Natriumhydrogensulfid

Excerpt from ERG Guide 135 [Substances - Spontaneously Combustible]:

Excerpt from ERG Guide 154 [Substances - Toxic and/or Corrosive (Non-Combustible)]:

Use water spray, foam, powder, carbon dioxide. In case of fire: keep drums, etc., cool by spraying with water. NO direct contact with water.

Half-upright position. Artificial respiration may be needed. Refer immediately for medical attention.

Rinse skin with plenty of water or shower. Refer immediately for medical attention.

Rinse with plenty of water (remove contact lenses if easily possible). Refer immediately for medical attention.

Rinse mouth. Give one or two glasses of water to drink. Do NOT induce vomiting. Refer immediately for medical attention.

· CALL 911. Then call emergency response telephone number on shipping paper. If shipping paper not available or no answer, refer to appropriate telephone number listed on the inside back cover.

· ELIMINATE all ignition sources (no smoking, flares, sparks or flames) from immediate area.

· CALL 911. Then call emergency response telephone number on shipping paper. If shipping paper not available or no answer, refer to appropriate telephone number listed on the inside back cover.

· ELIMINATE all ignition sources (no smoking, flares, sparks or flames) from immediate area.

Excerpt from ERG Guide 135 [Substances - Spontaneously Combustible]:

INHALATION: move victim from contaminated atmosphere; call physician; if breathing has ceased, start mouth-to-mouth resuscitation.

General First Aid:

General First Aid:

· Wear positive pressure self-contained breathing apparatus (SCBA).

· Wear positive pressure self-contained breathing apparatus (SCBA).

Excerpt from ERG Guide 135 [Substances - Spontaneously Combustible]:

Excerpt from ERG Guide 154 [Substances - Toxic and/or Corrosive (Non-Combustible)]:

Personal protection: particulate filter respirator adapted to the airborne concentration of the substance and filter respirator for inorganic gases and vapours adapted to the airborne concentration of the substance. Sweep spilled substance into covered plastic containers. 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.

Land spill - Dig a pit, pond, lagoon, holding area to contain liquid or solid material. Cover solids with a plastic sheet to prevent dissolving in rain or fire fighting water. /sodium hydrosulfide, solid/

Land spill - Dig a pit, pond, lagoon, holding area to contain liquid or solid material. Dike surface flow using soil, sand bags, foamed polyurethane, or foamed concrete. Absorb bulk liquid with fly ash or cement powder. /sodium hydrosulfide solution/

Water spill - Add soda ash (Na2CO3). Allow to aerate. Use mechanical dredges or lifts to remove immobilized masses of pollutants and precipitates.

Air spill - Apply water spray or mist to knock down vapors. /sodium hydrosulfide solution/

LC50 Fly inhalation 1500 mg/cu m/7 min. /Hydrogen sulfide/

TLm Gammarus 0.84 mg/l/96 hr. /Conditions of bioassay not specified/ /Hydrogen sulfide/

TLm Ephemera 0.316 mg/l/96 hr. /Hydrogen sulfide/

TLm Fathead minnow 0.0071-0.55 mg/l at 6-24 °C/96 hr flow through bioassay. /Hydrogen sulfide/

For more Ecotoxicity Values (Complete) data for SODIUM HYDROSULFIDE (6 total), please visit the HSDB record page.

Sore throat. Burning sensation. Shortness of breath. Laboured breathing. Unconsciousness.

Redness. Pain. Skin burns.

Redness. Pain. Burns.

Sore throat. Burns in mouth and throat. Abdominal pain. Vomiting. Shock or collapse.

Sodium sulfide contact with workmen's eyes has been noted to cause burns which may be slow healing, owing presumably to strong alkalinity.

Man: severe toxic effects: 200 ppm = 280 mg/cu m 1 min; symptoms of illness: 50 ppm = 70 mg/cu m unsatisfactory: 20 ppm = 28 mg/cu m lethal: 600 ppm, 30 min 800 ppm, immediately.

Hydrogen sulfide does two things: it directly irritates mucous membranes, including respiratory linings, and it inhibits cellular respiration. Direct irritation is probably the major cause of pulmonary edema, hyperemia, and dyspnea seen in animals that do not die outright. Thus hydrogen sulfide was classified earlier as one of the agents capable of causing interference with oxygen uptake from pulmonary alveoli. The exact means by which it produces pulmonary edema is not known, but it is not reasonable to attribute it to some unique mechanism set apart from the means by which any other irritant increases permeability of lung capillaries. /Hydrogen sulfide/

Twenty 6 month old male Sprague-Dawley rats were used in the study. Groups of five animals were exposed to an atmosphere of either 2,317 mg/cu m hydrogen sulfide, or no hydrogen sulfide, or were injected intraperitoneally with a solution containing 30 mg/kg sodium hydrosulfide or saline solution. The peracute lethal exposure to hydrogen sulfide produced pulmonary edema, similar to, but much more severe, than that which has been reported with sublethal concentrations of this gas. Peracute exposure resulted in rapid and massive accumulation of fluid in the lungs that the rat was unable to clear, resulting in massive alveolar flooding and finally death. The degree of pulmonary edema was further shown histologically by massive extravasation of fluids. The strong eosinophilic appearance of edematous fluid suggests that the extravasated fluid was rich in protein. The study also demonstrated that sodium hydrosulfide killed rats within the same post exposure time as hydrogen sulfide yet only the rats exposed to hydrogen sulfide had gross and histological evidence of pulmonary edema. The lack of clinical signs of respiratory distress during the agonic and unconscious state that preceded death suggest that lung structure was not notably compromised by sodium hydrosulfide. In contrast, the lungs of rats injected with sodium hydrosulfide or saline or exposed to air were unaffected. It was concluded that the edematogenic effect of hydrogen sulfide in the lungs cannot be reproduced by injection of sodium hydrosulfide. The severity of lung edema induced by a peracute exposure to hydrogen sulfide was extensive enough to account for death.

Administration of sodium hydrosulfide, an alkali salt of hydrogen sulfide at doses of 10 and 30 mg/kg, corresponding to sublethal and lethal doses (0.66 and 2.0 LD50) resulted in significant increases in regional catecholamine levels of the rat brain only after the dose of 2.0 LD50 of sodium hydrosulfide. Whereas the cortex and the cerebellum showed little or no change in catecholamine content, the hippocampus, striatum and brainstem all showed increases in noradrenaline and adrenaline. Additional analysis also showed that brainstem dopamine and 5-hydroxytryptamine levels (5-HT) increased as well. In vitro testing of sulfide for inhibition of monoamine oxidase activity showed the anion to be inhibitory with an IC50 of 39.1 + or - 3.6 uM. Inhibition of monoamine oxidase activity ex vivo could be demonstrated at a dose of 100 mg/kg but not at the lower dose of 30 mg/kg sodium hydrosulfide. Inhibition of enzyme activity could not be demonstrated at this lower dose, possibly due to the well known rapid intramitochondrial metabolism of sulfide. Correlation of synaptosomal and mitochondrial sulfide levels with enzyme inhibition data suggests that inhibition of monoamine oxidase may be an important contributing factor to the mechanism(s) underlying loss of central respiratory drive after fatal intoxication with hydrogen sulfide.

For advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious or in respiratory arrest. Positive-pressure ventilation techniques with a bag-valve-mask device may be beneficial. Monitor cardiac rhythm and treat arrhythmias if necessary ... . Start an IV with D5W TKO /SRP: To keep open, "minimal flow rate"/. Use lactated Ringer's if signs of hypovolemia are present. Watch for signs of fluid overload. Consider drug therapy for pulmonary edema ... . For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of pulmonary edema. Consider vasopressors to treat hypotension without signs of hypovolemia ... . Treat seizures with diazepam (Valium) ... . In severe cases use amyl nitrite and sodium nitrite ... as described for cyanide poisoning; omit the sodium thiosulfate injection. Early administration will be the most effective. DIRECT PHYSICIAN ORDER ONLY ... . Use proparacaine hydrochloride to assist eye irrigation ... . For basic treatment: Establish a patent airway. 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 pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with normal saline during transport ... . Treat with rapid rewarming techniques ... if frostbite occurs. /Hydrogen sulfide and related compounds/

LC50 Mouse inhalation 1500 mg/cu m/18 min. /Hydrogen sulfide/

LC50 Rat inhalation 1500 mg/cu m/14 min. /Hydrogen sulfide/

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 5000 lb or 2270 kg. The toll free number of the NRC is (800) 424-8802; In the Washington D.C. metropolitan area (202) 426-2675. The rule for determining when notification is required is stated in 40 CFR 302.4 (section IV. D.3.b).