안티몬 펜타염화물

Excerpt from ERG Guide 157 [Substances - Toxic and/or Corrosive (Non-Combustible / Water-Sensitive)]:

Excerpt from ERG Guide 157 [Substances - Toxic and/or Corrosive (Non-Combustible / Water-Sensitive)]:

· 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.

INHALATION: remove to clean air; rinse mouth and gargle with water; if overexposure is serious, get prompt medical attention.

Excerpt from ERG Guide 157 [Substances - Toxic and/or Corrosive (Non-Combustible / Water-Sensitive)]:

General First Aid:

General First Aid:

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

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

Suitable extinguishing media: Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide. Advice for firefighters: Wear self-contained breathing apparatus for firefighting if necessary.

Use appropriate extinguishing agents on nearby combustible fires. Use water spray to knock down acid vapors.

Separate from acids, alkalies. Store in a cool, dry, well-ventilated location.

Storage temp: ambient; venting: pressure-vacuum.

Keep container tightly closed in a dry and well-ventilated place. Containers which are opened must be carefully resealed and kept upright to prevent leakage. Store under inert gas. Reacts violently with water. Air sensitive.

ACCIDENTAL RELEASE MEASURES; Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid breathing vapours, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains. Discharge into the environment must be avoided. Methods and materials for containment and cleaning up: Soak up with inert absorbent material and dispose of as hazardous waste. Keep in suitable, closed containers for disposal.

Excerpt from ERG Guide 157 [Substances - Toxic and/or Corrosive (Non-Combustible / Water-Sensitive)]:

Excerpt from ERG Guide 157 [Substances - Toxic and/or Corrosive (Non-Combustible / Water-Sensitive)]:

SRP: Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in air, soil or water; effects on animal, aquatic and plant life; and conformance with environmental and public health regulations. If it is possible or reasonable use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity or environmental contamination.

After the material has been contained, remove it and the contaminated soil and place in plastic-lined impervious containers. If practical, transport material back to the supplier or chemical company to recover the heavy-metal content and for deactivation. If this is not practical, or facilities not available, the material should be encapsulated and buried in a specially designated chemical landfill. Alternatively, material is amenable to biological treatment at a municipal sewage treatment plant when first chemically treated and neutralized.

Product: Offer surplus and non-recyclable solutions to a licensed disposal company. Contact a licensed professional waste disposal service to dispose of this material. Dissolve or mix the material with a combustible solvent and burn in a chemical incinerator equipped with an afterburner and scrubber. Contaminated packaging: Dispose of as unused product.

Gloves must be inspected prior to use. Use proper glove removal technique (without touching glove's outer surface) to avoid skin contact with this product. Dispose of contaminated gloves after use in accordance with applicable laws and good laboratory practices. Wash and dry hands.

Handle in accordance with good industrial hygiene and safety practice. Wash hands before breaks and at the end of workday.

Avoid inhalation of vapor or mist.

ACCIDENTAL RELEASE MEASURES; Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid breathing vapours, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains. Discharge into the environment must be avoided.

For more Preventive Measures (Complete) data for Antimony pentachloride (8 total), please visit the HSDB record page.

Excerpt from ERG Guide 157 [Substances - Toxic and/or Corrosive (Non-Combustible / Water-Sensitive)]:

Excerpt from ERG Guide 157 [Substances - Toxic and/or Corrosive (Non-Combustible / Water-Sensitive)]:

Immediate precautionary measure

Immediate precautionary measure

Following oral exposure to antimony, administer charcoal as a slurry (240 mL water/30 g charcoal). Following inhalation exposure, 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 inhaled beta2 agonist and oral or parenteral corticosteroids. In case of eye exposure, irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes. Following dermal exposure, remove contaminated clothing and wash exposed area thoroughly with soap and water. A physician may need to examine the area if irritation or pain persists. (T36)

Tumor necrosis factor-alpha (TNF-alpha) is a mediator of inflammation and has an important role in human and experimental renal diseases. Pentoxifylline (PTX) has been shown to inhibit cytokine synthesis, including TNF-alpha. The aim of the present study was to examine the effect of PTX on meglumine antimonate (Sb(V)) and antimony pentachloride (SbCl(5))-induced renal toxicity in rats. Sixty Wistar rats were divided into six groups according to the treatment employed over the period of 7 days: group I-saline (NaCl 0.9%); group II-PTX plus saline; group III-meglumine antimonate (Sb(V)) plus saline; group IV-meglumine antimonate (Sb(V)) plus PTX; group V-SbCl(5) plus saline; group VI-SbCl(5) with PTX. The animals' urinary concentration ability was evaluated before and after the end of the treatment. Urine and blood osmolality, sodium and creatinine concentration, and urine volume per minute (V) were determined. Creatinine clearance (CrCl), fractional sodium excretion (FE(Na)), and urine to plasma osmolality ratio (U/P osm) were calculated. TNF-alpha concentration in blood was assessed. On the seventh day, the animals were sacrificed and their kidneys were submitted to histological analysis. The meglumine antimonate (Sb(V))-treated animals showed an impaired renal capacity to concentrate urine, with low values of the ratio U/P osm, reduction in CrCl, and an increment in TNF-alpha serum levels. PTX associated with meglumine antimonate (Sb(V)) reduced TNF-alpha serum levels and was effective in preventing renal functional alterations. Rats treated with SbCl(5) showed functional and histopathologic alterations compatible with acute tubular necrosis, and treatment with PTX did not prevent SbCl(5)-induced nephrotoxicity. PTX was effective in preventing renal functional alterations induced by meglumine antimonate (Sb(V)) in rats.

Dermal exposure to antimony can cause antimony spots (papules and pustules around sweat and sebaceous glands). Antimony poisoning can also lead to pneumoconiosis. Alterations in pulmonary function and other effects including chronic bronchitis, chronic emphysema, inactive tuberculosis, pleural adhesions, and irritation can result from inhalation of antimony. Increased blood pressure can also result from antimony poisoning. Myocardial depression, vasodilation and fluid loss may cause shock with hypotension, electrolyte disturbances and acute renal failure. Cerebral oedema, coma, convulsions, and death are possible. (L741)

IDENTIFICATION AND USE: Antimony pentachloride is a colorless to yellow oily liquid. It is used as catalyst when replacing a fluorine substituent with chlorine in organic compounds. It is also used in analysis (testing for alkaloids and cesium), dyeing intermediates, as chlorine carrier in organic chlorinations. HUMAN STUDIES: Severe burns of cornea caused by exposure to high concentration of vapor. Inhalation causes coughing, choking, and variable symptoms of headache, dizziness, and weakness followed by pulmonary edema, difficult breathing, cyanosis, and bloody sputum. Skin contact causes severe burns. Burns heal slowly with scar formation. May produce anemia and bloody urine. Two deaths from antimony pentachloride poisoning have been reported. ANIMAL STUDIES: Antimony pentachloride is moderately toxic following acute oral exposure. Inhalation exposure of rats to 0.037 mg antimony pentachloride/L air, 2 hours/day for 4 months led to partly reversible damage to the lungs, heart, liver, kidneys and thyroid gland as well as accumulation of antimony in the spleen, heart, lymph nodes and thyroid gland. According to the available genotoxicity studies, antimony pentachloride was negative in the Salmonella/microsome test in strains TA 98 and TA 100 with and without metabolic activation, and did not increase the sister chromatid exchange rate in mammalian cells in vitro. Of three spot tests with antimony pentachloride in Bacillus subtilis, two were positive and one was negative.

The inhalation data suggest that the myocardium is a target of antimony toxicity. It is possible that antimony affects circulating glucose by interfering with enzymes of the glycogenolysis and gluconeogenesis pathways. The mechanism of action of antimony remains unclear. However, some studies suggest that antimony combines with sulfhydryl groups including those in several enzymes important for tissue respiration. The antidotal action of BAL depends on its ability to prevent or break the union between antimony and vital enzymes. Moreover, the The cause of death is believed to be essentially the same as that in acute arsenic poisoning. Antimony pentachloride reacts with water to form hydrochloric acid which has a direct corrosive effect on mucous membranes. (L793, T18, L741, A238)

Abdominal pain, vomiting, diarrhea can result from inhalation of antimony. Dyspnea, headache, vomiting,cough, conjunctivitis, and bloody purulent discharge from nose can result from inhalation exposure. Skin or eye contact can cause pain and redness of the exposed surface. (T64, L741)

/SIGNS AND SYMPTOMS/ Severe burns of cornea ... caused by exposure to high concn of vapor ... .

/SIGNS AND SYMPTOMS/ Inhalation causes coughing, choking, and variable symptoms of headache, dizziness, and weakness followed by pulmonary edema, difficult breathing, cyanosis, and bloody sputum. Skin contact causes severe burns. Burns heal slowly with scar formation. May produce anemia and bloody urine.

/SIGNS AND SYMPTOMS/ Occupational exposures are usually by inhalation of dust containing ... antimony pentachloride ... . Effects may be acute, particularly from /pentachloride/ ... exposures, producing a rhinitis and even acute pulmonary edema.

/SIGNS AND SYMPTOMS/ In man, antimony-V-chloride is irritant or corrosive to the skin and mucous membranes of the respiratory tract and can cause pulmonary edema.

/CASE REPORTS/ The effects of poisoning with diborane, hydrogen-sulfide (H2S), chlorine, phosgene, carbon-monoxide, or antimony-pentachloride were examined in 55 patients with pulmonary edema. Most of the cases of intoxication resulted from accidental acute exposure to gaseous agents in industrial settings. Chlorine gas in low concentrations induced damage to the mucosa of the nose and throat because of the solubility of the gas in water. Greater concentrations gave rise to severe pulmonary congestion and edema due to the hydrolysis of chlorine to hydrochloric-acid in the parenchymal lung tissue. Phosgene produced irritation of the conjunctiva, nasal, and pharyngeal membranes at low concentrations. At higher exposures, bronchial, bronchiolar, and alveolar inflammatory reactions ensued. At low exposures to H2S, damage occurred in the conjunctiva, cornea, and pharyngeal membranes. A more prolonged exposure to low concentrations evoked damage to the respiratory tract and produced pulmonary edema. Following high exposure to H2S, central nervous system depression developed with respiratory and olfactory paralysis. All patients with diborane intoxication survived; there were two deaths from H2S poisoning and two deaths from antimony-pentachloride poisoning. All patients received oxygen therapy (at 60 to 80 percent), usually with intermittent positive pressure breathing. The authors conclude that narcotic agents should not be administered to patients with respiratory depression. Victims of poisonings such as those described should be treated in intensive care units.

/LABORATORY ANIMALS: Acute Exposure/ Antimony-V-chloride is moderately toxic following acute oral exposure (LD50 rat oral 1115 mg/kg body weight). According to an unclear citation in the literature, the 2-hour LC50 in the rat is 720 mg/cu m.

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ A limited subchronic study gave weak indications of partly reversible damage to the lungs, heart, liver, kidneys and thyroid gland as well as accumulation of antimony in the spleen, heart, lymph nodes and thyroid gland, following inhalation exposure of rats to 0.037 mg antimony-V-chloride/L air, 2 hours/day for 4 months.

/GENOTOXICITY/ The rec, Salmonella mutagenicity, and sister chromatid exchange (SCE) assays were conducted to evaluate the genotoxicity of three beryllium, three gallium, and four antimony compounds. Fifty milligrams samples of beryllium-chloride (BeCl2), beryllium-nitrate (Be(NO3)2), beryllium-oxide ((BeO), gallium-chloride (GaCl3), gallium-nitrate (Ga(NO3)3), gallium-oxide (GaO3), antimony-chloride (SbCl3), antimony-oxide (Sb2O3), antimony-pentachloride (SbCl5), and antimony-pentoxide (Sb2O5) were dissolved in distilled water and diluted serially two fold for the assays; both negative and positive controls were used. The rec assays involved spores of Bacillus-subtilis-M45 and Bacillus-subtilis-H17 and the SCE assays involved V79-Chinese-hamster cells. The Salmonella mutagenicity assays used the (TA100) and (TA98) strains and were conducted in the presence of rat liver-S9. In the rec assay, DNA damaging activity was exhibited by BeCl2, Be(NO3)2, GaCl3, Ga(NO3)3, SbCl3, SbCl5, and Sb2O3. None of the tested compounds were mutagenic to Salmonella and only SbCl3, Sb3O3, BeCl2, and Be(NO3)2 significantly induced sister chromatid exchanges. One of the antimony(III) compound, Sb2O3, was positive in both the rec and SCE assays at very low doses.

/GENOTOXICITY/ According to the available genotoxicity studies, antimony-V-chloride is negative in the Salmonella/microsome test in strains TA 98 and TA 100 with and without metabolic activation, and does not increase the sister chromatid exchange rate in mammalian cells in vitro. Of three spot tests with antimony-V-chloride in Bacillus subtilis, two were positive and one was negative. Overall, the genotoxic potential of the substance cannot be evaluated based on these studies.

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 if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on the 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. /Poisons A and B/

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 needed. 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 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 ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/

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 as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/

Call for medical aid. ... Move victim to fresh air. If breathing has stopped, give artificial respiration. If breathing is difficult, give oxygen. ... Remove contaminated clothing and shoes. Flush affected areas with plenty of water. If in eyes, hold eyelids open and flush with plenty of water. If swallowed and victim is conscious, have victim drink water or milk. Do not induce vomiting.

LC50 (rat) = 720 mg/m3/2h

LD50: 1115 mg/kg (Oral, Rat) (L792) LD50: 900 mg/kg (Oral, Guinea pig) (L792)

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. Antimony compounds are included on this list. /Antimony Componds/

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 1000 lb or 454 kg. The toll free number of the NRC is (800) 424-8802. The rule for determining when notification is required is stated in 40 CFR 302.4 (section IV. D.3.b).

Antimony pentachloride is designated as a hazardous substance under section 311(b)(2)(A) of the Federal Water Pollution Control Act and further regulated by the Clean Water Act Amendments of 1977 and 1978. These regulations apply to discharges of this substance. This designation includes any isomers and hydrates, as well as any solutions and mixtures containing this substance.

Toxic pollutant designated pursuant to section 307(a)(1) of the Federal Water Pollution Control Act and is subject to effluent limitations. /Antimony and compounds/