throats, coryza-like symptoms with lacrimation, a metallic taste in the mouth, and a garlicky breath odor are frequently reported.
    0.2.5) CARDIOVASCULAR
    A) Ingestion of sodium selenate caused diffuse T-wave flattening, T-wave inversions in the lateral and anterior leads, and a prolonged QT interval, all of which became maximal at three days after exposure and cleared over the following two weeks.
    0.2.6) RESPIRATORY
    A) Pulmonary edema has been noted. 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.
    B) Inhalation of selenium dusts can cause cough, nasal discharge, upper respiratory tract irritation, epistaxis, and olfactory fatigue. Transient dyspnea has been seen.
    0.2.7) NEUROLOGIC
    A) Dizziness, CNS depression, restlessness, sluggish pupillary reflexes, clouding of the sensorium, and coma have all been noted with selenium toxicity. SELENITE toxicity may include a lightheaded sensation. Inhalation of selenium dusts can cause headache. Acute ingestion of sodium selenate by an adolescent caused irritability.
    0.2.8) GASTROINTESTINAL
    A) Effects include nausea, vomiting, salivation, and gastrointestinal pain. A garlic odor on the breath may occur. Acute ingestion of sodium selenate caused a garlic odor of the breath and diarrhea.
    0.2.9) HEPATIC
    A) Elevation of liver function tests, especially bilirubin, persisted for 6 days after ingestion of sodium selenate. Fatty degeneration of the liver and cirrhosis has been reported.
    0.2.10) GENITOURINARY
    A) Mild tubular degeneration of the kidneys has been noted.
    0.2.14) DERMATOLOGIC
    A) Selenium compounds may cause dermatitis. SELENITE toxicity may include facial flushing.
    0.2.15) MUSCULOSKELETAL
    A) SELENITE toxicity may include muscle tenderness and tremors. Acute ingestion of sodium selenate caused muscle aches and pains.
    0.2.20) REPRODUCTIVE
    A) Selenium readily crosses the placenta; maternal and fetal levels are similar at term.
    B) Some spontaneous abortions and neonates born with bilateral talipes equinovarus (club foot deformity) have been noted in selenite-exposed female workers, suggesting that occupational exposure to selenium compounds may pose a human reproductive risk.
    C) Studies with potassium selenate and sodium selenite in rats, rabbits, mice, and hamsters have failed to produce teratogenic effects; an unspecified selenium salt caused teratogenic effects in sheep.
    D) Specific developmental abnormalities in the skin and skin appendages and effects on the newborn, including viability index and growth statistic changes have been observed in mouse studies.
    E) No adequate data are available on the possible effects of selenium on endocrine, or gonadal effects, or effects on fertility. No adequate data are available for effects of occupational exposure on pregnancy outcome although an unconfirmed association with spontaneous abortions has been suggested.
    F) Irregular menses have been reported in Japanese selenium rectifier workers.
    G) Selenium has been found in breast milk in varying amounts with an average of 0.02 ppm. No adverse effects have been reported in breast-fed infants.
    H) No information about possible male reproductive effects was found in available references at the time of this review.
    0.2.21) CARCINOGENICITY
    A) Data on carcinogenicity are inadequate for evaluation.
    B) In one study, exposure to selenium was protective against lung cancer in copper smelter workers.
    C) Current evidence indicates that selenium and its compounds are NOT carcinogenic in man. Selenium animal feed additives do not pose a cancer risk for humans.
    D) In a 26-year study of occupational selenium exposure, there was no difference between the observed and expected deaths from cancer.

Laboratory Monitoring

    A) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring complete blood count, urinalysis, and liver and kidney function tests is suggested for patients with significant exposure.
    B) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.
    C) Monitoring selenium blood levels may be useful to follow the course of the poisoning.
    D) Monitoring urine selenium excretion may be useful to follow the course of acute poisoning or for biological monitoring of exposed workers.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) Do NOT induce emesis.
    B) GASTRIC LAVAGE: Consider after ingestion of a potentially life-threatening amount of poison if it can be performed soon after ingestion (generally within 1 hour). Protect airway by placement in the head down left lateral decubitus position or by endotracheal intubation. Control any seizures first.
    1) CONTRAINDICATIONS: Loss of airway protective reflexes or decreased level of consciousness in unintubated patients; following ingestion of corrosives; hydrocarbons (high aspiration potential); patients at risk of hemorrhage or gastrointestinal perforation; and trivial or non-toxic ingestion.
    C) 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.
    D) If coma and respiratory depression occur, ensure airway patency and adequacy of respirations and oxygenation. Endotracheal intubation, administration of supplemental oxygen, and assisted ventilation may be required.
    E) ACUTE LUNG INJURY: Maintain ventilation and oxygenation and evaluate with frequent arterial blood gases and/or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed.
    F) In general, chelation or antagonist therapy with available agents HAS NOT BEEN RECOMMENDED in cases of poisoning with selenium compounds.
    G) An in-vitro study showed that hemoperfusion might have only a "moderate effect" on selenium blood levels in selenious acid poisoning. This procedure has not been utilized in human poisoning cases and cannot be recommended at this time. No mention of early exchange transfusion for the treatment of selenious acid poisoning has been made in the literature.
    H) Patients symptomatic following exposure should be observed in a controlled setting until all signs and symptoms have fully resolved.
    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.
    B) Initial respiratory tract irritation may appear to improve, but can then worsen between 2 and 12 hours after exposure. Severe chemical pneumonitis may then develop over the following one to three days.
    1) Early administration of supplemental oxygen seemed to mitigate the degree of chemical pneumonitis that developed in one incident. Patients with inhalation exposure should be treated with supplemental oxygen beginning as soon as possible after rescue and should have a prolonged period of observation in a controlled setting with careful monitoring for the development of chemical pneumonitis.
    C) If bronchospasm and wheezing occur, consider treatment with inhaled sympathomimetic agents.
    D) ACUTE LUNG INJURY: Maintain ventilation and oxygenation and evaluate with frequent arterial blood gases and/or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed.
    E) Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    F) If coma and respiratory depression occur, ensure airway patency and adequacy of respirations and oxygenation. Endotracheal intubation, administration of supplemental oxygen, and assisted ventilation may be required.
    G) In general, chelation or antagonist therapy with available agents HAS NOT BEEN RECOMMENDED in cases of poisoning with selenium compounds.
    H) Patients symptomatic following exposure should be observed in a controlled setting until all signs and symptoms have fully resolved.
    0.4.4) EYE EXPOSURE
    A) DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
    B) Because of the potential for serious eye irritation following direct contact with this agent, prolonged initial flushing and early ophthalmologic consultation are advisable.
    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).
    2) Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines.
    3) Treatment should include recommendations listed in the INHALATION EXPOSURE section when appropriate.

Range Of Toxicity

    A) The minimum lethal human dose to this agent has not been delineated.
    B) An adolescent patient ingested 400 mL of a 5 mg/mL sodium selenate-containing sheep dip preparation (2000 mg; 22.3 mg Se/kg) but survived. Three other patients aged 22 months to 18 years ingested up to 5 mL of similar sheep dip (up to 5 mg) and had no ill effects.
    C) Anemia and marked hepatic necrosis, hemorrhage, and cirrhosis were found in experimental animals fed 5 to 15 ppm of selenium chronically in the diet.

Clinical Effects

Summary Of Exposure

    A) Elemental selenium has a relatively low order of toxicity; selenium is an ESSENTIAL TRACE METAL, and CHRONIC DEFICIENCY can lead to fatal cardiomyopathies. Industrial workers exposed for up to 26 years had a normal death pattern. All selenium salts can produce toxicity by ingestion, inhalation, and percutaneous absorption, although specific information on the possible dermal absorption of sodium selenate was not found.
    B) Chronic selenium poisoning resembles chronic arsenic poisoning. Nausea, vomiting, white streaks of the nails, pallor, upper respiratory irritation, paronychiae, hair loss, skin rashes, irritability, fatigue, hyperreflexia, EKG changes, a garlic odor on the breath, and a metallic taste in the mouth may be noted with chronic selenium exposure.
    1) Screening laboratory values such as complete blood counts and liver and renal function tests are usually within normal limits. Liver and renal lesions have been seen in experimental animals.
    C) Acute poisonings with selenium metal and its salts are rare. SELENITE toxicity may include facial flushing, a lightheaded sensation, and muscle tenderness and tremors.
    1) Inhalation of selenium dusts may cause headache, cough, nasal discharge, upper respiratory tract irritation, epistaxis, and olfactory fatigue. Transient dyspnea has been seen.
    2) Severe eye irritation may be seen with selenium dust exposure.
    D) While chronic occupational selenium exposure has not been reported to result in disabling disease, paralysis and hemiplegia were noted in an endemic outbreak of dietary hyperselenosis in China.
    E) Acute ingestion of 2000 mg of sodium selenate by an adolescent caused a garlic odor of the breath, diarrhea, EKG changes indicating possible anterolateral myocardial damage, elevated liver function tests, muscle aches and pains, and irritability.
    F) Anemia and marked hepatic necrosis, hemorrhage, and cirrhosis were found in experimental animals fed 5 to 15 ppm of selenium chronically in the diet. These effects have not been reported in exposed humans.
    G) Sodium selenate releases toxic and irritating fumes of selenium and sodium oxide when heated to decomposition.

Heent

    3.4.1) SUMMARY
    A) Redness of the eyes and blurred vision have been noted. Severe eye irritation may be seen with selenium dust exposure. Inhalation of selenium dusts can cause nasal discharge, upper respiratory tract irritation, epistaxis, and olfactory fatigue.
    B) A burning sensation of the nostrils and local irritation have been noted, as well as sneezing and nasal congestion. Acute sore throats, coryza-like symptoms with lacrimation, a metallic taste in the mouth, and a garlicky breath odor are frequently reported.
    3.4.3) EYES
    A) CONJUNCTIVITIS - Redness of the eyes and blurred vision have been noted (Alderman & Bergin, 1986).
    1) Eye irritation may be seen with selenium fume exposure (Hathaway et al, 1996).
    3.4.5) NOSE
    A) IRRITATION - Inhalation of selenium dusts can cause nasal discharge, upper respiratory tract irritation, epistaxis, and olfactory fatigue (Ellenhorn, 1997; Proctor et al, 1988).
    B) BURNING SENSATION - A burning sensation of the nostrils and local irritation have been noted, as well as sneezing and nasal congestion (Alderman & Bergin, 1986).
    3.4.6) THROAT
    A) SORE THROAT - Acute sore throats, coryza-like symptoms with lacrimation, a metallic taste in the mouth, and a garlicky breath odor are frequently reported (Motley & Ellis, 1937).

Cardiovascular

    3.5.1) SUMMARY
    A) Ingestion of sodium selenate caused diffuse T-wave flattening, T-wave inversions in the lateral and anterior leads, and a prolonged QT interval, all of which became maximal at three days after exposure and cleared over the following two weeks.
    3.5.2) CLINICAL EFFECTS
    A) ELECTROCARDIOGRAM ABNORMAL
    1) Ingestion of sodium selenate caused diffuse T-wave flattening, T-wave inversions in the lateral and anterior leads, and a prolonged QT interval, all of which became maximal at three days after exposure and cleared over the following two weeks (Civil & McDonald, 1978).

Respiratory

    3.6.1) SUMMARY
    A) Pulmonary edema has been noted. 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.
    B) Inhalation of selenium dusts can cause cough, nasal discharge, upper respiratory tract irritation, epistaxis, and olfactory fatigue. Transient dyspnea has been seen.
    3.6.2) CLINICAL EFFECTS
    A) ACUTE LUNG INJURY
    1) Pulmonary edema has been noted. 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 to hydrogen selenide. Initially, the patient had severe coughing and wheezing which progressed to irreversible obstructive and restrictive lung disease (Schecter et al, 1980).
    B) METAL FEVER
    1) 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).
    2) TOMES Plus system users may refer to the METAL FUME FEVER MEDITEXT medical management for further information.
    C) IRRITATION SYMPTOM
    1) Inhalation of selenium dusts can cause cough, nasal discharge, upper respiratory tract irritation, epistaxis, and olfactory fatigue (Ellenhorn, 1997; Proctor et al, 1988). Transient dyspnea has been seen (Proctor et al, 1988).

Neurologic

    3.7.1) SUMMARY
    A) Dizziness, CNS depression, restlessness, sluggish pupillary reflexes, clouding of the sensorium, and coma have all been noted with selenium toxicity. SELENITE toxicity may include a lightheaded sensation. Inhalation of selenium dusts can cause headache. Acute ingestion of sodium selenate by an adolescent caused irritability.
    3.7.2) CLINICAL EFFECTS
    A) COMA
    1) Dizziness, CNS depression, restlessness, sluggish pupillary reflexes, clouding of the sensorium, and coma have all been noted with selenium toxicity.
    B) DIZZINESS
    1) SELENITE toxicity may include a lightheaded sensation (Ellenhorn, 1997).
    C) HEADACHE
    1) Inhalation of selenium dusts can cause headache (Ellenhorn & Barceloux, 1988; Proctor et al, 1988).
    D) FEELING NERVOUS
    1) Acute ingestion of 2000 mg of sodium selenate by an adolescent caused irritability (Civil & McDonald, 1978).

Gastrointestinal

    3.8.1) SUMMARY
    A) Effects include nausea, vomiting, salivation, and gastrointestinal pain. A garlic odor on the breath may occur. Acute ingestion of sodium selenate caused a garlic odor of the breath and diarrhea.
    3.8.2) CLINICAL EFFECTS
    A) NAUSEA AND VOMITING
    1) Effects include nausea, vomiting, salivation, and gastrointestinal pain (Diskin et al, 1979; Lombeck et al, 1987).
    B) DIARRHEA
    1) Acute ingestion of 2000 mg of sodium selenate by an adolescent caused a garlic odor of the breath and diarrhea (Civil & McDonald, 1978).

Hepatic

    3.9.1) SUMMARY
    A) Elevation of liver function tests, especially bilirubin, persisted for 6 days after ingestion of sodium selenate. Fatty degeneration of the liver and cirrhosis has 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).
    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 of the kidneys has been noted.
    3.10.2) CLINICAL EFFECTS
    A) RENAL TUBULAR DISORDER
    1) Mild tubular degeneration of the kidneys has been noted (Carter, 1966).

Dermatologic

    3.14.1) SUMMARY
    A) Selenium compounds may cause dermatitis. SELENITE toxicity may include facial flushing.
    3.14.2) CLINICAL EFFECTS
    A) DERMATITIS
    1) Selenium compounds may cause dermatitis (HSDB, 1999).
    B) FLUSHING
    1) SELENITE toxicity may include facial flushing (Ellenhorn, 1997).

Musculoskeletal

    3.15.1) SUMMARY
    A) SELENITE toxicity may include muscle tenderness and tremors. Acute ingestion of sodium selenate caused muscle aches and pains.
    3.15.2) CLINICAL EFFECTS
    A) TREMOR
    1) SELENITE toxicity may include muscle tenderness and tremors (Ellenhorn, 1997).
    B) MUSCLE PAIN
    1) Acute ingestion of 2000 mg of sodium selenate by an adolescent caused muscle aches and pains (Civil & McDonald, 1978).

Reproductive

    3.20.1) SUMMARY
    A) Selenium readily crosses the placenta; maternal and fetal levels are similar at term.
    B) Some spontaneous abortions and neonates born with bilateral talipes equinovarus (club foot deformity) have been noted in selenite-exposed female workers, suggesting that occupational exposure to selenium compounds may pose a human reproductive risk.
    C) Studies with potassium selenate and sodium selenite in rats, rabbits, mice, and hamsters have failed to produce teratogenic effects; an unspecified selenium salt caused teratogenic effects in sheep.
    D) Specific developmental abnormalities in the skin and skin appendages and effects on the newborn, including viability index and growth statistic changes have been observed in mouse studies.
    E) No adequate data are available on the possible effects of selenium on endocrine, or gonadal effects, or effects on fertility. No adequate data are available for effects of occupational exposure on pregnancy outcome although an unconfirmed association with spontaneous abortions has been suggested.
    F) Irregular menses have been reported in Japanese selenium rectifier workers.
    G) Selenium has been found in breast milk in varying amounts with an average of 0.02 ppm. No adverse effects have been reported in breast-fed infants.
    H) No information about possible male reproductive effects was found in available references at the time of this review.
    3.20.2) TERATOGENICITY
    A) PLACENTAL BARRIER
    1) Selenium readily crosses the placenta; maternal and fetal levels are similar at term (Alfthan, 1986).
    B) ABORTION
    1) Some spontaneous abortions and neonates born with bilateral talipes equinovarus (club foot deformity) have been noted in selenite-exposed female workers, suggesting that occupational exposure to selenium compounds may pose a human reproductive risk (Council on Scientific Affairs, 1985).
    C) ANIMAL STUDIES
    1) Studies with sodium selenite in rats, rabbits, mice, and hamsters have failed to produce teratogenic effects; an unspecified selenium salt caused teratogenic effects in sheep (Schardein, 1993).
    2) Specific developmental abnormalities in the skin and skin appendages and effects on the newborn, including viability index and growth statistic changes have been observed in mouse studies (RTECS, 1999).
    3) In hamsters, the incidence of resorptions and congenital anomalies, primarily encephaloceles, increased with administration of sodium selenate (Ferm et al, 1990).
    4) In a frog embryo teratogenesis assay, sodium selenate tested as having moderately positive teratogenic potential (DeYoung et al, 1991).
    3.20.3) EFFECTS IN PREGNANCY
    A) ABORTION
    1) No adequate data are available for occupational exposure on pregnancy outcome although an unconfirmed association with spontaneous abortions has been suggested (Barlow & Sullivan, 1982)
    B) MENSTRUAL DISORDER
    1) Irregular menses have been reported in Japanese selenium rectifier workers (HSDB, 1999).
    C) PLACENTAL BARRIER
    1) Selenium may be transferred to the fetus through the placenta (HSDB, 1999).
    D) ANIMAL STUDIES
    1) Sodium selenate fed to sheep at 24 or 29 ppm did not alter estrus behavior, estrogen/progesterone profiles, pregnancy rate, or lamb birth weights (Panter et al, 1995).
    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 in breast-fed infants. Selenium levels in breast milk are dependent on dietary intake (HSDB, 1999).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS13410-01-0 (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) Not Listed
    3.21.2) SUMMARY/HUMAN
    A) Data on carcinogenicity are inadequate for evaluation.
    B) In one study, exposure to selenium was protective against lung cancer in copper smelter workers.
    C) Current evidence indicates that selenium and its compounds are NOT carcinogenic in man. Selenium animal feed additives do not pose a cancer risk for humans.
    D) In a 26-year study of occupational selenium exposure, there was no difference between the observed and expected deaths from cancer.
    3.21.3) HUMAN STUDIES
    A) LACK OF INFORMATION
    1) Data on carcinogenicity are inadequate for evaluation (Barlow & Sullivan, 1982).
    B) CARCINOMA
    1) IARC (Sodium selenate) (RTECS, 1999)
    a) Animal: Inadequate evidence
    b) Group 3
    C) OTHER NON-SPECIFIC
    1) In one study, exposure to selenium was protective against lung cancer in copper smelter workers (Gerhardsson et al, 1986).
    D) OCCUPATIONAL EXPOSURE
    1) In a 26-year study of occupational selenium exposure, there was no difference between the observed and expected deaths from cancer (IARC, 1974).
    E) LACK OF EFFECT
    1) Current evidence indicates that selenium and its compounds are NOT carcinogenic in man (HSDB, 1999). Selenium animal feed additives do not pose a cancer risk for humans (Clayton & Clayton, 1981).
    3.21.4) ANIMAL STUDIES
    A) CARCINOMA
    1) Sodium selenate was designated carcinogenic in the rat by RTECS criteria with the presence of leukemia and tumors of the lungs, thorax or respiration (RTECS, 1999).
    2) Sodium selenate retarded leukemic tumor growth in mice (Milner & Hsu, 1981).
    3) Schroeder and Mitchner (1971) showed that there was an increased incidence of both benign and malignant tumors in rats fed selenate (0.28 mg/kg/day) that was not seen in rats fed the same dose of selenite.

Genotoxicity

    A) DNA repair has been observed in B. subtilis and S. typhimurium (Ames Test). Sodium selenate induced unscheduled DNA synthesis in human fibroblasts and rat liver cells.
    B) Sodium selenate induced mutations in S. typhimurium (Ames Test).
    C) In Chinese hamster cells, no increase in sister chromatid exchanges or growth inhibition were seen with sodium selenate.
    D) Sodium selenate did NOT cause chromosome damage in human HeLa cells.
    E) EPA GENETOX PROGRAM 1988 -
    1) Positive: Histidine reversion-Ames test
    2) Positive: In vitro UDS-human fibroblast

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring complete blood count, urinalysis, and liver and kidney function tests is suggested for patients with significant exposure.
    B) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.
    C) Monitoring selenium blood levels may be useful to follow the course of the poisoning.
    D) Monitoring urine selenium excretion may be useful to follow the course of acute poisoning or for biological monitoring of exposed workers.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Monitoring selenium blood levels may be useful to follow the course of the poisoning, although they may not correlate well with toxicity (Baselt & Cravey, 1989).
    a) A study of 10 individuals demonstrated a linear correlation of whole blood selenium levels with dietary intake.
    b) 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.
    c) Two individuals received 350 mcg and 600 mcg/day for 18 months; whole blood levels were 0.345 and 0.642 mg/mL, respectively.
    2) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring complete blood count and liver and kidney function tests is suggested for patients with significant exposure.
    4.1.3) URINE
    A) URINARY LEVELS
    1) Monitoring urine selenium excretion may be useful to follow the course of acute poisoning or for biological monitoring of exposed workers (Baselt & Cravey, 1989; Baselt, 1988). In one study of mildly symptomatic workers exposed to airborne selenium concentrations of 0.2 to 3.6 mg/m(3), urinary selenium concentrations ranged from less than 0.10 to 0.43 mg/L
    a) Urinary Concentrations (Baselt, 1988)
    1) Normal Persons: undetectable to 150 mcg/L (average: 34 mcg/L)
    2) Persons drinking high selenium content water: 22 to 203 mcg/L (average: 79 mcg/L)
    3) Asymptomatic exposed selenium workers: 120 to 350 mcg/L
    2) Over a wide range of selenium intakes, 50 to 70 percent of the total excreted selenium is present in the urine.
    a) The most reliable indication for determining urinary selenium content is the 24-hour excretion measurement.
    b) Normal values are stated as less than 30 mcg/L. In the intoxicated state or with exposure to high environmental selenium concentrations, urine can be used to monitor selenium status.
    c) 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).
    B) URINALYSIS
    1) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring urinalysis is suggested for patients with significant exposure.
    4.1.4) OTHER
    A) OTHER
    1) PULMONARY FUNCTION TESTS
    a) If respiratory tract irritation is present, it may be useful to monitor pulmonary function tests.
    2) MONITORING
    a) If respiratory tract irritation is present, monitor arterial blood gases and chest x-ray.
    3) Pulse oximetry may be useful in monitoring patients for hypoxia.
    4) HAIR
    a) Average hair selenium levels in the United States are 0 to 0.5 ppm.
    b) 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 child (Lombeck et al, 1987).

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) If respiratory tract irritation is present, monitor chest x-ray.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring complete blood count, urinalysis, and liver and kidney function tests is suggested for patients with significant exposure.
    B) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.
    C) Monitoring selenium blood levels may be useful to follow the course of the poisoning.
    D) Monitoring urine selenium excretion may be useful to follow the course of acute poisoning or for biological monitoring of exposed workers.

Oral Exposure

    6.5.2) PREVENTION OF ABSORPTION
    A) EMESIS/NOT RECOMMENDED
    1) Do NOT induce emesis.
    B) GASTRIC LAVAGE
    1) INDICATIONS: Consider gastric lavage with a large-bore orogastric tube (ADULT: 36 to 40 French or 30 English gauge tube {external diameter 12 to 13.3 mm}; CHILD: 24 to 28 French {diameter 7.8 to 9.3 mm}) after a potentially life threatening ingestion if it can be performed soon after ingestion (generally within 60 minutes).
    a) Consider lavage more than 60 minutes after ingestion of sustained-release formulations and substances known to form bezoars or concretions.
    2) PRECAUTIONS:
    a) SEIZURE CONTROL: Is mandatory prior to gastric lavage.
    b) AIRWAY PROTECTION: Place patients in the head down left lateral decubitus position, with suction available. Patients with depressed mental status should be intubated with a cuffed endotracheal tube prior to lavage.
    3) LAVAGE FLUID:
    a) Use small aliquots of liquid. Lavage with 200 to 300 milliliters warm tap water (preferably 38 degrees Celsius) or saline per wash (in older children or adults) and 10 milliliters/kilogram body weight of normal saline in young children(Vale et al, 2004) and repeat until lavage return is clear.
    b) The volume of lavage return should approximate amount of fluid given to avoid fluid-electrolyte imbalance.
    c) CAUTION: Water should be avoided in young children because of the risk of electrolyte imbalance and water intoxication. Warm fluids avoid the risk of hypothermia in very young children and the elderly.
    4) COMPLICATIONS:
    a) Complications of gastric lavage have included: aspiration pneumonia, hypoxia, hypercapnia, mechanical injury to the throat, esophagus, or stomach, fluid and electrolyte imbalance (Vale, 1997). Combative patients may be at greater risk for complications (Caravati et al, 2001).
    b) Gastric lavage can cause significant morbidity; it should NOT be performed routinely in all poisoned patients (Vale, 1997).
    5) CONTRAINDICATIONS:
    a) Loss of airway protective reflexes or decreased level of consciousness if patient is not intubated, following ingestion of corrosive substances, hydrocarbons (high aspiration potential), patients at risk of hemorrhage or gastrointestinal perforation, or trivial or non-toxic ingestion.
    C) ACTIVATED CHARCOAL/CATHARTIC
    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) MONITORING OF PATIENT
    1) Monitor EKG, vital signs, and urine output carefully.
    B) AIRWAY MANAGEMENT
    1) If coma and respiratory depression occur, ensure airway patency and adequacy of respirations and oxygenation. Endotracheal intubation, administration of supplemental oxygen, and assisted ventilation may be required.
    C) ACUTE LUNG INJURY
    1) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
    2) NON-PHARMACOLOGIC TREATMENT: The treatment of acute lung injury is primarily supportive (Cataletto, 2012). Maintain adequate ventilation and oxygenation with frequent monitoring of arterial blood gases and/or pulse oximetry. If a high FIO2 is required to maintain adequate oxygenation, mechanical ventilation and positive-end-expiratory pressure (PEEP) may be required; ventilation with small tidal volumes (6 mL/kg) is preferred if ARDS develops (Haas, 2011; Stolbach & Hoffman, 2011).
    a) To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)
    3) FLUIDS: Crystalloid solutions must be administered judiciously. Pulmonary artery monitoring may help. In general the pulmonary artery wedge pressure should be kept relatively low while still maintaining adequate cardiac output, blood pressure and urine output (Stolbach & Hoffman, 2011).
    4) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
    5) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
    6) CALFACTANT: In a multicenter, randomized, blinded trial, endotracheal instillation of 2 doses of 80 mL/m(2) calfactant (35 mg/mL of phospholipid suspension in saline) in infants, children, and adolescents with acute lung injury resulted in acute improvement in oxygenation and lower mortality; however, no significant decrease in the course of respiratory failure measured by duration of ventilator therapy, intensive care unit, or hospital stay was noted. Adverse effects (transient hypoxia and hypotension) were more frequent in calfactant patients, but these effects were mild and did not require withdrawal from the study (Wilson et al, 2005).
    7) However, in a multicenter, randomized, controlled, and masked trial, endotracheal instillation of up to 3 doses of calfactant (30 mg) in adults only with acute lung injury/ARDS due to direct lung injury was not associated with improved oxygenation and longer term benefits compared to the placebo group. It was also associated with significant increases in hypoxia and hypotension (Willson et al, 2015).
    D) CHELATION THERAPY
    1) In general, chelation or antagonist therapy with available agents HAS NOT BEEN RECOMMENDED in cases of poisoning with selenium compounds.
    2) Calcium Disodium EDTA -
    a) Animal studies have shown that while calcium disodium EDTA decreased selenium toxicity if given within 15 minutes of ingestion, after that time period administration of the chelating agent actually INCREASED selenium toxicity (Civil & McDonald, 1978). Both the chelating agent and its selenium chelate product are nephrotoxic (Civil & McDonald, 1978).
    b) Administration of calcium disodium EDTA is NOT RECOMMENDED IN HUMAN POISONING CASES.
    3) BAL - (Dimercaprol) -
    a) In animal studies, administration of BAL INCREASED the toxicity of selenium (Civil & McDonald, 1978).
    b) Administration of BAL is NOT RECOMMENDED IN HUMAN POISONING CASES.
    4) Ascorbic Acid
    a) Animal studies have shown that although ascorbic acid administration increases the excretion of selenium, it also INCREASES SELENIUM TOXICITY (Civil & McDonald, 1978).
    b) Administration of ascorbic acid is NOT RECOMMENDED IN HUMAN POISONING CASES.
    5) Others -
    a) Glutathione has been suggested as an antagonist in experimental animals but has not been tried for the treatment of human poisoning (Lombeck et al, 1987).
    b) Methionine was ineffective in treating experimental selenium poisoning (Lombeck et al, 1987).
    c) Bromobenzene may hasten selenium excretion in some experimental animals, but has NOT BEEN RECOMMENDED for treatment of human poisonings because of its toxicity and high incidence of severe adverse reactions (Finkel, 1983). It was not effective when administered orally to selenium-poisoned rats.
    d) Apparently no studies have been done using d-penicillamine or DMSA for the treatment of selenium poisoning. Severe gastrointestinal symptoms and early development of seizures, coma, or shock would limit the administration of these oral agents. The fact that other chelating agents increase selenium toxicity in experimental animals would argue against their administration.
    E) OBSERVATION REGIMES
    1) Patients symptomatic following exposure should be observed in a controlled setting until all signs and symptoms have fully resolved.

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) Move patient from the toxic environment to fresh air. Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for hypoxia, respiratory tract irritation, bronchitis, or pneumonitis.
    B) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    C) INITIAL TREATMENT: Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists, if bronchospasm develops. Consider systemic corticosteroids in patients with significant bronchospasm (National Heart,Lung,and Blood Institute, 2007). Exposed skin and eyes should be flushed with copious amounts of water.
    6.7.2) TREATMENT
    A) IRRITATION SYMPTOM
    1) Initial respiratory tract irritation may appear to improve, but can then worsen between 2 and 12 hours after exposure (Wilson, 1962). Severe chemical pneumonitis may then develop over the following one to three days (Wilson, 1962).
    2) Early administration of supplemental oxygen seemed to mitigate the degree of chemical pneumonitis that developed in one incident (Wilson, 1962).
    3) Patients with inhalation exposure should be treated with supplemental oxygen beginning as soon as possible after rescue and should have a prolonged period of observation in a controlled setting with careful monitoring for the development of chemical pneumonitis.
    B) BRONCHOSPASM
    1) If bronchospasm and wheezing occur, consider treatment with inhaled sympathomimetic agents.
    C) ACUTE LUNG INJURY
    1) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
    2) NON-PHARMACOLOGIC TREATMENT: The treatment of acute lung injury is primarily supportive (Cataletto, 2012). Maintain adequate ventilation and oxygenation with frequent monitoring of arterial blood gases and/or pulse oximetry. If a high FIO2 is required to maintain adequate oxygenation, mechanical ventilation and positive-end-expiratory pressure (PEEP) may be required; ventilation with small tidal volumes (6 mL/kg) is preferred if ARDS develops (Haas, 2011; Stolbach & Hoffman, 2011).
    a) To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)
    3) FLUIDS: Crystalloid solutions must be administered judiciously. Pulmonary artery monitoring may help. In general the pulmonary artery wedge pressure should be kept relatively low while still maintaining adequate cardiac output, blood pressure and urine output (Stolbach & Hoffman, 2011).
    4) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
    5) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
    6) CALFACTANT: In a multicenter, randomized, blinded trial, endotracheal instillation of 2 doses of 80 mL/m(2) calfactant (35 mg/mL of phospholipid suspension in saline) in infants, children, and adolescents with acute lung injury resulted in acute improvement in oxygenation and lower mortality; however, no significant decrease in the course of respiratory failure measured by duration of ventilator therapy, intensive care unit, or hospital stay was noted. Adverse effects (transient hypoxia and hypotension) were more frequent in calfactant patients, but these effects were mild and did not require withdrawal from the study (Wilson et al, 2005).
    7) However, in a multicenter, randomized, controlled, and masked trial, endotracheal instillation of up to 3 doses of calfactant (30 mg) in adults only with acute lung injury/ARDS due to direct lung injury was not associated with improved oxygenation and longer term benefits compared to the placebo group. It was also associated with significant increases in hypoxia and hypotension (Willson et al, 2015).
    D) OBSERVATION REGIMES
    1) Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    E) MONITORING OF PATIENT
    1) Monitor EKG, vital signs, and urine output carefully.
    F) AIRWAY MANAGEMENT
    1) If coma and respiratory depression occur, ensure airway patency and adequacy of respirations and oxygenation. Endotracheal intubation, administration of supplemental oxygen, and assisted ventilation may be required.
    G) CHELATION THERAPY
    1) In general, chelation or antagonist therapy with available agents HAS NOT BEEN RECOMMENDED in cases of poisoning with selenium compounds.
    2) Calcium Disodium EDTA -
    a) Animal studies have shown that while calcium disodium EDTA decreased selenium toxicity if given within 15 minutes of ingestion, after that time period administration of the chelating agent actually INCREASED selenium toxicity (Civil & McDonald, 1978). Both the chelating agent and its selenium chelate product are nephrotoxic (Civil & McDonald, 1978).
    b) Administration of calcium disodium EDTA is NOT RECOMMENDED IN HUMAN POISONING CASES.
    3) BAL - (Dimercaprol) -
    a) In animal studies, administration of BAL INCREASED the toxicity of selenium (Civil & McDonald, 1978).
    b) Administration of BAL is NOT RECOMMENDED IN HUMAN POISONING CASES.
    4) Ascorbic Acid -
    a) Animal studies have shown that although ascorbic acid administration increases the excretion of selenium, it also INCREASES SELENIUM TOXICITY (Civil & McDonald, 1978).
    b) Administration of ascorbic acid is NOT RECOMMENDED IN HUMAN POISONING CASES.
    5) Others -
    a) Glutathione has been suggested as an antagonist in experimental animals but has not been tried for the treatment of human poisoning (Lombeck et al, 1987).
    b) Methionine was ineffective in treating experimental selenium poisoning (Lombeck et al, 1987).
    c) Bromobenzene may hasten selenium excretion in some experimental animals, but has NOT BEEN RECOMMENDED for treatment of human poisonings because of its toxicity and high incidence of severe adverse reactions (Finkel, 1983). It was not effective when administered orally to selenium-poisoned rats.
    d) Apparently no studies have been done using d-penicillamine or DMSA for the treatment of selenium poisoning. Severe gastrointestinal symptoms and early development of seizures, coma, or shock would limit the administration of these oral agents. The fact that other chelating agents increase selenium toxicity in experimental animals would argue against their administration.
    H) OBSERVATION REGIMES
    1) Patients symptomatic following exposure should be observed in a controlled setting until all signs and symptoms have fully resolved.
    2) Patients with inhalation exposure should be treated with supplemental oxygen beginning as soon as possible after rescue and should have a prolonged period of observation in a controlled setting with careful monitoring for the development of chemical pneumonitis.
    I) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Eye Exposure

    6.8.1) DECONTAMINATION
    A) EYE IRRIGATION, ROUTINE: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, an ophthalmologic examination should be performed (Peate, 2007; Naradzay & Barish, 2006).
    6.8.2) TREATMENT
    A) OPHTHALMIC EXAMINATION AND EVALUATION
    1) CONSULTATION - Because of the potential for serious eye irritation following direct contact with this agent, prolonged initial flushing and early ophthalmologic consultation are advisable.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL DECONTAMINATION
    1) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).
    6.9.2) TREATMENT
    A) IRRITATION SYMPTOM
    1) Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines.
    B) SKIN ABSORPTION
    1) Systemic absorption may take place through the skin.
    C) GENERAL TREATMENT
    1) Treatment should include recommendations listed in the INHALATION EXPOSURE section when appropriate.
    D) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Enhanced Elimination

    A) HEMOPERFUSION
    1) An in-vitro study showed that hemoperfusion might have only a "moderate effect" on selenium blood levels in selenious acid poisoning (Koppel et al, 1987). This procedure has not been utilized in human poisoning cases and cannot be recommended at this time.
    B) EXCHANGE TRANSFUSION
    1) No mention of early exchange transfusion for the treatment of selenious acid poisoning has been made in the literature.

Range Of Toxicity

Summary

    A) The minimum lethal human dose to this agent has not been delineated.
    B) An adolescent patient ingested 400 mL of a 5 mg/mL sodium selenate-containing sheep dip preparation (2000 mg; 22.3 mg Se/kg) but survived. Three other patients aged 22 months to 18 years ingested up to 5 mL of similar sheep dip (up to 5 mg) and had no ill effects.
    C) Anemia and marked hepatic necrosis, hemorrhage, and cirrhosis were found in experimental animals fed 5 to 15 ppm of selenium chronically in the diet.

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) The minimum lethal human dose to this agent has not been delineated.

Maximum Tolerated Exposure

    A) SPECIFIC SUBSTANCE
    1) 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) An adolescent patient ingested 400 mL of a 5 mg/mL sodium selenate-containing sheep dip preparation (2000 mg; 22.3 mg Se/kg) but survived (Civil & McDonald, 1978).
    a) Three other patients aged 22 months to 18 years ingested up to 5 mL of similar sheep dip (up to 5 mg) and had no ill effects (Civil & McDonald, 1978).
    2) A report by Yang et al (1983) from the Republic of China described a major outbreak of apparent selenium toxicity. The disease was characterized by the loss of hair and nails and skin lesions on the back of the hands and feet, and outer side of the legs.
    a) In regions of China with the most intense exposure, the residents had symptoms of a toxic polyneuritis. Individual daily selenium intake in the area ranged from 3.2 mg to 6.69 mg (average 4.99 mg), and whole blood levels of selenium ranged from 1.33 mcg/mL to 7.5 mcg/mL (average 3.2 mcg/mL) (Yang et al, 1983). An average daily intake of 0.1 milligram of selenium was noted for persons who were unaffected (Proctor et al, 1988).
    C) ANIMAL DATA
    1) Anemia and marked hepatic necrosis, hemorrhage, and cirrhosis were found in experimental animals fed 5 to 15 ppm of selenium chronically in the diet (Proctor et al, 1988).

Workplace Standards

    A) ACGIH TLV Values for CAS13410-01-0 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    B) NIOSH REL and IDLH Values for CAS13410-01-0 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    C) Carcinogenicity Ratings for CAS13410-01-0 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
    3) 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): Not Listed
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS13410-01-0 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: (RTECS, 1999)
    1) LD50- (ORAL)RAT:
    a) 1600 mcg/kg

Physicochemical

Physical Characteristics

    A) Sodium selenate exists as white crystals (Budavari, 1996).

Molecular Weight

    A) 188.94 (Budavari, 1996)

References

General Bibliography

    1) 40 CFR 372.28: Environmental Protection Agency - Toxic Chemical Release Reporting, Community Right-To-Know, Lower thresholds for chemicals of special concern. National Archives and Records Administration (NARA) and the Government Printing Office (GPO). Washington, DC. Final rules current as of Apr 3, 2006.
    2) 40 CFR 372.65: Environmental Protection Agency - Toxic Chemical Release Reporting, Community Right-To-Know, Chemicals and Chemical Categories to which this part applies. National Archives and Records Association (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Apr 3, 2006.
    3) 49 CFR 172.101 - App. B: Department of Transportation - Table of Hazardous Materials, Appendix B: List of Marine Pollutants. National Archives and Records Administration (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Aug 29, 2005.
    4) 62 FR 58840: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 1997.
    5) 65 FR 14186: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.
    6) 65 FR 39264: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.
    7) 65 FR 77866: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.
    8) 66 FR 21940: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2001.
    9) 67 FR 7164: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2002.
    10) 68 FR 42710: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2003.
    11) 69 FR 54144: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2004.
    12) AIHA: 2006 Emergency Response Planning Guidelines and Workplace Environmental Exposure Level Guides Handbook, American Industrial Hygiene Association, Fairfax, VA, 2006.
    13) Alderman LC & Bergin JJ: Hydrogen selenide poisoning: an illustrative case with review of the literature. Arch Environ Health 1986; 41:354-358.
    14) Alfthan G: Selenium status of nonpregnant, pregnant women and neonates. Acta Pharmacol Toxicol 1986; 59(Suppl 7):142.
    15) American Conference of Governmental Industrial Hygienists : ACGIH 2010 Threshold Limit Values (TLVs(R)) for Chemical Substances and Physical Agents and Biological Exposure Indices (BEIs(R)), American Conference of Governmental Industrial Hygienists, Cincinnati, OH, 2010.
    16) Artigas A, Bernard GR, Carlet J, et al: The American-European consensus conference on ARDS, part 2: ventilatory, pharmacologic, supportive therapy, study design strategies, and issues related to recovery and remodeling.. Am J Respir Crit Care Med 1998; 157:1332-1347.
    17) Barlow SM & Sullivan FM: Reproductive Hazards of Industrial Chemicals: an Evaluation of Animal and Human Studies, Academic Press, London, UK, 1982.
    18) Baselt RC & Cravey RH: Disposition of Toxic Drugs and Chemicals in Man, 3rd ed, Year Book Medical Publishers, Chicago, IL, 1989, pp 756-758.
    19) Baselt RC: Biological Monitoring Methods for Industrial Chemicals, 2nd ed, PSG Publishing Company, Littleton, MA, 1988, pp 261-264.
    20) Biswas S, Talukder G, & Sharma A: Selenium salts and chromosome damage. Mutat Res 1997; 390:201-205.
    21) Brower RG, Matthay AM, & Morris A: Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Eng J Med 2000; 342:1301-1308.
    22) Budavari S: The Merck Index, 11th ed, Merck & Co, Inc, Rahway, NJ, 1989, pp 1368.
    23) Budavari S: The Merck Index, 12th ed, Merck & Co, Inc, Rahway, NJ, 1996, pp 8815.
    24) Buell DN: Potential hazards of selenium as a chemopreventive agent. Sem Oncol 1983; 10:311-321.
    25) Burgess JL, Kirk M, Borron SW, et al: Emergency department hazardous materials protocol for contaminated patients. Ann Emerg Med 1999; 34(2):205-212.
    26) Caravati EM, Knight HH, & Linscott MS: Esophageal laceration and charcoal mediastinum complicating gastric lavage. J Emerg Med 2001; 20:273-276.
    27) Cataletto M: Respiratory Distress Syndrome, Acute(ARDS). In: Domino FJ, ed. The 5-Minute Clinical Consult 2012, 20th ed. Lippincott Williams & Wilkins, Philadelphia, PA, 2012.
    28) Chyka PA, Seger D, Krenzelok EP, et al: Position paper: Single-dose activated charcoal. Clin Toxicol (Phila) 2005; 43(2):61-87.
    29) Civil IDS & McDonald MJA: Acute selenium poisoning: case report. NZ Med J 1978; 87:354-356.
    30) Clayton GD & Clayton FE: Patty's Industrial Hygiene and Toxicology, Vol 2A, Toxicology, 3rd ed, John Wiley & Sons, New York, NY, 1981, pp 2130-2132.
    31) Council on Scientific Affairs: Effects of Toxic Chemicals on the Reproductive System, American Medical Association, Chicago, IL, 1985.
    32) DFG: List of MAK and BAT Values 2002, Report No. 38, Deutsche Forschungsgemeinschaft, Commission for the Investigation of Health Hazards of Chemical Compounds in the Work Area, Wiley-VCH, Weinheim, Federal Republic of Germany, 2002.
    33) DeYoung DJ, Bantle JA, & Fort DJ: Assessment of the developmental toxicity of ascorbic acid, sodium selenate, coumarin, serotonin, and 13-cis retinoic acid using FETAX. Drug Chem Toxicol 1991; 127-141.
    34) Diskin CJ, Tomasso CL, & Alper JC: Long-term selenium exposure. Arch Intern Med 1979; 139:824-826.
    35) EPA: EPA chemical profile on sodium selenate, Environmental Protection Agency, Washington, DC, 1985.
    36) EPA: Search results for Toxic Substances Control Act (TSCA) Inventory Chemicals. US Environmental Protection Agency, Substance Registry System, U.S. EPA's Office of Pollution Prevention and Toxics. Washington, DC. 2005. Available from URL: http://www.epa.gov/srs/.
    37) Ellenhorn MJ & Barceloux DG: Selenium, in: Medical Toxicology: Diagnosis and Treatment of Human Poisoning, Elsevier, New York, NY, 1988, pp 1059-1060.
    38) Ellenhorn MJ: Ellenhorn's Medical Toxicology. Diagnosis and Treatment of Human Poisoning, Williams & Wilkins, Baltimore, MD, 1997, pp 1607-1608.
    39) Elliot CG, Colby TV, & Kelly TM: Charcoal lung. Bronchiolitis obliterans after aspiration of activated charcoal. Chest 1989; 96:672-674.
    40) FDA: Poison treatment drug product for over-the-counter human use; tentative final monograph. FDA: Fed Register 1985; 50:2244-2262.
    41) Ferm VH, Hanlon DP, & Willhite CC: Embryotoxicity and dose-response relationships of selenium in hamsters. Reprod Toxicol 1990; 4:183-190.
    42) Finkel AJ: Hamilton and Hardy's Industrial Toxicology, 4th ed, John Wright, PSG Inc, Boston, MA, 1983, pp 123-125.
    43) Gerhardsson L, Brune D, & Nordberg GF: Selenium and other trace elements in lung tissue in smelter workers: relationship to the occurrence of lung cancer. ACTA Pharmacol Toxicol 1986; 59(Suppl 7):256-259.
    44) Golej J, Boigner H, Burda G, et al: Severe respiratory failure following charcoal application in a toddler. Resuscitation 2001; 49:315-318.
    45) Graff GR, Stark J, & Berkenbosch JW: Chronic lung disease after activated charcoal aspiration. Pediatrics 2002; 109:959-961.
    46) HSDB : Hazardous Substances Data Bank. National Library of Medicine. Bethesda, MD (Internet Version). Edition expires 1993; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    47) Haas CF: Mechanical ventilation with lung protective strategies: what works?. Crit Care Clin 2011; 27(3):469-486.
    48) Harris CR & Filandrinos D: Accidental administration of activated charcoal into the lung: aspiration by proxy. Ann Emerg Med 1993; 22:1470-1473.
    49) Hathaway GJ, Proctor NH, & Hughes JP: Chemical Hazards of the Workplace, 4th ed, Van Nostrand Reinhold Company, New York, NY, 1996, pp 551-552.
    50) Henschler D & Kirschner U: Zur resorption und toxicitat von selensulfid. Arch Toxicol (Berl) 1969; 24:341-344.
    51) IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: 1,3-Butadiene, Ethylene Oxide and Vinyl Halides (Vinyl Fluoride, Vinyl Chloride and Vinyl Bromide), 97, International Agency for Research on Cancer, Lyon, France, 2008.
    52) IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Formaldehyde, 2-Butoxyethanol and 1-tert-Butoxypropan-2-ol, 88, International Agency for Research on Cancer, Lyon, France, 2006.
    53) IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Household Use of Solid Fuels and High-temperature Frying, 95, International Agency for Research on Cancer, Lyon, France, 2010a.
    54) IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Smokeless Tobacco and Some Tobacco-specific N-Nitrosamines, 89, International Agency for Research on Cancer, Lyon, France, 2007.
    55) IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Some Non-heterocyclic Polycyclic Aromatic Hydrocarbons and Some Related Exposures, 92, International Agency for Research on Cancer, Lyon, France, 2010.
    56) IARC: List of all agents, mixtures and exposures evaluated to date - IARC Monographs: Overall Evaluations of Carcinogenicity to Humans, Volumes 1-88, 1972-PRESENT. World Health Organization, International Agency for Research on Cancer. Lyon, FranceAvailable from URL: http://monographs.iarc.fr/monoeval/crthall.html. As accessed Oct 07, 2004.
    57) IARC: Selenium and Selenium Compounds, in: IARC Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man: Some Aziridines, N-, S-, and O-mustards and Selenium, 9, International Agency for Research on Cancer, World Health Organization, Geneva, Switzerland, 1974, pp 245-260.
    58) International Agency for Research on Cancer (IARC): IARC monographs on the evaluation of carcinogenic risks to humans: list of classifications, volumes 1-116. International Agency for Research on Cancer (IARC). Lyon, France. 2016. Available from URL: http://monographs.iarc.fr/ENG/Classification/latest_classif.php. As accessed 2016-08-24.
    59) International Agency for Research on Cancer: IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. World Health Organization. Geneva, Switzerland. 2015. Available from URL: http://monographs.iarc.fr/ENG/Classification/. As accessed 2015-08-06.
    60) Kollef MH & Schuster DP: The acute respiratory distress syndrome. N Engl J Med 1995; 332:27-37.
    61) Koppel C, Baudisch H, & Koppel I: Fatal poisoning with selenium dioxide. Clin Toxicol 1986; 24:21-35.
    62) Lo LW, Koropatnick J, & Stich HF: The mutagenicity and cytotoxicity of selenite, "activated" selenite and selenate for normal and DNA repair-deficient human fibroblasts. Mutat Res 1978; 49:305-312.
    63) Lombeck I, Menzel H, & Frosch D: Acute selenium poisoning of a 2-year-old child. Eur J Pediatr 1987; 146:308-312.
    64) Matoba R, Kimura H, & Uchima E: An autopsy case of acute selenium (selenious acid) poisoning and selenium levels in human tissues. Forens Sci Internat 1986; 31:87-92.
    65) Milner JA & Hsu CY: Inhibitory effects of selenium on the growth of L1210 leukemic cells. Cancer Res 1981; 41:1652-1656.
    66) Motley HL & Ellis MM: Acute sore throats following exposure to selenium. JAMA 1937; 109:1718-1719.
    67) NFPA: Fire Protection Guide to Hazardous Materials, 13th ed., National Fire Protection Association, Quincy, MA, 2002.
    68) NHLBI ARDS Network: Mechanical ventilation protocol summary. Massachusetts General Hospital. Boston, MA. 2008. Available from URL: http://www.ardsnet.org/system/files/6mlcardsmall_2008update_final_JULY2008.pdf. As accessed 2013-08-07.
    69) NRC: Acute Exposure Guideline Levels for Selected Airborne Chemicals - Volume 1, Subcommittee on Acute Exposure Guideline Levels, Committee on Toxicology, Board on Environmental Studies and Toxicology, Commission of Life Sciences, National Research Council. National Academy Press, Washington, DC, 2001.
    70) NRC: Acute Exposure Guideline Levels for Selected Airborne Chemicals - Volume 2, Subcommittee on Acute Exposure Guideline Levels, Committee on Toxicology, Board on Environmental Studies and Toxicology, Commission of Life Sciences, National Research Council. National Academy Press, Washington, DC, 2002.
    71) NRC: Acute Exposure Guideline Levels for Selected Airborne Chemicals - Volume 3, Subcommittee on Acute Exposure Guideline Levels, Committee on Toxicology, Board on Environmental Studies and Toxicology, Commission of Life Sciences, National Research Council. National Academy Press, Washington, DC, 2003.
    72) NRC: Acute Exposure Guideline Levels for Selected Airborne Chemicals - Volume 4, Subcommittee on Acute Exposure Guideline Levels, Committee on Toxicology, Board on Environmental Studies and Toxicology, Commission of Life Sciences, National Research Council. National Academy Press, Washington, DC, 2004.
    73) Naradzay J & Barish RA: Approach to ophthalmologic emergencies. Med Clin North Am 2006; 90(2):305-328.
    74) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,2,3-Trimethylbenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2006k. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d68a&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    75) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,2,4-Trimethylbenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2006m. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d68a&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    76) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,2-Butylene Oxide (Proposed). United States Environmental Protection Agency. Washington, DC. 2008d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648083cdbb&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    77) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,2-Dibromoethane (Proposed). United States Environmental Protection Agency. Washington, DC. 2007g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064802796db&disposition=attachment&contentType=pdf. As accessed 2010-08-18.
    78) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,3,5-Trimethylbenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2006l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d68a&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    79) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 2-Ethylhexyl Chloroformate (Proposed). United States Environmental Protection Agency. Washington, DC. 2007b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648037904e&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    80) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Acrylonitrile (Proposed). United States Environmental Protection Agency. Washington, DC. 2007c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648028e6a3&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    81) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Adamsite (Proposed). United States Environmental Protection Agency. Washington, DC. 2007h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    82) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Agent BZ (3-quinuclidinyl benzilate) (Proposed). United States Environmental Protection Agency. Washington, DC. 2007f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803ad507&disposition=attachment&contentType=pdf. As accessed 2010-08-18.
    83) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Allyl Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2008. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648039d9ee&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    84) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Aluminum Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    85) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Arsenic Trioxide (Proposed). United States Environmental Protection Agency. Washington, DC. 2007m. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480220305&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    86) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Automotive Gasoline Unleaded (Proposed). United States Environmental Protection Agency. Washington, DC. 2009a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7cc17&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    87) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Biphenyl (Proposed). United States Environmental Protection Agency. Washington, DC. 2005j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064801ea1b7&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    88) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Bis-Chloromethyl Ether (BCME) (Proposed). United States Environmental Protection Agency. Washington, DC. 2006n. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648022db11&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    89) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Boron Tribromide (Proposed). United States Environmental Protection Agency. Washington, DC. 2008a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803ae1d3&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    90) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Bromine Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2007d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648039732a&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    91) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Bromoacetone (Proposed). United States Environmental Protection Agency. Washington, DC. 2008e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809187bf&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    92) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Calcium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    93) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Carbonyl Fluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2008b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803ae328&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    94) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Carbonyl Sulfide (Proposed). United States Environmental Protection Agency. Washington, DC. 2007e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648037ff26&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    95) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Chlorobenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2008c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803a52bb&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    96) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Cyanogen (Proposed). United States Environmental Protection Agency. Washington, DC. 2008f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809187fe&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    97) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Dimethyl Phosphite (Proposed). United States Environmental Protection Agency. Washington, DC. 2009. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7cbf3&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    98) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Diphenylchloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    99) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethyl Isocyanate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648091884e&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    100) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethyl Phosphorodichloridate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480920347&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    101) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethylbenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2008g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809203e7&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    102) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethyldichloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    103) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Germane (Proposed). United States Environmental Protection Agency. Washington, DC. 2008j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963906&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    104) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Hexafluoropropylene (Proposed). United States Environmental Protection Agency. Washington, DC. 2006. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064801ea1f5&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    105) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ketene (Proposed). United States Environmental Protection Agency. Washington, DC. 2007. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ee7c&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    106) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Magnesium Aluminum Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    107) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Magnesium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    108) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Malathion (Proposed). United States Environmental Protection Agency. Washington, DC. 2009k. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809639df&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    109) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Mercury Vapor (Proposed). United States Environmental Protection Agency. Washington, DC. 2009b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a8a087&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    110) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyl Isothiocyanate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008k. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963a03&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    111) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyl Parathion (Proposed). United States Environmental Protection Agency. Washington, DC. 2008l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963a57&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    112) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyl tertiary-butyl ether (Proposed). United States Environmental Protection Agency. Washington, DC. 2007a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064802a4985&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    113) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methylchlorosilane (Proposed). United States Environmental Protection Agency. Washington, DC. 2005. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5f4&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    114) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyldichloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    115) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyldichlorosilane (Proposed). United States Environmental Protection Agency. Washington, DC. 2005a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c646&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    116) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Mustard (HN1 CAS Reg. No. 538-07-8) (Proposed). United States Environmental Protection Agency. Washington, DC. 2006a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d6cb&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    117) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Mustard (HN2 CAS Reg. No. 51-75-2) (Proposed). United States Environmental Protection Agency. Washington, DC. 2006b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d6cb&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    118) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Mustard (HN3 CAS Reg. No. 555-77-1) (Proposed). United States Environmental Protection Agency. Washington, DC. 2006c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d6cb&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    119) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Tetroxide (Proposed). United States Environmental Protection Agency. Washington, DC. 2008n. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648091855b&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    120) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Trifluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2009l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963e0c&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    121) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Parathion (Proposed). United States Environmental Protection Agency. Washington, DC. 2008o. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963e32&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    122) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Perchloryl Fluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2009c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7e268&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    123) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Perfluoroisobutylene (Proposed). United States Environmental Protection Agency. Washington, DC. 2009d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7e26a&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    124) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phenyl Isocyanate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008p. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096dd58&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    125) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phenyl Mercaptan (Proposed). United States Environmental Protection Agency. Washington, DC. 2006d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020cc0c&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    126) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phenyldichloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007k. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    127) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phorate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008q. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096dcc8&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    128) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phosgene (Draft-Revised). United States Environmental Protection Agency. Washington, DC. 2009e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a8a08a&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    129) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phosgene Oxime (Proposed). United States Environmental Protection Agency. Washington, DC. 2009f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7e26d&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    130) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Potassium Cyanide (Proposed). United States Environmental Protection Agency. Washington, DC. 2009g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7cbb9&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    131) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Potassium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    132) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Propargyl Alcohol (Proposed). United States Environmental Protection Agency. Washington, DC. 2006e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ec91&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    133) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Selenium Hexafluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2006f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ec55&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    134) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Silane (Proposed). United States Environmental Protection Agency. Washington, DC. 2006g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d523&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    135) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Sodium Cyanide (Proposed). United States Environmental Protection Agency. Washington, DC. 2009h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7cbb9&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    136) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Sodium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    137) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Strontium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    138) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Sulfuryl Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2006h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ec7a&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    139) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Tear Gas (Proposed). United States Environmental Protection Agency. Washington, DC. 2008s. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096e551&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    140) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Tellurium Hexafluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2009i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7e2a1&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    141) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Tert-Octyl Mercaptan (Proposed). United States Environmental Protection Agency. Washington, DC. 2008r. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096e5c7&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    142) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Tetramethoxysilane (Proposed). United States Environmental Protection Agency. Washington, DC. 2006j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d632&disposition=attachment&contentType=pdf. As accessed 2010-08-17.
    143) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Trimethoxysilane (Proposed). United States Environmental Protection Agency. Washington, DC. 2006i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d632&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    144) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Trimethyl Phosphite (Proposed). United States Environmental Protection Agency. Washington, DC. 2009j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7d608&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    145) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Trimethylacetyl Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2008t. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096e5cc&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    146) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Zinc Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    147) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for n-Butyl Isocyanate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008m. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064808f9591&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    148) National Heart,Lung,and Blood Institute: Expert panel report 3: guidelines for the diagnosis and management of asthma. National Heart,Lung,and Blood Institute. Bethesda, MD. 2007. Available from URL: http://www.nhlbi.nih.gov/guidelines/asthma/asthgdln.pdf.
    149) National Institute for Occupational Safety and Health: NIOSH Pocket Guide to Chemical Hazards, U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, Cincinnati, OH, 2007.
    150) National Research Council : Acute exposure guideline levels for selected airborne chemicals, 5, National Academies Press, Washington, DC, 2007.
    151) National Research Council: Acute exposure guideline levels for selected airborne chemicals, 6, National Academies Press, Washington, DC, 2008.
    152) National Research Council: Acute exposure guideline levels for selected airborne chemicals, 7, National Academies Press, Washington, DC, 2009.
    153) National Research Council: Acute exposure guideline levels for selected airborne chemicals, 8, National Academies Press, Washington, DC, 2010.
    154) Noda M, Takano T, & Sakurai H: Mutagenic activity of selenium compounds. Mutat Res 1979; 66:175-179.
    155) None Listed: Position paper: cathartics. J Toxicol Clin Toxicol 2004; 42(3):243-253.
    156) Paton GR & Allison AC: Chromosome damage in human cell cultures induced by metal salts. Mutat Res 1972; 16:332-336.
    157) Peate WF: Work-related eye injuries and illnesses. Am Fam Physician 2007; 75(7):1017-1022.
    158) Pollack MM, Dunbar BS, & Holbrook PR: Aspiration of activated charcoal and gastric contents. Ann Emerg Med 1981; 10:528-529.
    159) Proctor NH, Hughes JP, & Fischman ML: Chemical Hazards of the Workplace, 2nd ed, JB Lippincott Co, Philadelphia, PA, 1988, pp 437-438.
    160) RTECS : Registry of Toxic Effects of Chemical Substances. National Institute for Occupational Safety and Health. Cincinnati, OH (Internet Version). Edition expires 1990; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    161) Rau NR, Nagaraj MV, Prakash PS, et al: Fatal pulmonary aspiration of oral activated charcoal. Br Med J 1988; 297:918-919.
    162) Robberecht HJ & Deelstra HA: Selenium in human urine: concentration levels and medical implications. Clin Chem Acta 1984; 136:107-120.
    163) Russell GR, Nader CJ, & Partick EJ: Induction of DNA repair by some selenium compounds. Cancer Lett 1980; 10:75-81.
    164) Sax NI & Lewis RJ: Dangerous Properties of Industrial Materials, 7th ed, Van Nostrand Reinhold Company, New York, NY, 1989, pp 1504.
    165) Sax NI & Lewis RJ: Hawley's Condensed Chemical Dictionary, 11th ed, Van Nostrand Reinhold Company, New York, NY, 1987, pp 1072.
    166) Schardein JL: Chemically Induced Birth Defects, 2nd ed, Marcel Dekker, Inc, New York, NY, 1993, pp 738-739.
    167) Schellmann B, Raithel HJ, & Schaller KH: Acute fatal selenium poisoning: Toxicological and occupational medical aspects. Arch Toxicol 1986; 59:61-63.
    168) Sirianni SR & Huang CC: Induction of sister chromatid exchanges by various selenium compounds in Chinese hamster cells in the presence and absence of S9 mixture. Cancer Lett 1983; 18:109-116.
    169) Sittig M: Handbook of Toxic and Hazardous Chemicals and Carcinogens, 3rd ed, Noyes Publications, Park Ridge, NJ, 1991, pp 1418-1421.
    170) Stolbach A & Hoffman RS: Respiratory Principles. In: Nelson LS, Hoffman RS, Lewin NA, et al, eds. Goldfrank's Toxicologic Emergencies, 9th ed. McGraw Hill Medical, New York, NY, 2011.
    171) U.S. Department of Energy, Office of Emergency Management: Protective Action Criteria (PAC) with AEGLs, ERPGs, & TEELs: Rev. 26 for chemicals of concern. U.S. Department of Energy, Office of Emergency Management. Washington, DC. 2010. Available from URL: http://www.hss.doe.gov/HealthSafety/WSHP/Chem_Safety/teel.html. As accessed 2011-06-27.
    172) U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project : 11th Report on Carcinogens. U.S. Department of Health and Human Services, Public Health Service, National Toxicology Program. Washington, DC. 2005. Available from URL: http://ntp.niehs.nih.gov/INDEXA5E1.HTM?objectid=32BA9724-F1F6-975E-7FCE50709CB4C932. As accessed 2011-06-27.
    173) U.S. Environmental Protection Agency: Discarded commercial chemical products, off-specification species, container residues, and spill residues thereof. Environmental Protection Agency's (EPA) Resource Conservation and Recovery Act (RCRA); List of hazardous substances and reportable quantities 2010b; 40CFR(261.33, e-f):77-.
    174) U.S. Environmental Protection Agency: Integrated Risk Information System (IRIS). U.S. Environmental Protection Agency. Washington, DC. 2011. Available from URL: http://cfpub.epa.gov/ncea/iris/index.cfm?fuseaction=iris.showSubstanceList&list_type=date. As accessed 2011-06-21.
    175) U.S. Environmental Protection Agency: List of Radionuclides. U.S. Environmental Protection Agency. Washington, DC. 2010a. Available from URL: http://www.gpo.gov/fdsys/pkg/CFR-2010-title40-vol27/pdf/CFR-2010-title40-vol27-sec302-4.pdf. As accessed 2011-06-17.
    176) U.S. Environmental Protection Agency: List of hazardous substances and reportable quantities. U.S. Environmental Protection Agency. Washington, DC. 2010. Available from URL: http://www.gpo.gov/fdsys/pkg/CFR-2010-title40-vol27/pdf/CFR-2010-title40-vol27-sec302-4.pdf. As accessed 2011-06-17.
    177) U.S. Environmental Protection Agency: The list of extremely hazardous substances and their threshold planning quantities (CAS Number Order). U.S. Environmental Protection Agency. Washington, DC. 2010c. Available from URL: http://www.gpo.gov/fdsys/pkg/CFR-2010-title40-vol27/pdf/CFR-2010-title40-vol27-part355.pdf. As accessed 2011-06-17.
    178) U.S. Occupational Safety and Health Administration: Part 1910 - Occupational safety and health standards (continued) Occupational Safety, and Health Administration's (OSHA) list of highly hazardous chemicals, toxics and reactives. Subpart Z - toxic and hazardous substances. CFR 2010 2010; Vol6(SEC1910):7-.
    179) U.S. Occupational Safety, and Health Administration (OSHA): Process safety management of highly hazardous chemicals. 29 CFR 2010 2010; 29(1910.119):348-.
    180) United States Environmental Protection Agency Office of Pollution Prevention and Toxics: Acute Exposure Guideline Levels (AEGLs) for Vinyl Acetate (Proposed). United States Environmental Protection Agency. Washington, DC. 2006. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d6af&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    181) Vale JA, Kulig K, American Academy of Clinical Toxicology, et al: Position paper: Gastric lavage. J Toxicol Clin Toxicol 2004; 42:933-943.
    182) Vale JA: Position Statement: gastric lavage. American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. J Toxicol Clin Toxicol 1997; 35:711-719.
    183) Willson DF, Truwit JD, Conaway MR, et al: The adult calfactant in acute respiratory distress syndrome (CARDS) trial. Chest 2015; 148(2):356-364.
    184) Wilson DF, Thomas NJ, Markovitz BP, et al: Effect of exogenous surfactant (calfactant) in pediatric acute lung injury. A randomized controlled trial. JAMA 2005; 293:470-476.
    185) Wilson HM: Selenium oxide poisoning. N Carolina Med J 1962; 23:73-75.
    186) Yang G, Wang S, & Zhou R: Endemic selenium intoxication of humans in China. Am J Clin Nutr 1983; 37:872-881.