Dimethyl selenide

If material on fire or involved in fire: Extinguish fire using agent suitable for type of surrounding fire. Material itself does not burn or burns with difficulty. Keep run-off water out of sewers and water sources. /Selenium compound, solid, nos/

Personnel protection: Wear appropriate chemical protective clothing. Wear positive pressure self-contained breathing apparatus when fighting fires involving this material. /Selenium compound, solid, nos/

SRP: Wastewater from contaminant suppression, cleaning of protective clothing/equipment, or contaminated sites should be contained and evaluated for subject chemical or decomposition product concentrations. Concentrations shall be lower than applicable environmental discharge or disposal criteria. Alternatively, pretreatment and/or discharge to a permitted wastewater treatment facility is acceptable only after review by the governing authority and assurance that "pass through" violations will not occur. Due consideration shall be given to remediation worker exposure (inhalation, dermal and ingestion) as well as fate during treatment, transfer and disposal. If it is not practicable to manage the chemical in this fashion, it must be evaluated in accordance with EPA 40 CFR Part 261, specifically Subpart B, in order to determine the appropriate local, state and federal requirements for disposal.

Eye Exposure: If selenium or its inorganic compounds get into the eyes, wash eyes immediately with large amounts of water, lifting the lower and upper lids occasionally. Get medical attention immediately. /Selenium and its inorganic salts/

Personnel protection: Avoid breathing vapors. Keep upwind. Do not handle broken packages unless wearing appropriate personal protective equipment. /Selenium compound, solid, nos/

The worker should immediately wash the skin when it becomes contaminated. /Selenium/

Work clothing that becomes wet or significantly contaminated should be removed or replaced. /Selenium/

8 hr Time Weighted Avg (TWA): 0.2 mg/cu m. /Selenium and compounds, as Se/

Excursion Limit Recommendation: Excursions in worker exposure levels may exceed 3 times the TLV-TWA for no more than a total of 30 minutes during a work day, and under no circumstances should they exceed 5 times the TLV-TWA, provided that the TLV-TWA is not exceeded. /Selenium and compounds, as Se/

Wear appropriate personal protective clothing to prevent skin contact. /Selenium/

Facilities for quickly drenching the body should be provided within the immediate work area for emergency use where there is a possibility of exposure. [Note: It is intended that these facilities provide a sufficient quantity or flow of water to quickly remove the substance from any body areas likely to be exposed. The actual determination of what constitutes an adequate quick drench facility depends on the specific circumstances. In certain instances, a deluge shower should be readily available, whereas in others, the availability of water from a sink or hose could be considered adequate.] /Selenium/

Respirator Recommendations: Up to 1 mg/cu m: /Selenium/ [Table#7712]

Respirator Recommendations: Emergency or planned entry into unknown concentrations or IDLH conditions: /Selenium/ [Table#7713]

Respirator Recommendations: Escape conditions: /Selenium/ [Table#7714]

The anticarcinogenic activity of selenium in animal models is well established. The active forms of selenium involved have not been identified to date, but conversion of selenium via hydrogen selenide (H2Se) to methylated forms such as dimethylselenide and trimethylselenonium ion is an important metabolic fate. By controlling the entry of selenium into various points within this pathway through selection of appropriate starting compounds, it is possible to pinpoint more closely the form(s) of selenium responsible for its anticarcinogenic activity. Selenobetaine in the chloride form [(CH3)2Se+CH2COOH] and its methyl ester are extensively metabolized in the rat to mono-, di-, and trimethylated selenides, largely bypassing the inorganic H2Se intermediary pool. The chemopreventive efficacy of these selenobetaines was determined at 1 and 2 ppm selenium supplemented in the diet throughout the duration of the experiment using the dimethylbenz(a)anthracene induced mammary tumor model in rats. There was a dose-dependent inhibitory response to both compounds, and they appeared to be slightly more active than selenite. These doses were without any adverse effects on the animals. Coadministration of selenobetaine with arsenite (5 ppm arsenic) enhanced the tumor-suppressive effect of selenobetaine, although arsenic by itself was totally inactive. Arsenite is known to inhibit certain steps in selenium methylation. The substantial prophylactic efficacy of methylated selenides and the enhancement by arsenite suggest that partially methylated forms of selenium may be directly involved in the anticarcinogenic action of selenium.

2-month-old male rats kept on a standard laboratory diet containing 0.06 ug Se/g dry weight were found to be more sensitive to the toxic action of selenite than female rats of corresponding age. This sex-dependent difference was not found in 20-day-old animals. Previous sc administration of 1 umol of selenium in the form of sodium selenite lowered the sensitivity of male rats to the toxic effects of selenite. The protective effect of this dose persisted for 18 days. A similar protective action against the lethal effects of selenite in adult male rats was exhibited by sodium selenate, selenomethionine, and dimethylselenide, all in an amount equal to 1 umol of selenium; pretreatment with trimethylselenonium iodide showed only an insignificant mortality decrease. Three days intake of deionized water with an addition of 0.1 or 1.0 ug selenium/mL also protected male rats against lethal doses of selenite. Peroral pretreatment of adult females did not decrease their sensitivity to the lethal effects of selenite.

TERRESTRIAL FATE: In soils, elemental selenium and inorganic selenium compounds can be methylated by microorganisms and subsequently volatilize to the atmosphere(1,2); dimethylselenide and dimethyl diselenide are the principal products(2).

AQUATIC FATE: Biological methylation of selenium may occur in aquatic environments; inorganic selenium undergoes biological methylation to dimethyl selenide and dimethyl diselenide(1,2).

ATMOSPHERIC FATE: Volatile dimethyl selenide and dimethyl diselenide are expected to exist in the gaseous state in the atmosphere(1,2). Dimethylselenide reacted with ozone in the gas phase to form dimethyl selenoxide as the major product with a yield of approximately 90%(3).

About 87-96% of the total dimethylselenide injected into dry soil was volatilized to air; in moist and flooded soils, 20-88% and 4.3-16.8% were volatilized to air, respectively(1).

The Kd values measured in unamended, manure-amended and gluten-amended Hanford sandy loam at 4 °C were 0.038, 0.091 and 0.045, respectively; there was no detection at temperatures of 21 and 40 °C, or in Losthill clay loam under the same conditions(1).

Dimethylselenide is produced naturally in soil and sediments from inorganic selenium species(1,2).

Biomethylation of selenium (Se) by freshwater green algae, Ankistrodesmus sp., Chlorella vulgaris and Selenastrum sp., which had been isolated from the Tone River and Lake Kasumigaura in Japan, were investigated. All of the three algae produced methylated Se compounds from the corresponding inorganic compounds. The formation of trimethylselenonium ion (TMSe) by algae reached a plateau 2-4 d after culturing and the amount of Se and TMSe /in the culture/ was less than about 0.001% of the added Se. TMSe was also found in the algae and was in the range from 0.04 to 0.3% of total-Se accumulated in the algae. Dimethylselenide (DMSe) was found in the headspace gases of the cultured flask and was in the range from 0.001 to 0.016% of the added Se. Total-Se accumulated in the algae was in the range from 0.002 to 0.2% of added Se. The presence of arsenic in the medium inhibited DMSe formation in the algae. Green algae in the freshwater ecosystems might be related to methylation of Se, and biomethyl.

Selenium is found in the -2 (selenide) oxidation state(1,2). Natural atmospheric releases of selenium result from volatilization, as a result of biomethylation, by plants and bacteria and from volcanic eruptions(3).

All nutritional selenium sources are transformed into the assumed common intermediate selenide for the syntheses of selenoproteins for utilization and/or of selenosugar for excretion. Methylselenol [monomethylselenide, MMSe] is the assumed intermediate leading to other methylated metabolites, dimethylselenide (DMSe) and trimethylselenonium (TMSe) for excretion, and also to the intermediate selenide from methylselenocysteine and methylseleninic acid (MSA). Here, related methylation and demethylation reactions were studied in vitro by providing chemically reactive starting substrates (76Se-selenide, 77Se-MMSe and 82Se-DMSe) which were prepared in situ by the reduction of the corresponding labeled proximate precursors (76Se-selenite, 77Se-MSA and 82Se-dimethylselenoxide (DMSeO), respectively) with glutathione, the three substrates being incubated simultaneously in rat organ supernatants and homogenates. The resulting chemically labile reaction products were detected simultaneously by speciation analysis with HPLC-ICP-MS after converting the products and un-reacted substrates to the corresponding oxidized derivatives (selenite, MSA and DMSeO). The time-related changes in selenium isotope profiles showed that demethylation of MMSe to selenide was efficient but that of DMSe to MMSe was negligible, whereas methylation of selenide to MMSe, and MMSe to DMSe were efficient, and that of DMSe to TMSe occurred less efficiently. The present methylation and demethylation reactions on equilibrium between selenide, MMSe and DMSe without producing selenosugar and selenoproteins indicated that DMSe rather than TMSe is produced as the end product, suggesting that DMSe is to be excreted more abundantly than TMSe. Organ-dependent differences in the methylation and demethylation reactions were characterized for the liver, kidney and lung.

Dimethylselenide was detected in air samples collected at 13 sites in Bordeaux, France from September 1995 to May 1996 at concentrations (as metal) of 0.7 to 8.7 ng/cu m(1). Dimethylselenium was detected in air samples collected near water bodies in Belgium at concentrations of 0.47 (Campus lake), 1.41 (smelter), 2.40 (sewage treatment plant #2) ng/cu m; it was detected at concentrations less than 0.15 ng/cu m at sewage treatment plate #1, and Borek and Breeven fishing ponds(2).

/OTHER TOXICITY INFORMATION/ Metabolic pathways and toxic effects of long-term selenium exposure in animal models and humans have both similarities and significant differences. In animal models the target organ is the liver, in which chronic cirrhosis develops. In /humans/ the target organ appears to be the lung, which manifests acute "rose cold," or, as in /a/ patient, a chronic granulomatous hypersensitivity. /The/ data indicate not only a different target organ than would have been predicted from animal models, but also a difference in the distribution of selenium in human tissues. Long-term use of selenium favors production of dimethylselenide, which is excreted by the lungs and should be considered a pulmonary toxin. ...

/OTHER TOXICITY INFORMATION/ Selenium (Se) is an essential trace element, and its low status in humans has been linked to increased risk of various diseases, such as cancer and heart disease. In recent years, Se research has attracted tremendous interest because of its important role in antioxidant selenoproteins for protection against oxidative stress initiated by excess reactive oxygen species (ROS) and reactive nitrogen species (NOS). The synthesis of selenoproteins requires a unique incorporation of amino acid selenocysteine (Sec) into proteins directed by the UGA codon, which is also a termination codon. Interest in Se research has led to the discovery of at least 30 selenoproteins; however, the biochemical functional roles of some of these selenoproteins are still unknown. Besides in the form of selenoproteins, Se can exist in many different chemical forms in biological materials either as organic Se compounds, such as selenomethionine and dimethylselenide, and inorganic selenites and selenates. In foods, Se is predominantly present as selenomethionine, which is an important source of dietary Se in humans, and also as a chemical form that is commonly used for Se supplements in clinical trials.

Degradation of dimethylselenide, measured by a first-order rate constant, varied with soil type and organic amendment and was dependent on temperature but independent of soil moisture content over the range of 10% (by weight) to saturation(1). Degradation proceeded rapidly in a Hanford sandy loam, with a half-life of 9 hours; the half-life in a Losthill clay loam was 875 hours(1). In Arlington sandy loam, 68% of the applied dimethylselenide was degraded at 20 °C after 18 days; approximately 81% was degraded at 30 and 40 °C(2).

Biomethylation of selenium was optimal in a well-mixed, aerobic system amended with a protein source; removal, via volatilization of dimethyl selenide, ranged between 8 and 100% for peptone-amended evaporation pond waters containing between 2.2 and 0.02 ug/L Se, respectively(1). Microbial methylation of selenium can be stimulated in Se-contaminated sediments by specific organic amendments, such as addition of protein sources(2). Three freshwater green algae, isolated from the Tone River and Lake Kasumigaura in Japan, produced methylated selenium compounds from inorganic selenium compounds; trimethylselenonium ion and dimethyl selenide were identified as products(3). A variety of organisms, including benthic microflora are capable of methylating selenium(4). Microbes present in lake sediments methylated organic and inorganic selenium compounds including sodium selenite and sodium selenate; gaseous dimethyl selenide and dimethyl diselenide were produced(4). Dimethylselenide, dimethyl diselenide, and another selenium compound tentatively identified as dimethyl selenone were evolved from brown-black loamy soil collected 1 cm under the ground surface inside selenium smelter grounds in Belgium, at rates of 8.2, 4.3, and 1.9 ng Se/day, respectively; this was attributed to natural biomethylation of selenium in the soils(5).

Selenium volatilizes from soils at rates that are modified by temperature, moisture, time, season or year, concentration of water soluble selenium, and microbiological activity. Conversion of inorganic and organic selenium compounds to volatile selenium compounds (such as dimethyl selenide, dimethyl diselenide, and an unknown compound) by microorganisms has been observed in lake sediments of the Sudbury area of Ontario. This conversion may have been effected by pure cultures of Aeromonas, Flavobacterium, Pseudomonas, or an unidentified fungus, all of which are found in methylated lake sediments. Production of volatile selenium is temperature dependent. Compared with the amount of dimethyl Se produced at an incubation temperature of 20 °C, 25% less was produced at 10 °C and 90% less at 4 °C.

/LABORATORY ANIMALS: Acute Exposure/ In pigs and other food producing animals, relatively little is known about the mode of action of excess selenium. This study reports the cardiovascular effects brought about in anesthetized Landrace pigs by 2 mg selenium/kg body weight intravenously as either sodium selenite or dimethylselenide. Sodium selenite dosing was characterized by a dramatic fall in systemic blood pressure with an increase in cardiac output and heart frequency. The only significant change elicited by dimethylselenide was a linear rise of cardiac output. Neither of the tested compounds significantly affected pulmonary arterial pressure. These results suggest that under the experimental conditions in this study, sodium selenite induces a vasculogenic shock without primarily affecting cardiac performance. The lack of detrimental effects on cardiovascular parameters with dimethylselenide indicates the importance of methylation in detoxifying excess selenium.

/LABORATORY ANIMALS: Acute Exposure/ A characteristic sign of acute selenium poisoning in animals is the odor due to the pulmonary excretion of dimethyl selenide. Other signs of acute selenium poisoning in dogs and rats include: vomiting, dyspnea, tetanic spasms, and death from respiratory failure.

/LABORATORY ANIMALS: Acute Exposure/ /This/ investigation was undertaken to examine the biochemical changes occurring in blood and tissues of Landrace pigs given intravenously 2 mg selenium/kg b.w. as either sodium selenite or dimethylselenide. NADP-isocitric dehydrogenase, lactic dehydrogenase and succinic dehydrogenase activities were evaluated in subcellular fractions from liver, heart (right and left ventricle) kidney and longissimus dorsi. Other tested parameters included plasma cations and proteins, blood urea nitrogen, hematocrit as well as selected serum enzymes. The marked inhibition of succinic dehydrogenase along with the rise of the two other dehydrogenases and the modification of the plasma cation profile suggest that in swine sodium selenite may act by determining a shift toward anaerobiosis accompanied by alterations in cell membrane permeability. Comparatively, dimethylselenide was found to affect the tissue enzymes to a similar but less severe extent and appeared devoid of significant effects on the remaining parameters.

/LABORATORY ANIMALS: Acute Exposure/ A total of 60 adult Fischer 344 male rats were exposed to dimethylselenide (DMSe) vapor at 1607, 4499, or 8034 ppm for 1 hr (20 rats/group). In addition, 26 unexposed rats were used as controls. The exposed rats were observed frequently during the 7 d following exposure and appeared normal. The animals were sacrificed at either 1 or 7 d after inhalation and the major tissues were grossly examined and weighed. Selenium levels were found to be elevated only in the lung at d 1. At d 1, significant changes in organ weights were an increase in the lung weight at exposure levels of 1607 and 8034 ppm of DMSe and in liver weight at 4499 and 8034 ppm. At d 1, significant changes in the lung were an increase in protein at 1607 and 8034 ppm of DMSe, and an increase in RNA and a reduction in DNA at 4499 ppm DMSe. The only change in the liver was a reduction in DNA at 4499 ppm. At 7 d, the protein content and RNA content of spleen were increased. Lung, liver, kidney, spleen, thymus, lymph nodes, pancreas, and adrenal gland were examined microscopically and found to be normal. All of these observed responses were minor and did not severely impact the health of the rats. Overall, the data indicate that the inhalation of DMSe for 1 hr has relatively low toxicity in rats even at high concentrations.

Inorganic selenium /converted/ to less toxic methylated compounds such as dimethylselenide (DMSe) and trimethylselenonium (TMSe). This study investigated the role of vitamin B12, a cofactor of methionine synthetase, in selenium methylation in the rat. Vitamin B12-depleted rats expired 16% of dosed 75Se-selenite as DMSe compared to 45% for control rats and excreted less TMSe in the urine (6.1% of dose) than control (9% of dose) rats. At the same time, higher (p < 0.05) tissue (liver, kidney, muscle) selenium levels and lower (p < 0.05) blood selenium levels were found in vitamin B12-deficient rats. Primary hepatocytes from vitamin B12-deficient rats volatilized 15% of selenite in incubation medium in 5 hr as compared to 49% in hepatocytes from control rats. Hepatocytes from vitamin B12-deficient rats were less resistant to selenite toxicity. In vitro methylation of selenium with liver extract from vitamin B12-deficient rats showed one-third to one-half the rate of volatilization of selenium as compared to control rats. S-adenosylmethionine was required for this reaction. These results show that vitamin B12 deficiency significantly decreases the ability of rats to methylate selenium.

/SRP:/ Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand-valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR as necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Selenium and Related Compounds/

/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if necessary. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for shock and treat if necessary ... . Monitor for pulmonary edema and treat if necessary ... . Treat seizures if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 ml/kg up to 200 ml of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool. Administer activated charcoal ... . /Selenium and Related Compounds/

/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... .Monitor cardiac rhythm and treat arrhythmias if necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's (LR) if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Consider vasopressors if patient is hypotensive with a normal fluid volume. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Selenium and Related Compounds/

Emergency and supportive measures. Maintain an open airway and assist ventilation if necessary. Administer supplemental oxygen. Treat coma, convulsions, bronchospasm, hypotension, and pulmonary edema if they occur. Since hypotension is often multifactorial, evaluate and optimize volume status, peripheral vascular resistance, and myocardial contractility. Observe for at least 6 hours after exposure. ... /Selenium/

Decontamination: Inhalation. Immediately remove the victim from exposure and give supplemental oxygen if available. Skin and eyes. Remove contaminated clothing and wash exposed skin with soap and copious water. Irrigate exposed eyes with copious tepid water or saline. Ingestion. Ingestion of elemental selenium or selenium salts does not usually benefit from GI decontamination. In light of the risk of severe corrosive GI injury, gastric lavage plus activated charcoal may be of value for ingestion s of selenious acid seen within 1 hour. Invitro experiments indicate that vitamin C can reduce selenium salts to elemental selenium, which poorly absorbed. Its use has not been studied in vivo, but oral or nasogastric administration of several grams of ascorbic acid has been recommended. /Selenium/

LD50 Rat intraperitoneal 2200 mg/kg

LD50 Mouse intraperitoneal 1800 mg/kg

LD50 Rat ip 1600 mg/kg

D010; A solid waste containing selenium (such as dimethylselenide) 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. Selenium cmpds are included on this list. /Selenium cmpds/

(AZ) ARIZONA 10 ug/L /Selenium/

(NY) NEW YORK 10 ug/L /Selenium/

(AZ) ARIZONA 45 ug/L /Selenium/

(CT) CONNECTICUT 10 ug/L /Selenium/

(ME) MAINE 35 ug/L /Selenium/

(MN) MINNESOTA 30 ug/L /Selenium/