Selenious Acid

3.004 at 59 °F (EPA, 1998) - Denser than water; will sink

3.004 @ 15 °C/4 °C

3.0 g/cm³

3 @25 °C

White hygroscopic crystals.

Transparent, colorless, crystals.

Hexagonal prisms.

soluble

90 parts/100 parts water @ 0 °C; 400 parts @ 90 °C

Very sol in alcohol; insol in ammonia

167 g/100 cc water @ 20 °C

Solubility in water, g/100ml at 20 °C: 167

FDA approved drugs -> Active ingredient

FDA approved drugs -> Active ingredient

When heated to decomp ... emits toxic fumes of /selenium/.

70 °C

Decomposes at 158 °F (EPA, 1998)

70 °C with decomposition.

2 mmHg at 59 °F (EPA, 1998)

2 mm Hg at 15 °C; 4.5 mm Hg at 35 °C; 7 mm Hg at 40.3 °C

Vapor pressure, Pa at 15 °C: 266

2 [mm Hg] @15 °C

Selenious acid appears as colorless solid, transparent, colorless crystals. Used as a reagent for alkaloids and as an oxidizing agent. Isotope is used in labeling radiopharmaceuticals. (EPA, 1998)

Deliquescent solid; [Merck Index] Colorless or white hygroscopic solid; [HSDB] Colorless or white odorless crystalline solid; [MSDSonline]

Solid

COLOURLESS HYGROSCOPIC CRYSTALS.

2.46

K1= 0.0024; K2= 4.8X10-9

DELIQUESCENT; GIVES OFF WATER UPON HEATING & SELENIUM OXIDE SUBLIMES; OXIDIZED TO SELENIC ACID BY STRONG OXIDIZING AGENTS ... REDUCED TO SELENIUM BY MOST REDUCING AGENTS ... .

Heat of formation, -531.3 kJ/mol @ 25 °C /endothermic/

Danger

H301+H331 (10.8%): Toxic if swallowed or if inhaled [Danger Acute toxicity, oral; acute toxicity, inhalation]

P260, P261, P264, P270, P271, P273, P301+P316, P304+P340, P316, P319, P321, P330, P391, P403+P233, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 231 reports by companies from 20 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Danger

H314: Causes severe skin burns and eye damage [Danger Skin corrosion/irritation]

Chemical: Selenious acid (H2SeO3)

Regulation (EC) No 1831/2003 (amended)

Status: Active Update: 17-08-2017 https://echa.europa.eu/registration-dossier/-/registered-dossier/5196

Selenious acid: Does not have an individual approval but may be used under an appropriate group standard

The New Jersey Worker and Community Right to Know Act requires public and private employers to provide information about hazardous substances at their workplaces. (N.J.S.A. 34:5A-1 et. seq.)

When heated to decomposition it emits toxic fumes of selenium. Avoid heating. (EPA, 1998)

Not combustible. Gives off irritating or toxic fumes (or gases) in a fire.

A corrosive substance that can cause injury to the skin, eyes, and respiratory tract; Inhalation may cause pulmonary edema; May cause skin sensitization; May cause impairment of the CNS and liver; [ICSC] Can cause irritation and burns to skin; After a suicidal ingestion of Gun Blue, the patient had pulmonary edema and acute tubular necrosis; Selenium levels in tissues were 9-90 times normal; In another poisoning case, a 2 year old girl ingested about 11 mL of gun blueing agent; Plasma selenium levels were 20 times normal 5 hours after ingestion, but she survived; [HSDB]; A corrosive substance that can cause injury to the skin, eyes, and respiratory tract; Inhalation may cause chemical pneumonitis; [MSDSonline] See Selenium.

WHO; Evaluation of The Available Toxicity Data On Selenium (1987). Properties and analysis; sources, levels and transport in the environment; human exposure; metabolism; animal studies; effects on man; evaluation of the health risks; quantitative assessment of exposure.

NTIS; Govt Reports Announcements & Index (GRA&I), Issue 14 (1987). This bibliography contains citations concerning the toxicity, carcinogenicity, environmental pollution, and other hazards and adverse effects of selenium. The detection, characterization, analytical methods, and removal from the environment are discussed. Pollution from coal fired and geothermal power plants are considered. (This updated bibliography contains 349 citations, none of which are new entries to the previous edition.)

Najael; Revue g'en'erale de s'ecurite - RGS 63: 65-72 (1987). Information note on the harmful effects of selenium compounds. Physical and chemical properties of selenium and its principal compounds; uses; pathology and toxicology (irritation of the skin and mucous membranes; these irritations are compensable under French law); radioactive selenium; fire hazards; French regulations; protection.

Environ Health Criteria: Selenium 58 (0): 1-306 (1987)

For more Special Reports (Complete) data for SELENIOUS ACID (8 total), please visit the HSDB record page.

U204; As stipulated in 40 CFR 261.33, when selenious acid, as a commercial chemical product or manufacturing chemical intermediate or an off-specification commercial chemical product or a manufacturing chemical intermediate, becomes a waste, it must be managed according to Federal and/or State hazardous waste regulations. Also defined as a hazardous waste is any residue, contaminated soil, water, or other debris resulting from the cleanup of a spill, into water or on dry land, of this waste. Generators of small quantities of this waste may qualify for partial exclusion from hazardous waste regulations (40 CFR 261.5).

D010; A solid waste containing selenium (such as selenious acid) may or may not become characterized as a hazardous waste when subjected to the Toxicity Characteristic Leaching Procedure listed in 40 CFR 261.24, and if so characterized, must be managed as a hazardous waste.

SELENIOUS ACID decomposes when heated to toxic and volatile selenium dioxide. Serves as an oxidizing agent. Reacts exothermically with many reducing agents including hydroiodic acid, sulfurous acid, sodium hyposulfite, hydroxylamine salts, hydrazine salts, hypophosphorous acid, phosphorous acid [Merck]. Oxidizes many organic substances. Is oxidized to selenic acid by strong oxidizing agents.

Listed as a hazardous air pollutant (HAP) generally known or suspected to cause serious health problems. The Clean Air Act, as amended in 1990, directs EPA to set standards requiring major sources to sharply reduce routine emissions of toxic pollutants. EPA is required to establish and phase in specific performance based standards for all air emission sources that emit one or more of the listed pollutants. Selenious acid is included on this list.

To extinguish a fire involving this chemical you may use a dry chemical, carbon dioxide, foam or halon extinguisher; a water spray may also be used. (NTP, 1992)

In case of fire in the surroundings, use appropriate extinguishing media.

Fresh air, rest. Half-upright position. Artificial respiration may be needed. Refer for medical attention.

Remove contaminated clothes. Rinse skin with plenty of water or shower. Refer for medical attention .

First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then refer for medical attention.

Rinse mouth. Do NOT induce vomiting. Refer for medical attention .

Signs and Symptoms of Selenious Acid Exposure: Signs and symptoms of acute selenious acid exposure include the following: garlic odor on breath, drooling, nasal irritation and burning sensation in nostrils, vomiting, hypotension (low blood pressure), dizziness, and poor reflexes. Pulmonary edema, cardiopulmonary arrest, and coma are possible complications. Contact with selenious acid often results in skin irritation and burns.

Avoid inhalation and skin contact. Ventilate area of spill. Collect spilled material in most convenient and safe manner and deposit in sealed containers for reclamation or disposal in a secured disposal landfill. Liquid containing selenium inorganic compounds should be absorbed in vermiculite, dry sand, earth or similar material. (EPA, 1998)

Generators of waste (equal to or greater than 100 kg/mo) containing this contaminant, EPA hazardous waste number U204, D010, must conform with USEPA regulations in storage, transportation, treatment and disposal of waste.

Poor candidate for incineration.

Evacuate danger area! Consult an expert! Personal protection: complete protective clothing including self-contained breathing apparatus. Cover the spilled material with dry lime or soda ash. Carefully collect remainder. Then store and dispose of according to local regulations.

SRP: The scientific literature for the use of contact lenses in industry is conflicting. The benefit or detrimental effects of wearing contact lenses depend not only upon the substance, but also on factors including the form of the substance, characteristics and duration of the exposure, the uses of other eye protection equipment, and the hygiene of the lenses. However, there may be individual substances whose irritating or corrosive properties are such that the wearing of contact lenses would be harmful to the eye. In those specific cases, contact lenses should not be worn. In any event, the usual eye protection equipment should be worn even when contact lenses are in place.

Inhalation studies on rats show that 94% of selenious acid deposited in the lung was absorbed within four hours. A model based on these rat studies predicted that organ concentration in man due to inhalation of selenious acid ... in urban atmospheres will not contribute significantly to human body burdens.

EYES: irrigate opened eyes for several minutes under running water. INGESTION: do not induce vomiting. Rinse mouth with water (never give anything by mouth to an unconscious person). Seek immediate medical advice. SKIN: should be treated immediately by rinsing the affected parts in cold running water for at least 15 minutes, followed by thorough washing with soap and water. If necessary, the person should shower and change contaminated clothing and shoes, and then must seek medical attention. INHALATION: supply fresh air. If required provide artificial respiration.

The chemopreventive efficacies of selenate, selenite, selenium dioxide, selenomethionine and selenocystine were examined during the promotion phase of carcinogenesis in the 7,12-dimethylbenz(a)anthracene-induced mammary tumor model in rats. Each agent was added to the diet of a final concentration of 3 ppm selenium. In general, there was no significant difference in the potency of these five selenium compounds in inhibiting the development of mammary tumors. The interaction of vitamin E (500 ppm) with either selenite or selenomethionine was further characterized in a second carcinogenesis study. Results of this experiment suggested that vitamin E enhanced the protective effect of selenite but not that of selenomethionine. In an attempt to explore the synergistic mechanism of selenium and vitamin E, the effects of these two agents on mitogen induced blastogenesis and natural killer cytotoxic activity were also investigated. No consistent changes in these in vitro immune functions were detected resulting from supranutritional feeding of either selenite or vitamin E or both. ... /Selenite/

The objectives of this study were a) to compare the efficacy of inorganic or organic selenium compounds in protecting against mammary tumorigenesis induced by 7,12-dimethylbenz(a)anthracene (DMBA); in rats and b) to study the interaction of vitamin C with either selenite (inorganic) or seleno-DL-methionine (organic) in chemoprevention. Control Sprague Dawley rats were fed a purified 55 corn oil diet containing 0.1 ppm selenium. Selenite or seleno-DL-methionine was added to the basal diet in concentrations of 2, 3, or 4 ppm starting 1 week after DMBA administration. The inhibitory response in mammary tumorigenesis with selenium supplementation was dose dependent. Both selenium compounds were found to be equally efficacious in prophylaxis, although at the 4 ppm level a slight reduction in growth was observed. /Selenite/

The effects of cadmium, mercury (Hg), and three different chemicals forms of selenium (selenite, selenocystine, and selenomethionine) on ram spermatozoal motility and oxygen comsumption in vitro were studied over a 4 mo period. Concentrations of 10(-6) to 10(-2) M cadmium and mercury were injurious to spermatozoa as indicated by depressed motility and reduced oxygen uptake. Equimolar concentrations of selenium as selenite, selenocystine, or selenomethioine counteracted the toxicity of cadmium and mercury at low concentrations (10(-5) and 10(-6) M) but not at higher concentrations (10(-4) to 10(-2) M). ... /Selenite/

Chronic oral exposure to high concentrations of selenium compounds can produce a disease called selenosis. The major signs of selenosis are hair loss, nail brittleness, and neurological abnormalities (such as numbness and other odd sensations in the extremities). Animal studies have shown that selenium may also affect sperm production and the female reproductive cycle. (L619)

The substance can be absorbed into the body by inhalation of its aerosol and by ingestion.

Oral (L619) ; inhalation (L619) ; dermal (L619)

Selenium readily substitutes for sulfur in biomolecules and in many biochemical reactions, especially when the concentration of selenium is high and the concentration of sulfur is low. Inactivation of the sulfhydryl enzymes necessary for oxidative reactions in cellular respiration, through effects on mitochondrial and microsomal electron transport, might contribute to acute selenium toxicity. Selenomethionine (a common organic selenium compound) also appears to randomly substitute for methionine in protein synthesis. This substitution may affect the structure and functionability of the protein, for example, by altering disulfide bridges. Inorganic forms of selenium appear to react with tissue thiols by redox catalysis, resulting in formation of reactive oxygen species and causing damage by oxidative stress. (L619)

Burning sensation. Cough. Laboured breathing. Sore throat. Shortness of breath. Symptoms may be delayed.

Redness. Pain. Blisters. Skin burns.

Redness. Pain. Severe deep burns.

Abdominal pain. Burning sensation. Sore throat. Diarrhoea. Nausea. Vomiting. Shock or collapse.

Short-term oral exposure to high concentrations of selenium may cause nausea, vomiting, and diarrhea. Brief exposures to high levels of elemental selenium or selenium dioxide in air can result in respiratory tract irritation, bronchitis, difficulty breathing, and stomach pains. Longer-term exposure to either of these air-borne forms can cause respiratory irritation, bronchial spasms, and coughing. (L619)

Selenious acid

Dermal

5 x 10 ^-3 mg/kg-day

The following medical procedures should be made available to each employee who is exposed to selenium and its inorganic compounds at potentially hazardous levels: 1. Initial Medical Examination: A complete history and physical examination: The purpose is to detect existing conditions that might place the exposed employee at increased risk, and to establish a baseline for future health monitoring. Persons with a history of asthma, allergies, or known sensitization to selenium, or with a history of other chronic respiratory disease, gastrointestinal disturbances, disorders of liver or kidneys or recurrent dermatitis would be expected to be at increased risk from exposure. Examination of the eyes, respiratory system, liver, kidneys, and blood should be stressed. The skin should be examined for evidence of chronic disorders. Special consideration should be given to women of childbearing age since the possibility that selenium may be teratogenic might place these women in a high risk group. Urinalysis: Proper function of the kidneys is necessary to validate levels of selenium in the urine. A urinalysis should be obtained to include at a minimum specific gravity, albumin, glucose, and a microscopic /examination of/ centrifuged sediment. Liver function tests: Selenium causes liver damage and tumors in animals. A profile of liver function should be obtained by using a medically acceptable array of biochemical tests. The aforementioned medical examinations should be repeated on an annual basis. /Selenium and its inorganic compounds/

U204; As stipulated in 40 CFR 261.33, when selenious acid, as a commercial chemical product or manufacturing chemical intermediate or an off-specification commercial chemical product or a manufacturing chemical intermediate, becomes a waste, it must be managed according to Federal and/or State hazardous waste regulations. Also defined as a hazardous waste is any residue, contaminated soil, water, or other debris resulting from the cleanup of a spill, into water or on dry land, of this waste. Generators of small quantities of this waste may qualify for partial exclusion from hazardous waste regulations (40 CFR 261.5).

D010; A solid waste containing selenium (such as selenious acid) may or may not become characterized as a hazardous waste when subjected to the Toxicity Characteristic Leaching Procedure listed in 40 CFR 261.24, and if so characterized, must be managed as a hazardous waste.

Listed as a hazardous air pollutant (HAP) generally known or suspected to cause serious health problems. The Clean Air Act, as amended in 1990, directs EPA to set standards requiring major sources to sharply reduce routine emissions of toxic pollutants. EPA is required to establish and phase in specific performance based standards for all air emission sources that emit one or more of the listed pollutants. Selenious acid is included on this list.

Persons in charge of vessels or facilities are required to notify the National Response Center (NRC) immediately, when there is a release of this designated hazardous substance, in an amount equal to or greater than its reportable quantity of 10 lb or 4.54 kg. The toll free telephone number of the NRC is (800) 424-8802; In the Washington metropolitan area (202) 426-2675. The rule for determining when notification is required is stated in 40 CFR 302.6 (section IV. D.3.b).

Releases of CERCLA hazardous substances are subject to the release reporting requirement of CERCLA section 103, codified at 40 CFR part 302, in addition to the requirements of 40 CFR part 355. Selenious acid is an extremely hazardous substance (EHS) subject to reporting requirements when stored in amounts in excess of its threshold planning quantity (TPQ) of 1,000/10,000 lbs.

(AZ) ARIZONA 45 ug/l /Selenium/

(ME) MAINE 35 ug/l /Selenium/

(MN) MINNESOTA 30 ug/l /Selenium/

/SELENIUM/ ... IS ... AN ESSENTIAL ELEMENT IN PREVENTING LIVER NECROSIS IN RATS & EXUDATIVE DIATHESIS IN CHICKS ... IT IS A ... REQUIREMENT FOR MAX GROWTH. ... DIETARY FACTOR KNOWN AS FACTOR 3 IS AN ORG CMPD CONTAINING SELENIUM & ... IS REPLACEABLE BY SELENITE IN UG QUANTITIES ... /SELENIUM CMPD/

Selenium is a component glutathione peroxidase, which protects cells from oxidative damage caused by peroxidases produced during cellular metabolism. Selenium is needed to maintain the circulatory system. It also keeps the heart muscle and skin tissue healthy. It may also help in the prevention of cancer due to its stimulation of antioxidant activity and protection of cell membranes,. Selenious acid preserves vitamin E, which improves the cell's antioxidant defense, and plays an important role in the structure of teeth. Prolonged TPN (total parenteral nutrition) support in humans has resulted in selenium deficiency symptoms which include muscle pain and tenderness. The symptoms have been reported to respond to supplementation of TPN solutions with selenium [DB11135],. Pediatric conditions, Keshan disease, and Kwashiorkor have been associated with low dietary intake of selenium. The conditions are endemic to geographical areas marked by low selenium content in the soil. Dietary supplementation with selenium salts has been reported to reduce the incidence of the conditions among affected children.

Sodium selenite likely has the same mechanism of action as [DB11135]. The most important physiological role of sodium selenite is associated with its presence as an active component of many enzymes and proteins, in addition to its antioxidative role. Selenium has been shown to activate anticancer agents, prevent heart and vascular diseases, exhibit anti-proliferative and anti-inflammatory properties, and to stimulate the immune system. Its anticancer properties may be explained by the oxidation of free sulfhydryl groups. Tumor cells express free sulfhydryl groups (–SH) on the surface of their cell membranes and contribute to uncontrolled cell division. Only those compounds that can oxidize these groups to disulfides (S–S) may inhibit this process. Some organic forms of selenium, including selenocysteine, methylseleninic acid, and Se-methylselenocysteine have been established to be antioxidants. However, their anticancer mechanism is still not well understood. Selenious acid, during an in vitro study, was found to stimulate hemoglobin synthesis in three different malignant erythroleukemia cell lines (MEL). It has also been shown to increase the release of interleukin 2 in a dose-dependent manner. Interleukin-2 is made by a type of T lymphocyte (white blood cell). It increases the growth and activity of other T-lymphocytes and B-lymphocytes and this contributes to the development of the immune system.

SELENIOUS ACID STIMULATED HEMOGLOBIN SYNTHESIS IN 3 DIFFERENT MALIGNANT MURINE ERYTHROLEUKEMIA (MEL) CELL LINES.

30 days in beagle dogs.

BEAGLE DOGS WERE GIVEN 20-60 UG SELENIUM/KG BODY WT BY INHALATION OF SELENIOUS ACID. VIRTUALLY ALL OF THE INHALED AEROSOL WAS RAPIDLY ABSORBED INTO THE BLOOD FROM THE LUNG, GI TRACT, AND DIRECTLY THROUGH THE NASAL MEMBRANES. THE LONG TERM COMPONENT OF THE WHOLE BODY RETENTION FUNCTION HAD A HALF LIFE OF APPROX 30 DAYS & ACCOUNTED FOR APPROX 20% OF THE INITIAL SELENIUM DEPOSITED.

Absorbed selenium, from both inorganic sources such as selenite and organic sources including selenomethionine, is metabolized to hydrogen selenide, and subsequently incorporated into essential selenoproteins. In vivo, selenium compounds are generally metabolized to reduced states. For example, quadrivalent selenium (Se+4) in selenite often undergoes reduction to Se−2, metabolized firstly to H2Se and, finally, being methylated to various excretory forms. Selenious acid to oxidize sulfurous acid: H2SeO3 + 2H2SO3 → Se0 + 2H2SO4 + H2O. Se may also produce reactive oxygen species and, thereby, exert cancer-selective cytotoxicity. Selenodiglutathione (SDG) is a primary Se metabolite conjugated to two glutathione (GSH) moieties. Selenodiglutathione increases intracellular selenium accumulation and is significantly more toxic than selenous acid (H2SeO3).. The liver is the central organ for selenium regulation and produces excretory selenium forms to regulate whole-body selenium.

Selenium may be absorbed through inhalation and ingestion, while some selenium compounds may also be absorbed dermally. Once in the body, selenium is distributed mainly to the liver and kidney. Selenium is an essential micronutrient and is a component of glutathione peroxidase, iodothyronine 5'-deiodinases, and thioredoxin reductase. Organic selenium is first metabolized into inorganic selenium. Inorganic selenium is reduced stepwise to the intermediate hydrogen selenide, which is either incorporated into selenoproteins after being transformed to selenophosphate and selenocysteinyl tRNA or excreted into the urine after being transformed into methylated metabolites of selenide. Elemental selenium is also methylated before excretion. Selenium is primarily eliminated in the urine and feces, but certain selenium compounds may also be exhaled. (L619)

The absorption of selenite following oral administration approximately 40-70% of an oral dose, based on studies done in humans. Selenoprotein P, the plasma form of selenium, contains at least 40% of the total selenium in plasma. Deletion of the gene for selenoprotein P in mouse models alters the distribution of selenium in body tissues suggesting that selenoprotein P is necessary for selenium transport.

Selenium is eliminated mainly in the urine. However, significant endogenous losses through the feces can also occur. The rate of excretion varies with the chemical form of selenium used in supplementation and the route of administration. Other minor routes of elimination are lungs and skin. Analysis of 72-hour urine sampling from a study of 48 Norwegian women given a 200 μg supplement of selenium in the form of selenite indicated approximately 50% absorption of selenite.

Following oral intake and absorption, selenium from sodium selenite is found in the highest concentrations in the liver and kidneys of humans and animals. In one study, tissue samples taken at autopsy from 46 healthy individuals killed in accidents and from 75 corpses of victims of various diseases to analyze selenium levels and distribution. The per-weight-unit basis of selenium levels ng/gm in wet in tissues decreased in the following order: kidney (469) > liver > spleen > pancreas > heart > brain > lung > bone > skeletal muscle. The highest proportion of body selenium was found in skeletal muscles (27.5%),. Significantly less selenium was measured in bones (16%) and blood (10%). In the tissues of cancer corpses, the selenium levels were lower than levels in the control group. The lowest selenium concentrations were measured in alcoholic livers.

Inhalation studies on rats show that 94% of selenious acid deposited in the lung was absorbed within four hours. The corresponding value for elemental selenium was 57%. Skin absorption was also noted in this study. A model based on these rat studies predicted that organ concentration in man due to inhalation of selenious acid ... in urban atmospheres will not contribute significantly to human body burdens.

BEAGLE DOGS WERE GIVEN 20-60 UG SELENIUM/KG BODY WT BY INHALATION OF SELENIOUS ACID. VIRTUALLY ALL OF THE INHALED AEROSOL WAS RAPIDLY ABSORBED INTO THE BLOOD FROM THE LUNG, GI TRACT, AND DIRECTLY THROUGH THE NASAL MEMBRANES. SELENIUM THAT WAS ABSORBED INTO THE SYSTEMIC CIRCULATION WAS TRANSLOCATED TO THE LIVER, KIDNEY, PELT, AND BLOOD. LONG TERM RETENTION WAS PRIMARILY IN LIVER, PELT, AND BLOOD.

BY 4 HR AFTER INHALATION OF SELENIUM AEROSOLS, 57% OF SELENIUM DEPOSITED IN LUNG WAS ABSORBED INTO THE BLOOD. OF SELENIOUS ACID INSTILLED INTO NASAL PASSAGES, 16% OF SELENIUM WAS ABSORBED. GI ABSORPTION WAS 50% FOR SELENIUM. FOLLOWING INHALATION OR INJECTION OF SELENIUM, MOST WAS EXCRETED IN URINE. SIGNIFICANTLY MORE APPEARED IN FECES OF ANIMALS RECEIVING SELENIUM BY GAVAGE. /SELENIUM CMPD/

Used as a reagent for alkaloids, an oxidizing agent, and a medication; A gun-blueing agent (Super Blue or Gun Blue) contains 4% selenious acid and 2.5% cupric sulfate in hydrochloric acid; [HSDB]

AS REAGENT FOR ALKALOIDS; AS OXIDIZING AGENT

(75)SELENIOUS ACID IS REDUCED IN AN AQ BUFFERED SOLN WITH NABH4 WITH THE FINAL PH ADJUSTMENT TO 6.5-7.0 TO YIELD QUANT NAH(75)SE WHICH IS USED TO INTRODUCE (75)SE INTO RADIOPHARMACEUTICALS.

MEDICATION

Selenous acid is used in organic synthesis. (L736)

PREPD BY DISSOLVING SELENIUM DIOXIDE IN HOT WATER AND COOLING.

ACTION OF HOT NITRIC ACID ON SELENIUM