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STIBINE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Stibine is a poisonous gas which causes hemolysis. It is formed when acid solutions of antimony compounds are treated with reducing agents.

Specific Substances

    1) Antimonous Hydrous
    2) Hydrogen Antimonide
    3) Antimony Trihydride
    4) CAS 7803-52-3
    5) Molecular Formula: SbH3
    1.2.1) MOLECULAR FORMULA
    1) H3-Sb

Available Forms Sources

    A) FORMS
    1) Stibine is a colorless gas with a disagreeable odor similar to that of hydrogen sulfide (Lewis, 1992; HSDB , 2000). It is the volatile anhydride of antimony (Beliles, 1994; HSDB , 2000).
    B) SOURCES
    1) Stibine can be generated when an acid reacts with metal containing antimony, is produced as a by-product of the processing of antimony-containing metal, and is produced in lead acid battery manufacture or results from overcharging storage batteries, but it is less stable and less readily formed than arsine (Webster, 1946; Jones & Gamble, 1984; Beliles, 1994; HSDB , 2000).
    2) Stibine, in addition to arsine and hydrogen sulfide, can be released into the work environment when hardening antimony alloys in water (Nau et al, 1944; (HSDB , 2000).
    3) The primary areas of exposure are in the metallurgy industry, welding, soldering, etching of zinc, chemical laboratories, and filling of hydrogen balloons (Stokinger, 1981).
    C) USES
    1) Stibine is used as a fumigating agent. High purity stibine is used as an n-type gas phase dopant for silicon in semiconductors (Lewis, 1992; HSDB , 2000).

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Human exposures have been uncommon and have often involved exposure to arsine and hydrogen sulfide, in addition to stibine. The principal effect of stibine is hemolysis, with secondary effects involving the kidneys and liver. It is anticipated to cause pulmonary irritation, based on animal studies.
    B) Exposed humans have experienced headache, weakness, nausea, lumbar pain, jaundice, and hematuria. Signs and symptoms similar to those occurring in shock, seizures and death are suggested effects which are anticipated to occur with severe exposures.
    C) Animals exposed to stibine have pulmonary irritation, congestion and edema, hemolysis, secondary renal effects, anemia, and fatty liver changes.
    0.2.3) VITAL SIGNS
    A) Effects similar to those encountered in shock have been suggested effects. The pulse may be weak and irregular. Dyspnea and/or slowed respirations may be present.
    0.2.6) RESPIRATORY
    A) Pulmonary irritation is a possible effect based principally on results in animal studies.
    0.2.7) NEUROLOGIC
    A) Severe headache is a common early symptom of stibine poisoning. Seizures may develop in severe exposures.
    0.2.8) GASTROINTESTINAL
    A) Nausea and abdominal pain are common.
    0.2.9) HEPATIC
    A) Jaundice has been reported.
    0.2.10) GENITOURINARY
    A) Abdominal and lumbar pain are common. Hematuria is an early sign of stibine-induced hemolysis.
    0.2.13) HEMATOLOGIC
    A) Stibine causes hemolysis. Anemia and significant weakness may be present.

Laboratory Monitoring

    A) Monitor complete blood count, reticulocyte count, liver function tests, creatinine, and creatinine clearance.

Treatment Overview

    0.4.3) INHALATION EXPOSURE
    A) Human exposures to stibine gas are uncommon. More human cases need to be described before an accurate picture of the intoxication can be drawn. Treatment is primarily supportive as necessary. Insure adequate hydration by starting intravenous fluids. Severe hemolytic anemia can occur. Maintaining adequate urine output may prevent renal damage by disposition of hemoglobin and hemoglobin breakdown products. Exchange transfusion should be considered.
    B) 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.
    C) If major hemolysis has occurred, exchange transfusion may be performed to remove plasma hemoglobin in conjunction with hemodialysis to preserve renal function.
    D) ECG - An ECG should be performed because cardiac conduction abnormalities may occur.
    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.
    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).

Range Of Toxicity

    A) Concentrations which are lethal in humans are not known. Exposure to a concentration of 5 parts per million or greater may result in adverse health effects or death.

Clinical Effects

Summary Of Exposure

    A) Human exposures have been uncommon and have often involved exposure to arsine and hydrogen sulfide, in addition to stibine. The principal effect of stibine is hemolysis, with secondary effects involving the kidneys and liver. It is anticipated to cause pulmonary irritation, based on animal studies.
    B) Exposed humans have experienced headache, weakness, nausea, lumbar pain, jaundice, and hematuria. Signs and symptoms similar to those occurring in shock, seizures and death are suggested effects which are anticipated to occur with severe exposures.
    C) Animals exposed to stibine have pulmonary irritation, congestion and edema, hemolysis, secondary renal effects, anemia, and fatty liver changes.

Vital Signs

    3.3.1) SUMMARY
    A) Effects similar to those encountered in shock have been suggested effects. The pulse may be weak and irregular. Dyspnea and/or slowed respirations may be present.
    3.3.2) RESPIRATIONS
    A) Effects similar to those occurring in shock have been suggested following poisoning (HSDB , 2000). Dyspnea and/or slowed respirations may be present (Stokinger, 1981).
    3.3.5) PULSE
    A) Symptoms of shock may occur with poisoning (HSDB , 2000).

Heent

    3.4.3) EYES
    A) IRRITATION - Stibine is not considered an eye irritant (US DHHS, 1981).
    3.4.5) NOSE
    A) ODOR - Stibine has a disagreeable odor (HSDB , 2000). The threshold for odor detection is not known (US DHHS, 1981).

Respiratory

    3.6.1) SUMMARY
    A) Pulmonary irritation is a possible effect based principally on results in animal studies.
    3.6.2) CLINICAL EFFECTS
    A) IRRITATION SYMPTOM
    1) Pulmonary irritation is a suggested effect, based on animal studies (US DHHS, 1981; Hathaway et al, 1996). No case studies were found which described pulmonary irritation in stibine-exposed humans.
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) IRRITATION
    a) Stibine may cause pulmonary irritation (Webster, 1946; Hathaway et al, 1996).
    2) PULMONARY EDEMA
    a) Pulmonary congestion and edema have been reported in cats and dogs exposed to stibine (Webster, 1946; Hathaway et al, 1996).

Neurologic

    3.7.1) SUMMARY
    A) Severe headache is a common early symptom of stibine poisoning. Seizures may develop in severe exposures.
    3.7.2) CLINICAL EFFECTS
    A) SEIZURE
    1) Seizures may occur with significant exposures to stibine (IRPTC, 1984).
    B) HEADACHE
    1) Headache is an early sign of acute stibine poisoning (HSDB , 2000) and can be severe (Nau et al, 1944; Dernehl et al, 1944).

Gastrointestinal

    3.8.1) SUMMARY
    A) Nausea and abdominal pain are common.
    3.8.2) CLINICAL EFFECTS
    A) NAUSEA
    1) Nausea and abdominal pain are common (Dernehl et al, 1944; Nau et al, 1944 Hathaway et al, 1996).

Hepatic

    3.9.1) SUMMARY
    A) Jaundice has been reported.
    3.9.2) CLINICAL EFFECTS
    A) JAUNDICE
    1) Jaundice secondary to hemolysis developing within hours of exposure has been reported (Nau et al, 1944; (Hathaway et al, 1996).

Genitourinary

    3.10.1) SUMMARY
    A) Abdominal and lumbar pain are common. Hematuria is an early sign of stibine-induced hemolysis.
    3.10.2) CLINICAL EFFECTS
    A) BLOOD IN URINE
    1) Hematuria or hemoglobinuria is common and may be an early sign of stibine-induced hemolysis (Nau & Anderson, 1944; Dernehl et al, 1944).
    B) PAIN
    1) Abdominal and lumbar pain are common (Dernehl et al, 1944; Nau et al, 1944; (Hathaway et al, 1996).
    3.10.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) HEMOLYSIS
    a) Hemoglobinuria occurs within 10 to 20 hours in guinea pigs exposed to 65 ppm of stibine for one hour (Webster, 1946; HSDB , 2000). One or two days later the urine clears. Dogs and cats failed to develop hemoglobinuria, despite apparent susceptibility to stibine (Webster, 1946; Hathaway et al, 1996; HSDB , 2000).
    2) ANURIA
    a) Anuria or oliguria are common in exposed laboratory animals (Webster, 1946; HSDB , 2000).

Hematologic

    3.13.1) SUMMARY
    A) Stibine causes hemolysis. Anemia and significant weakness may be present.
    3.13.2) CLINICAL EFFECTS
    A) HEMOLYSIS
    1) Stibine is highly hemolytic (Nau et al, 1944; Dernehl et al, 1944; Hathaway et al, 2000).
    B) ANEMIA
    1) Anemia may be present (Nau et al, 1944; (Dernehl et al, 1984; HSDB , 2000).
    C) FATIGUE
    1) Weakness is common (Dernehl et al, 1944; Nau et al, 1944; (Hathaway et al, 1996), possibly due to massive hemolysis.
    3.13.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) HEMOLYSIS
    a) Stibine is a powerful hemolytic agent in laboratory animals, causing death within a few hours up to a day (Webster, 1946; Hathaway et al, 1996).
    2) ANEMIA
    a) Hemoglobinuria occurs within 10 to 20 hours in guinea pigs exposed to 65 ppm of stibine for one hour. One or two days later the urine clears and a significant drop in red blood count occurs. Anemia develops a few days later (Webster, 1946; Hathaway et al, 1996; HSDB , 2000).
    3) ERYTHROCYTES ABNORMAL
    a) The erythrocytes develop a spherical morphology with spicules extending around the periphery within minutes of exposure and generally precedes hemolysis in the laboratory animals. The effects on erythrocyte morphology resemble the effects of phenylhydrazine (Webster, 1946).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) DISCOLORATION OF SKIN
    1) Although not yet reported with stibine, bronze skin has been reported in severe cases of hemolysis due to arsine.

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS7803-52-3 (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
    3.21.3) HUMAN STUDIES
    A) LACK OF INFORMATION
    1) No information concerning possible carcinogenicity of stibine in humans or animals was found (IARC, 1987; US DHHS, 1994; HSDB , 2000; RTECS , 2000).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor complete blood count, reticulocyte count, liver function tests, creatinine, and creatinine clearance.
    4.1.2) SERUM/BLOOD
    A) HEMATOLOGIC
    1) Stibine may cause hemolytic anemia. Obtain several complete blood counts. The presence of serum hemoglobin should be determined.
    B) BLOOD/SERUM CHEMISTRY
    1) Routine liver and renal function tests results should be monitored.
    4.1.3) URINE
    A) URINALYSIS
    1) Obtain a urine sample and evaluate for hematuria.
    B) OTHER
    1) Monitor urine output and creatinine clearance.

Methods

    A) SPECTROSCOPY/SPECTROMETRY
    1) A spectrochemical method for analysis of antimony in biologic materials has been published by Kinser et al (1965). It has a lower limit of detection of 50 ppm in 2 mg of ash.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) Monitor complete blood count, reticulocyte count, liver function tests, creatinine, and creatinine clearance.

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) SEIZURE
    1) SUMMARY
    a) Attempt initial control with a benzodiazepine (eg, diazepam, lorazepam). If seizures persist or recur, administer phenobarbital or propofol.
    b) Monitor for respiratory depression, hypotension, and dysrhythmias. Endotracheal intubation should be performed in patients with persistent seizures.
    c) Evaluate for hypoxia, electrolyte disturbances, and hypoglycemia (or, if immediate bedside glucose testing is not available, treat with intravenous dextrose).
    2) DIAZEPAM
    a) ADULT DOSE: Initially 5 to 10 mg IV, OR 0.15 mg/kg IV up to 10 mg per dose up to a rate of 5 mg/minute; may be repeated every 5 to 20 minutes as needed (Brophy et al, 2012; Prod Info diazepam IM, IV injection, 2008; Manno, 2003).
    b) PEDIATRIC DOSE: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed (Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
    c) Monitor for hypotension, respiratory depression, and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after repeated doses of diazepam .
    3) NO INTRAVENOUS ACCESS
    a) DIAZEPAM may be given rectally or intramuscularly (Manno, 2003). RECTAL DOSE: CHILD: Greater than 12 years: 0.2 mg/kg; 6 to 11 years: 0.3 mg/kg; 2 to 5 years: 0.5 mg/kg (Brophy et al, 2012).
    b) MIDAZOLAM has been used intramuscularly and intranasally, particularly in children when intravenous access has not been established. ADULT DOSE: 0.2 mg/kg IM, up to a maximum dose of 10 mg (Brophy et al, 2012). PEDIATRIC DOSE: INTRAMUSCULAR: 0.2 mg/kg IM, up to a maximum dose of 7 mg (Chamberlain et al, 1997) OR 10 mg IM (weight greater than 40 kg); 5 mg IM (weight 13 to 40 kg); INTRANASAL: 0.2 to 0.5 mg/kg up to a maximum of 10 mg/dose (Loddenkemper & Goodkin, 2011; Brophy et al, 2012). BUCCAL midazolam, 10 mg, has been used in adolescents and older children (5-years-old or more) to control seizures when intravenous access was not established (Scott et al, 1999).
    4) LORAZEPAM
    a) MAXIMUM RATE: The rate of intravenous administration of lorazepam should not exceed 2 mg/min (Brophy et al, 2012; Prod Info lorazepam IM, IV injection, 2008).
    b) ADULT DOSE: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist (Manno, 2003; Brophy et al, 2012).
    c) PEDIATRIC DOSE: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue (Brophy et al, 2012; Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008; Sreenath et al, 2009; Chin et al, 2008).
    5) PHENOBARBITAL
    a) ADULT LOADING DOSE: 20 mg/kg IV at an infusion rate of 50 to 100 mg/minute IV. An additional 5 to 10 mg/kg dose may be given 10 minutes after loading infusion if seizures persist or recur (Brophy et al, 2012).
    b) Patients receiving high doses will require endotracheal intubation and may require vasopressor support (Brophy et al, 2012).
    c) PEDIATRIC LOADING DOSE: 20 mg/kg may be given as single or divided application (2 mg/kg/minute in children weighing less than 40 kg up to 100 mg/min in children weighing greater than 40 kg). A plasma concentration of about 20 mg/L will be achieved by this dose (Loddenkemper & Goodkin, 2011).
    d) REPEAT PEDIATRIC DOSE: Repeat doses of 5 to 20 mg/kg may be given every 15 to 20 minutes if seizures persist, with cardiorespiratory monitoring (Loddenkemper & Goodkin, 2011).
    e) MONITOR: For hypotension, respiratory depression, and the need for endotracheal intubation (Loddenkemper & Goodkin, 2011; Manno, 2003).
    f) SERUM CONCENTRATION MONITORING: Monitor serum concentrations over the next 12 to 24 hours. Therapeutic serum concentrations of phenobarbital range from 10 to 40 mcg/mL, although the optimal plasma concentration for some individuals may vary outside this range (Hvidberg & Dam, 1976; Choonara & Rane, 1990; AMA Department of Drugs, 1992).
    6) OTHER AGENTS
    a) If seizures persist after phenobarbital, propofol or pentobarbital infusion, or neuromuscular paralysis with general anesthesia (isoflurane) and continuous EEG monitoring should be considered (Manno, 2003). Other anticonvulsants can be considered (eg, valproate sodium, levetiracetam, lacosamide, topiramate) if seizures persist or recur; however, there is very little data regarding their use in toxin induced seizures, controlled trials are not available to define the optimal dosage ranges for these agents in status epilepticus (Brophy et al, 2012):
    1) VALPROATE SODIUM: ADULT DOSE: An initial dose of 20 to 40 mg/kg IV, at a rate of 3 to 6 mg/kg/minute; may give an additional dose of 20 mg/kg 10 minutes after loading infusion. PEDIATRIC DOSE: 1.5 to 3 mg/kg/minute (Brophy et al, 2012).
    2) LEVETIRACETAM: ADULT DOSE: 1000 to 3000 mg IV, at a rate of 2 to 5 mg/kg/min IV. PEDIATRIC DOSE: 20 to 60 mg/kg IV (Brophy et al, 2012; Loddenkemper & Goodkin, 2011).
    3) LACOSAMIDE: ADULT DOSE: 200 to 400 mg IV; 200 mg IV over 15 minutes (Brophy et al, 2012). PEDIATRIC DOSE: In one study, median starting doses of 1.3 mg/kg/day and maintenance doses of 4.7 mg/kg/day were used in children 8 years and older (Loddenkemper & Goodkin, 2011).
    4) TOPIRAMATE: ADULT DOSE: 200 to 400 mg nasogastric/orally OR 300 to 1600 mg/day orally divided in 2 to 4 times daily (Brophy et al, 2012).
    B) MONITORING OF PATIENT
    1) Obtain baseline CBC, urinalysis, serum hemoglobin, and renal and hepatic function tests.
    2) ECG - Obtain a baseline electrocardiogram following a moderate to severe exposure. Conduction abnormalities may occur.
    C) EXCHANGE TRANSFUSION
    1) HEMOLYSIS - If severe hemolysis has occurred, exchange transfusion may be performed to remove the plasma hemoglobin, in conjunction with hemodialysis to preserve renal function.
    2) Remember that other factors can cause hemolysis and should be considered; these include arsine, G6PD deficiency, binge drinking, hereditary spherocytosis and elliptocytosis, sickle cell disease, artificial heart valves, arsine and others. Also, rhabdomyolysis and traumatic muscle damage can produce myoglobinuria. Non-hemolytic anemias can be present from myriad causes.
    3) If mixed metal exposures occur, potential cross-over toxicity characteristic of other metals should be kept in mind by metal, organ system, and toxic characteristics.

Range Of Toxicity

Summary

    A) Concentrations which are lethal in humans are not known. Exposure to a concentration of 5 parts per million or greater may result in adverse health effects or death.

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) The minimum lethal human dose to this agent has not been delineated.
    B) ACUTE
    1) Exposure to five parts per million is anticipated to cause immediate adverse health effects or death (NIOSH , 1996).

Maximum Tolerated Exposure

    A) GENERAL/SUMMARY
    1) The maximum tolerated human exposure to this agent has not been delineated.
    B) ACUTE
    1) Exposure to five parts per million is anticipated to cause immediate adverse health effects or death (NIOSH , 1996).

Workplace Standards

    A) ACGIH TLV Values for CAS7803-52-3 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.
    a) Adopted Value
    1) Antimony hydride
    a) TLV:
    1) TLV-TWA: 0.1 ppm
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: Not Listed
    2) Codes: Not Listed
    3) Definitions: Not Listed
    c) TLV Basis - Critical Effect(s): Hemolysis; kidney dam; LRT irr
    d) Molecular Weight: 124.78
    1) For gases and vapors, to convert the TLV from ppm to mg/m(3):
    a) [(TLV in ppm)(gram molecular weight of substance)]/24.45
    2) For gases and vapors, to convert the TLV from mg/m(3) to ppm:
    a) [(TLV in mg/m(3))(24.45)]/gram molecular weight of substance
    e) Additional information:

    B) NIOSH REL and IDLH Values for CAS7803-52-3 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Stibine
    2) REL:
    a) TWA: 0.1 ppm (0.5 mg/m(3))
    b) STEL:
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s):
    3) IDLH:
    a) IDLH: 5 ppm
    b) Note(s): Not Listed

    C) Carcinogenicity Ratings for CAS7803-52-3 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Antimony hydride
    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 ; Listed as: Stibine
    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 CAS7803-52-3 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Stibine
    2) Table Z-1 for Stibine:
    a) 8-hour TWA:
    1) ppm: 0.1
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3: 0.5
    a) Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.
    3) Ceiling Value:
    4) Skin Designation: No
    5) Notation(s): Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: RTECS, 2000

Pharmacology Toxicology

Toxicologic Mechanism

    A) Stibine hemolyzes red blood cells, causes secondary renal and hepatic effects, and causes pulmonary irritation in animals (Webster, 1946; Hathaway et al, 1996).

Physicochemical

Physical Characteristics

    A) Stibine is said to have a very unpleasant sulfide-like odor (Stokinger, 1981; Budavari, 1996).
    B) Stibine is a colorless gas with a disagreeable odor similar to that of hydrogen sulfide (Lewis, 1992; Budavari, 1996).

Ph

    1) No information found at the time of this review.

Molecular Weight

    A) 124.78 (HSDB , 2000)

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) 49 CFR 172.101: Department of Transportation - Table of Hazardous Materials. National Archives and Records Administration (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Aug 11, 2005.
    5) 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.
    6) 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.
    7) 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.
    8) 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.
    9) 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.
    10) 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.
    11) 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.
    12) 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.
    13) AAR: Emergency Handling of Hazardous Materials in Surface Transportation, Bureau of Explosives, Association of American Railroads, Washington, DC, 1987, pp 651.
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