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OSMIUM TETROXIDE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Osmium tetroxide is an oxidation product of osmium metal (ACGIH, 2001a; Budavari, 2001).

Specific Substances

    1) Osmic acid
    2) Osmic acid anhydride
    3) Osmine tetroxide
    4) Osmium oxide
    5) Osmium tetraoxide
    6) Osmium tetroxide
    7) Perosmic acid anhydride
    8) Perosmic acid
    9) Perosmic oxide
    1.2.1) MOLECULAR FORMULA
    1) O4-Os

Available Forms Sources

    A) FORMS
    1) Osmium tetroxide exists as a colorless to pale yellow crystalline solid (HSDB, 2004; NIOSH ICSC, 1999).
    B) SOURCES
    1) Osmium tetroxide can be prepared by heating finely divided osmium metal in a stream of air or oxygen (Budavari, 2001).
    2) The compound may also be formed through oxidation of osmium containing solutions with aqua regia or nitric acid (HSDB, 2004; Bingham et al, 2001).
    3) At room temperature, powdered osmium metal can slowly oxidize to osmium tetroxide (HSDB, 2004; Bingham et al, 2001).
    C) USES
    1) Osmium tetroxide is an oxidation product of osmium metal used as a fat fixing and staining agent for adipose tissues in pathological laboratories; in photography; as a catalyst in organic synthesis for chlorate, peroxide, periodate, and other oxidations; and as an oxidizing agent to convert olefins to glycols (ACGIH, 2001; Budavari, 2001).
    2) Osmium tetroxide was formerly used in taking fingerprints, but this use was discontinued because it caused dermatitis (Harbison, 1998).
    3) Osmium tetroxide has been used by intra-articular injection to perform chemical synovectomies in patients with degenerative joint diseases such as rheumatoid arthritis (Bessant et al, 2003). This use has been discontinued in the US because the injection also causes necrosis of the articular cartilage (Mitchell et al, 1973).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Osmium tetroxide causes irritation or damage to the eyes, skin, and respiratory tract. Pulmonary edema may occur. Excessive lacrimation and a sensation of seeing halos around lights has been described. A burning sensation in the chest may occur. Excessive lacrimation, conjunctivitis, visual disturbances, headache, nose and throat irritation, and cough have been reported in exposed workers. CNS depression may be seen.
    0.2.8) GASTROINTESTINAL
    A) Irritation or burns might occur following ingestion.
    0.2.20) REPRODUCTIVE
    A) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.
    B) Osmium tetroxide has caused paternal effects on reproduction and spermatogenesis in rats and mice.

Laboratory Monitoring

    A) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring complete blood count, urinalysis, and liver and kidney function tests is suggested for patients with significant exposure.
    B) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) GASTRIC LAVAGE: Consider after ingestion of a potentially life-threatening amount of poison if it can be performed soon after ingestion (generally within 1 hour). Protect airway by placement in the head down left lateral decubitus position or by endotracheal intubation. Control any seizures first.
    1) CONTRAINDICATIONS: Loss of airway protective reflexes or decreased level of consciousness in unintubated patients; following ingestion of corrosives; hydrocarbons (high aspiration potential); patients at risk of hemorrhage or gastrointestinal perforation; and trivial or non-toxic ingestion.
    B) ACTIVATED CHARCOAL: Administer charcoal as a slurry (240 mL water/30 g charcoal). Usual dose: 25 to 100 g in adults/adolescents, 25 to 50 g in children (1 to 12 years), and 1 g/kg in infants less than 1 year old.
    C) Observe patients with ingestion carefully for the possible development of esophageal or gastrointestinal tract irritation or burns. If signs or symptoms of esophageal irritation or burns are present, consider endoscopy to determine the extent of injury.
    0.4.3) INHALATION EXPOSURE
    A) 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.
    B) ACUTE LUNG INJURY: Maintain ventilation and oxygenation and evaluate with frequent arterial blood gases and/or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed.
    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) Rabbits exposed by inhalation to 130 mg/m(3) or more for 30 minutes died of pulmonary edema. A 4-hour inhalation exposure to 40 ppm has caused death in rats and mice.

Clinical Effects

Summary Of Exposure

    A) Osmium tetroxide causes irritation or damage to the eyes, skin, and respiratory tract. Pulmonary edema may occur. Excessive lacrimation and a sensation of seeing halos around lights has been described. A burning sensation in the chest may occur. Excessive lacrimation, conjunctivitis, visual disturbances, headache, nose and throat irritation, and cough have been reported in exposed workers. CNS depression may be seen.

Heent

    3.4.3) EYES
    A) CONJUNCTIVITIS - Vapor exposure can cause eye irritation, excessive lacrimation, photophobia, conjunctivitis, and a "gritty" sensation (Proctor, 1988; ACGIH, 1986; Grant, 1986).
    B) VISUAL CHANGES - Visual changes have been described in workers exposed to the vapors (ACGIH, 1986; Proctor, 1988). A sensation of seeing halos or colored rings around lights has been described (Proctor, 1988; Grant, 1986).
    1) These symptoms have not developed until after 2 hours of exposure in some cases (ACGIH, 1986) and normally spontaneously resolve after 24 hours when exposure is terminated (Finkel, 1983). Visual acuity usually remains normal (Grant, 1986).
    C) EYE SPLASHES - Direct eye contact with a single drop of a 1 percent osmium tetroxide solution caused severe and permanent corneal damage in experimental animals (Proctor, 1988; Grant, 1986). A brown staining of the cornea and conjunctiva may be noted (Grant, 1986).
    3.4.5) NOSE
    A) IRRITATION of the mucosa of the nose and throat may occur (ACGIH, 1986). Symptoms may not develop until after up to 2 hours of exposure and may not resolve for as late as 12 hours after cessation of exposure (ACGIH, 1986).
    3.4.6) THROAT
    A) IRRITATION of the mucosa of the nose and throat may occur (ACGIH, 1986). Symptoms may not develop until after up to 2 hours of exposure and may not resolve for as late as 12 hours after cessation of exposure (ACGIH, 1986).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) IRRITATION SYMPTOM
    1) Irritation of the respiratory tract with coughing may occur with vapor exposure at concentrations of 0.1 to 0.6 mg/m(3) (ACGIH, 1986).
    B) BRONCHOSPASM
    1) Exposed workers have developed chest tightness or an asthmatic-like bronchitis, and at least one case of possible related chronic bronchitis has been described (Finkel, 1983; Grant, 1986). The bronchitic symptoms persisted for 12 to 24 hours after cessation of exposure in some cases (Finkel, 1983).
    C) PNEUMONIA
    1) Suppurative bronchopneumonia and bronchitis were noted at autopsy in a single fatal human case following vapor inhalation (Finkel, 1983).
    D) ACUTE LUNG INJURY
    1) More severe or prolonged exposure can result in pulmonary edema (ACGIH, 1986). Experimental animals exposed to 130 mg/m(3) or more developed pulmonary edema and bronchopneumonia and died within 4 days of exposure (Proctor, 1988; ACGIH, 1986).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) HEADACHE
    1) Frontal headache has been described by workers exposed to between 0.1 and 0.6 mg/m(3) (Proctor, 1988; ACGIH, 1986).
    B) COMA
    1) Inhalation exposure to concentrations that later caused death from pulmonary injury first produced a semicomatose state in experimental animals (Clayton & Clayton, 1982).

Gastrointestinal

    3.8.1) SUMMARY
    A) Irritation or burns might occur following ingestion.
    3.8.2) CLINICAL EFFECTS
    A) DRUG-INDUCED GASTROINTESTINAL DISTURBANCE
    1) Unspecified, self-limited gastrointestinal complaints have been noted in some workers with chronic exposure (Finkel, 1983; ITI, 1985).
    B) GASTRITIS
    1) Human ingestion exposures have not been reported, but irritation or burns of the esophagus or gastrointestinal tract may be predicted to occur based on this agent's other irritant properties.

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) TOXIC NEPHROPATHY
    1) Mild kidney injury developed in experimental animals with fatal osmium tetroxide exposure (Proctor, 1988).
    a) There was evidence of fatty degeneration of the renal tubules in a single fatal human case following vapor inhalation (Finkel, 1983).
    2) A single patient with rheumatoid arthritis who underwent chemical synovectomy by intra-articular injection of osmium tetroxide developed nephrotic syndrome 2 months later (Honkanen et al, 1987). It is unclear whether or not there was any relationship between the osmium tetroxide injection and the development of the nephrotic syndrome, although transient hematuria and proteinuria had been previously described during osmium tetroxide therapy (Honkanen et al, 1987).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) DERMATITIS
    1) Osmium tetroxide has a caustic action on the skin and can result in eczema, possible ulceration, and dermatitis (Proctor, 1988; ITI, 1985). A greenish or blackish discoloration of the skin may result from direct contact (EPA, 1985).

Musculoskeletal

    3.15.2) CLINICAL EFFECTS
    A) INJECTION SITE REACTION
    1) CARTILAGE NECROSIS - When used as an intra-articular injection to produce chemical synovectomy in conditions such as rheumatoid arthritis, osmium tetroxide has caused both synovial and articular cartilage necrosis (Mitchell et al, 1973).

Reproductive

    3.20.1) SUMMARY
    A) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.
    B) Osmium tetroxide has caused paternal effects on reproduction and spermatogenesis in rats and mice.
    3.20.2) TERATOGENICITY
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the teratogenic potential of this agent.
    3.20.3) EFFECTS IN PREGNANCY
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS20816-12-0 (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

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring complete blood count, urinalysis, and liver and kidney function tests is suggested for patients with significant exposure.
    B) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring complete blood count and liver and kidney function tests is suggested for patients with significant exposure.
    4.1.3) URINE
    A) URINALYSIS
    1) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring urinalysis is suggested for patients with significant exposure.
    4.1.4) OTHER
    A) OTHER
    1) PULMONARY FUNCTION TESTS
    a) If respiratory tract irritation is present, it may be useful to monitor pulmonary function tests.
    2) PULMONARY FUNCTION TESTS
    a) If respiratory tract irritation is present, monitor arterial blood gases and chest x-ray.

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) If respiratory tract irritation is present, monitor chest x-ray.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Patients symptomatic following exposure should be observed in a controlled setting until all signs and symptoms have fully resolved.

Monitoring

    A) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring complete blood count, urinalysis, and liver and kidney function tests is suggested for patients with significant exposure.
    B) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.

Oral Exposure

    6.5.2) PREVENTION OF ABSORPTION
    A) EMESIS/NOT RECOMMENDED
    1) Inducing emesis SHOULD MOST LIKELY BE AVOIDED.
    B) GASTRIC LAVAGE
    1) INDICATIONS: Consider gastric lavage with a large-bore orogastric tube (ADULT: 36 to 40 French or 30 English gauge tube {external diameter 12 to 13.3 mm}; CHILD: 24 to 28 French {diameter 7.8 to 9.3 mm}) after a potentially life threatening ingestion if it can be performed soon after ingestion (generally within 60 minutes).
    a) Consider lavage more than 60 minutes after ingestion of sustained-release formulations and substances known to form bezoars or concretions.
    2) PRECAUTIONS:
    a) SEIZURE CONTROL: Is mandatory prior to gastric lavage.
    b) AIRWAY PROTECTION: Place patients in the head down left lateral decubitus position, with suction available. Patients with depressed mental status should be intubated with a cuffed endotracheal tube prior to lavage.
    3) LAVAGE FLUID:
    a) Use small aliquots of liquid. Lavage with 200 to 300 milliliters warm tap water (preferably 38 degrees Celsius) or saline per wash (in older children or adults) and 10 milliliters/kilogram body weight of normal saline in young children(Vale et al, 2004) and repeat until lavage return is clear.
    b) The volume of lavage return should approximate amount of fluid given to avoid fluid-electrolyte imbalance.
    c) CAUTION: Water should be avoided in young children because of the risk of electrolyte imbalance and water intoxication. Warm fluids avoid the risk of hypothermia in very young children and the elderly.
    4) COMPLICATIONS:
    a) Complications of gastric lavage have included: aspiration pneumonia, hypoxia, hypercapnia, mechanical injury to the throat, esophagus, or stomach, fluid and electrolyte imbalance (Vale, 1997). Combative patients may be at greater risk for complications (Caravati et al, 2001).
    b) Gastric lavage can cause significant morbidity; it should NOT be performed routinely in all poisoned patients (Vale, 1997).
    5) CONTRAINDICATIONS:
    a) Loss of airway protective reflexes or decreased level of consciousness if patient is not intubated, following ingestion of corrosive substances, hydrocarbons (high aspiration potential), patients at risk of hemorrhage or gastrointestinal perforation, or trivial or non-toxic ingestion.
    C) ACTIVATED CHARCOAL/CATHARTIC
    1) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.3) TREATMENT
    A) IRRITATION SYMPTOM
    1) Observe patients with ingestion carefully for the possible development of esophageal or gastrointestinal tract irritation or burns. If signs or symptoms of esophageal irritation or burns are present, consider endoscopy to determine the extent of injury.
    B) MONITORING OF PATIENT
    1) Monitor renal function tests and urinalysis.
    C) AIRWAY MANAGEMENT
    1) If CNS and respiratory depression are present, ensure airway patency and adequacy of respirations and oxygenation.
    2) Endotracheal intubation, supplemental oxygen, and assisted ventilation could be required.
    D) OBSERVATION REGIMES
    1) Carefully observe patients with ingestion exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.

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) IRRITATION SYMPTOM
    1) Respiratory tract irritation, if severe, can progress to noncardiogenic pulmonary edema which may be delayed in onset up to 24 to 72 hours after exposure in some cases.
    2) There are no controlled studies indicating that early administration of corticosteroids can prevent the development of noncardiogenic pulmonary edema in patients with inhalation exposure to respiratory irritant substances, and long-term use may cause adverse effects (Boysen & Modell, 1989).
    a) However, based on anecdotal experience, some clinicians do recommend early administration of corticosteroids (such as methylprednisolone 1 gram intravenously as a single dose) in an attempt to prevent the later development of pulmonary edema.
    1) Anecdotal experience with dimethyl sulfate inhalation showed possible benefit of methylprednisolone in the TREATMENT of noncardiogenic pulmonary edema (Ip et al, 1989).
    3) Anecdotal experience also indicated that systemic corticosteroids may have possible efficacy in the TREATMENT of drug-induced noncardiogenic pulmonary edema (Zitnik & Cooper, 1990; Stentoft, 1990; Chudnofsky & Otten, 1989) or noncardiogenic pulmonary edema developing after cardiopulmonary bypass (Maggart & Stewart, 1987).
    4) It is not clear from the published literature that administration of systemic corticosteroids early following inhalation exposure to respiratory irritant substances can PREVENT the development of noncardiogenic pulmonary edema. The decision to administer or withhold corticosteroids in this setting must currently be made on clinical grounds.
    B) BRONCHOSPASM
    1) If bronchospasm and wheezing occur, consider treatment with inhaled sympathomimetic agents.
    C) ACUTE LUNG INJURY
    1) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
    2) NON-PHARMACOLOGIC TREATMENT: The treatment of acute lung injury is primarily supportive (Cataletto, 2012). Maintain adequate ventilation and oxygenation with frequent monitoring of arterial blood gases and/or pulse oximetry. If a high FIO2 is required to maintain adequate oxygenation, mechanical ventilation and positive-end-expiratory pressure (PEEP) may be required; ventilation with small tidal volumes (6 mL/kg) is preferred if ARDS develops (Haas, 2011; Stolbach & Hoffman, 2011).
    a) To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)
    3) FLUIDS: Crystalloid solutions must be administered judiciously. Pulmonary artery monitoring may help. In general the pulmonary artery wedge pressure should be kept relatively low while still maintaining adequate cardiac output, blood pressure and urine output (Stolbach & Hoffman, 2011).
    4) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
    5) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
    6) CALFACTANT: In a multicenter, randomized, blinded trial, endotracheal instillation of 2 doses of 80 mL/m(2) calfactant (35 mg/mL of phospholipid suspension in saline) in infants, children, and adolescents with acute lung injury resulted in acute improvement in oxygenation and lower mortality; however, no significant decrease in the course of respiratory failure measured by duration of ventilator therapy, intensive care unit, or hospital stay was noted. Adverse effects (transient hypoxia and hypotension) were more frequent in calfactant patients, but these effects were mild and did not require withdrawal from the study (Wilson et al, 2005).
    7) However, in a multicenter, randomized, controlled, and masked trial, endotracheal instillation of up to 3 doses of calfactant (30 mg) in adults only with acute lung injury/ARDS due to direct lung injury was not associated with improved oxygenation and longer term benefits compared to the placebo group. It was also associated with significant increases in hypoxia and hypotension (Willson et al, 2015).
    D) OBSERVATION REGIMES
    1) Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    E) GENERAL TREATMENT
    1) Treatment is SYMPTOMATIC and SUPPORTIVE.
    F) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Eye Exposure

    6.8.1) DECONTAMINATION
    A) EYE IRRIGATION, ROUTINE: 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, an ophthalmologic examination should be performed (Peate, 2007; Naradzay & Barish, 2006).
    6.8.2) TREATMENT
    A) OPHTHALMIC EXAMINATION AND EVALUATION
    1) Due to the potential for serious and permanent corneal injury with direct eye splashes, prolonged initial flushing and early ophthalmologic consultation are advisable.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL DECONTAMINATION
    1) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).
    6.9.2) TREATMENT
    A) IRRITATION SYMPTOM
    1) Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Enhanced Elimination

    A) EXTRACORPOREAL ELIMINATION
    1) No studies have addressed the utilization of extracorporeal elimination techniques in poisoning with this agent.

Range Of Toxicity

Summary

    A) Rabbits exposed by inhalation to 130 mg/m(3) or more for 30 minutes died of pulmonary edema. A 4-hour inhalation exposure to 40 ppm has caused death in rats and mice.

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) The minimum lethal human dose to this agent has not been delineated.
    B) ANIMAL DATA
    1) Rabbits exposed by inhalation to 130 mg/m(3) or more for 30 minutes died of pulmonary edema within 4 days of exposure (ACGIH, 2001a).
    2) A 4-hour inhalation exposure to 40 ppm has caused death in rats and mice (Bingham et al, 2001).

Maximum Tolerated Exposure

    A) CONCENTRATION LEVEL
    1) The highest concentration of osmium tetroxide that is tolerable for 6 hours without producing harmful effects is 0.001 mg/m(3) (ACGIH, 2001a).
    2) Workers exposed to between 0.1 and 0.6 mg/m(3) osmium tetroxide for 2 hours complained of excessive lacrimation, visual disturbances, conjunctivitis, headache, and cough (ACGIH, 2001a).
    3) Osmium tetroxide concentrations of 0.1 mg/m(3) or greater are associated with eye irritation in humans (ACGIH, 2001a).

Workplace Standards

    A) ACGIH TLV Values for CAS20816-12-0 (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) Osmium tetroxide, as Os
    a) TLV:
    1) TLV-TWA: 0.0002 ppm
    2) TLV-STEL: 0.0006 ppm
    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): Eye, URT, and skin irr
    d) Molecular Weight: 254.2
    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 CAS20816-12-0 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Osmium tetroxide
    2) REL:
    a) TWA: 0.002 mg/m(3) (0.0002 ppm)
    b) STEL: 0.006 mg/m(3) (0.0006 ppm)
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s):
    3) IDLH: Not Listed

    C) Carcinogenicity Ratings for CAS20816-12-0 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Osmium tetroxide, as Os
    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: Osmium tetroxide
    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 CAS20816-12-0 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Osmium tetroxide (as Os)
    2) Table Z-1 for Osmium tetroxide (as Os):
    a) 8-hour TWA:
    1) ppm:
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3: 0.002
    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) LD50- (INTRAPERITONEAL)MOUSE:
    1) 13.5 mg/kg (RTECS, 2004)
    B) LD50- (ORAL)MOUSE:
    1) 162 mg/kg (RTECS, 2004)
    C) LD50- (INTRAPERITONEAL)RAT:
    1) 14.1 mg/kg (RTECS, 2004)
    D) TCLo- (INHALATION)HUMAN:
    1) 133 mcg/m(3) -- lacrimation, structural or functional change in trachea or bronchi(RTECS, 2004)

Pharmacology Toxicology

Toxicologic Mechanism

    A) Osmium tetroxide is a direct irritant of the eyes, skin, and mucous membranes (Proctor, 1988; ACGIH, 1986). It has caused kidney injury by an unknown mechanism (Honkenen, 1987).

Physicochemical

Physical Characteristics

    A) Osmium tetroxide is a noncombustible, colorless to pale yellow, crystalline solid or crystalline mass with a disagreeable, pungent, irritating, acrid, bromine- or chlorine-like odor (HSDB, 2004; ACGIH, 2001; Budavari, 2001; Lewis, 2000; Hathaway et al, 1991).
    B) It sublimes easily and releases a poisonous and irritating vapor (ACGIH, 2001; Lewis, 1998; Grant & Schuman, 1993).

Molecular Weight

    A) 254.23

Other

    A) ODOR THRESHOLD
    1) air: 1.9 x 10(-3) ppm v/v (HSDB, 2004; Pohanish, 2002)
    2) water: 0.012 ppm w/v (HSDB, 2004)

References

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