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SULFURYL FLUORIDE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Sulfuryl fluoride is an odorless, colorless gas, and not very reactive. It is mainly used in its gaseous state for its fumigant insecticide effects. When heated to decomposition, it emits very toxic fumes of fluorine and sulfur oxides.

Specific Substances

    1) Sulfuryl fluoride
    2) Fluorure de sulfuryle (French)
    3) Sulfuric oxyfluoride
    4) Sulphuryl fluoride
    5) Vikane
    6) Vikane fumigant
    7) STCC 4904578
    8) NIOSH/RTECS WT 5075000
    9) Molecular Formula: S-O2-F2
    10) CAS 2699-79-8
    11) References: RTECS, 1988
    1.2.1) MOLECULAR FORMULA
    1) S-O2-F2

Available Forms Sources

    A) FORMS
    1) Sulfuryl fluoride is a colorless, odorless, nonflammable gas which is not very reactive and is not hydrolyzed by water (Budavari, 1996; ITI, 1995; ACGIH, 1991; Lewis, 2000).
    a) This material may be shipped as a liquified gas under its own vapor pressure (AAR, 1998). The gas is heavier than air (AAR, 1998).
    B) SOURCES
    1) Sulfuryl fluoride is prepared by heating Ba(SO3F)2 (Budavari, 1996).
    C) USES
    1) Sulfuryl fluoride is used as a fumigant insecticide and in organic synthesis for dyestuffs and pharmaceuticals (Scheffrahn et al, 1989; ITI, 1995; ACGIH, 1991; Budavari, 1996). Scheffrahn et al (1989) studied the residue fluoride levels in frozen foodstuffs fumigated with conventional amounts of sulfuryl fluoride (that used to fumigate food establishments) and determined the residues would probably not exceed 1 ppm.
    2) Sulfuryl fluoride is frequently used as a "tent fumigant" where an entire structure is enclosed in plastic sheeting and the agent used to fill the plastic tent (Scheuerman, 1986).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) INHALATION - Sulfuryl fluoride is heavier than air and prolonged breathing may result in fatal hypoxia. Nose, throat, and respiratory tract irritation may occur. Death has resulted from pulmonary edema and respiratory arrest following inhalation exposure.
    B) TOPICAL - Contact with escaping liquefied gas may cause frostbite injury. Eye irritation may occur with direct corneal contact.
    C) Paresthesias or seizures may develop. Nausea, vomiting, abdominal pain, diffuse rhonchi, hypotension, carpopedal spasm, dysrhythmias, and pruritus may occur.
    D) EXPERIMENTAL ANIMALS - In experimental animals CNS depression, tremors, seizures, pulmonary edema, and liver and kidney injury have been reported.
    0.2.5) CARDIOVASCULAR
    A) Cardiac dysrhythmias and hypotension may develop in patients with patients with severe poisoning.
    0.2.6) RESPIRATORY
    A) Dyspnea, irritation, and pulmonary edema can occur.
    0.2.7) NEUROLOGIC
    A) Weakness, restlessness, seizures, and CNS depression may occur. Long-term exposure may be associated with olfactory deficits and subclinical CNS effects.
    0.2.8) GASTROINTESTINAL
    A) Nausea, vomiting, drooling, and fecal incontinence may occur following acute ingestion exposure.
    0.2.20) REPRODUCTIVE
    A) Inhalation exposure to sulfuryl fluoride was not teratogenic or embryotoxic in rats or rabbits.

Laboratory Monitoring

    A) Serum fluoride and calcium levels may be useful following ingestion or significant inhalation exposure.
    B) 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.
    C) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.

Treatment Overview

    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) Endotracheal intubation, supplemental oxygenation, and assisted ventilation may be required. Calcium replacement therapy may be needed.
    C) 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.
    D) SEIZURES: Administer a benzodiazepine; DIAZEPAM (ADULT: 5 to 10 mg IV initially; repeat every 5 to 20 minutes as needed. CHILD: 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) or LORAZEPAM (ADULT: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist. CHILD: 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).
    1) Consider phenobarbital or propofol if seizures recur after diazepam 30 mg (adults) or 10 mg (children greater than 5 years).
    2) Monitor for hypotension, dysrhythmias, respiratory depression, and need for endotracheal intubation. Evaluate for hypoglycemia, electrolyte disturbances, and hypoxia.
    E) Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    F) VENTRICULAR DYSRHYTHMIAS SUMMARY
    1) Obtain an ECG, institute continuous cardiac monitoring and administer oxygen. Evaluate for hypoxia, acidosis, and electrolyte disorders (particularly hypokalemia, hypocalcemia, and hypomagnesemia). Lidocaine and amiodarone are generally first line agents for stable monomorphic ventricular tachycardia, particularly in patients with underlying impaired cardiac function. Amiodarone should be used with caution if a substance that prolongs the QT interval and/or causes torsades de pointes is involved in the overdose. Unstable rhythms require immediate cardioversion.
    G) TORSADES DE POINTES: Hemodynamically unstable patients require electrical cardioversion. Treat stable patients with magnesium (first-line agent) and/or atrial overdrive pacing. Correct electrolyte abnormalities (ie, hypomagnesemia, hypokalemia, hypocalcemia) and hypoxia, if present.
    1) MAGNESIUM SULFATE/DOSE: ADULT: 1 to 2 grams diluted in 10 milliliters D5W IV/IO over 15 minutes. An optimal dose has not been established. Followed if needed by a second 2 gram bolus and an infusion of 0.5 to 1 gram/hour, if dysrhythmias recur. CHILDREN: 25 to 50 mg/kg diluted to 10 mg/mL; infuse IV over 5 to 15 minutes.
    2) OVERDRIVE PACING: Begin at 130 to 150 beats per minute, decrease as tolerated.
    3) Avoid class Ia (eg, quinidine, disopyramide, procainamide), class Ic (eg, flecainide, encainide, propafenone) and most class III antidysrhythmics (eg, N-acetylprocainamide, sotalol).
    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) Rewarming and a variety of topical treatments have been recommended for treating frostbite injuries (See Main Section).

Range Of Toxicity

    A) Two fatalities occurred in a couple who lived in an 80,000 cubic foot house fumigated with 250 pounds of sulfuryl fluoride. Following fumigation, no one should enter the area without a self-contained breathing apparatus until measured air concentrations are below 5 ppm.

Clinical Effects

Summary Of Exposure

    A) INHALATION - Sulfuryl fluoride is heavier than air and prolonged breathing may result in fatal hypoxia. Nose, throat, and respiratory tract irritation may occur. Death has resulted from pulmonary edema and respiratory arrest following inhalation exposure.
    B) TOPICAL - Contact with escaping liquefied gas may cause frostbite injury. Eye irritation may occur with direct corneal contact.
    C) Paresthesias or seizures may develop. Nausea, vomiting, abdominal pain, diffuse rhonchi, hypotension, carpopedal spasm, dysrhythmias, and pruritus may occur.
    D) EXPERIMENTAL ANIMALS - In experimental animals CNS depression, tremors, seizures, pulmonary edema, and liver and kidney injury have been reported.

Heent

    3.4.2) HEAD
    A) ANIMAL STUDIES
    1) Fluorosis of the teeth was reported in some animals with chronic exposure (ACGIH, 1991; Mattsson et al, 1988). This effect has not been reported in exposed humans.
    3.4.3) EYES
    A) Eye irritation may occur (HSDB , 2001; Sittig, 1991). Eye irritation is not as severe as that found after sulfuryl chloride exposure (Grant & Schuman, 1993).
    3.4.5) NOSE
    A) Irritation of the mucosa of the nose and throat may occur following inhalation exposures (HSDB , 2001; Sittig, 1991; Gosselin et al, 1984).
    3.4.6) THROAT
    A) Irritation of the mucosa of the nose and throat may occur following inhalation exposures (HSDB , 2001; Sittig, 1991; Gosselin et al, 1984).

Cardiovascular

    3.5.1) SUMMARY
    A) Cardiac dysrhythmias and hypotension may develop in patients with patients with severe poisoning.
    3.5.2) CLINICAL EFFECTS
    A) CARDIAC ARREST
    1) CASE REPORT - Cardiopulmonary arrest occurred in one victim who developed pulmonary edema following inhalation exposure (CDC, 1987).
    B) CONDUCTION DISORDER OF THE HEART
    1) Ventricular and supraventricular dysrhythmias have been reported in humans with sulfuryl fluoride intoxication.
    2) CASE REPORT - An elderly woman developed fatal ventricular tachycardia secondary to sulfuryl fluoride intoxication (HSDB , 2001) CDC, 1987).
    3) CASE REPORT - A 19-year-old woman developed supraventricular tachycardia 6 hours after exposure to high airborne levels of sulfuryl fluoride (Scheuerman, 1986). Several hours later the patient developed severe cardiac dysrhythmias and died. Serum fluoride level was 20 milligrams/liter; serum calcium was not obtained.
    C) HYPOTENSIVE EPISODE
    1) CASE REPORT - Hypotension was reported in one fatal case (Scheuerman, 1986).
    3.5.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) CIRCULATORY FAILURE
    a) Experimental animals exposed to low concentrations of sulfuryl fluoride first had parasympathetic responses followed by cardiovascular collapse and pulmonary edema (Scheuerman, 1986).

Respiratory

    3.6.1) SUMMARY
    A) Dyspnea, irritation, and pulmonary edema can occur.
    3.6.2) CLINICAL EFFECTS
    A) DISORDER OF RESPIRATORY SYSTEM
    1) Respiratory tract irritation may occur (Sittig, 1991). Cough, hyperventilation, and chest discomfort develop (Scheuerman, 1986). Rales may be noted on physical examination (Scheuerman, 1986).
    B) ACUTE LUNG INJURY
    1) Diffuse rhonchi, respiratory tract irritation with dyspnea, and death from pulmonary edema have occurred following inhalation exposure (CDC, 1987; (Taxay, 1966; Sittig, 1991; Scheuerman, 1986). Delayed pulmonary damage may occur with no warning symptoms following exposure to the fumigant vapor (Grant & Schuman, 1993).
    C) INJURY DUE TO ASPHYXIATION
    1) Sulfuryl fluoride gas is heavier than air and can cause asphyxial hypoxic death (AAR, 1998).
    D) HYPOXEMIA
    1) CASE REPORT - An elderly couple died following exposure to sulfuryl fluoride after their house was fumigated. The man experienced severe dyspnea and cough and then a generalized seizure followed by cardiac arrest. The wife had dyspnea and was admitted to hospital; diffuse pulmonary infiltrates were seen on chest x-ray. The wife died in ventricular fibrillation (CDC, 1987).
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) CYANOSIS
    a) Rats exposed to high concentrations (10,000 ppm) of sulfuryl fluoride became cyanotic. Some had seizures followed by 15 to 30 seconds of apnea (Nitschke et al, 1986).
    2) PULMONARY HEMORRHAGE
    a) Experimental animals fatally exposed to higher concentrations of sulfuryl fluoride had pulmonary congestion and alveolar hemorrhage (Eisenbrandt & Nitschke, 1989). Mild pulmonary inflammation was found in rats exposed to an airborne concentration of 300 ppm for 6 hours/day, 5 days/week for 13 weeks (Mattsson et al, 1988).

Neurologic

    3.7.1) SUMMARY
    A) Weakness, restlessness, seizures, and CNS depression may occur. Long-term exposure may be associated with olfactory deficits and subclinical CNS effects.
    3.7.2) CLINICAL EFFECTS
    A) CENTRAL NERVOUS SYSTEM DEFICIT
    1) Central nervous system depression may occur at high concentrations (Hathaway et al, 1996; Lewis, 2000).
    B) SEIZURE
    1) Weakness, restlessness, and generalized seizures have been reported in humans exposed by inhalation (HSDB , 2001) CDC, 1987).
    C) PARESTHESIA
    1) Overexposure may result in paresthesias (HSDB , 2001). Transient paresthesias in one leg has been noted in a human (Taxay, 1966).
    D) CEREBRAL EDEMA
    1) Cerebral edema was found at autopsy in one fatal case (Scheuerman, 1986).
    E) TETANY
    1) Carpal-pedal tetany developed as a pre-mortem event in one fatal case (Scheuerman, 1986) and might have been a manifestation of hypocalcemia.
    F) CENTRAL NERVOUS SYSTEM FINDING
    1) Fumigation workers with median sulfuryl fluoride exposure of 2.85 years had significantly reduced performance on the pattern memory test and in testing of olfaction (Calvert et al, 1998).
    a) No pattern of widespread cognition deficits was found. These workers were also exposed to methyl bromide (Calvert et al, 1998).
    3.7.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) NEUROPATHY
    a) RABBITS exposed to airborne concentrations of 300 to 600 ppm of sulfuryl fluoride for 2 weeks had neurophysiologic changes characterized by focal malacia and vacuolation (Eisenbrandt & Nitschke, 1989).
    2) SEIZURES
    a) Tremors, seizures and CNS depression have occurred in exposed experimental animals (Hathaway et al, 1996; ACGIH, 1991) O'Donoghue, 1985; (Nitschke et al, 1986).
    3) EEG ABNORMAL
    a) Rats exposed to acute lethal concentrations of sulfuryl fluoride had only minor changes on the EEG; decreased power and some sharp waves. In rats exposed to an airborne concentration of 300 ppm minimal vacuolation was found in the area of the caudateputamen nuclei. No necrosis or neuronal destruction was found (Mattsson et al, 1988).

Gastrointestinal

    3.8.1) SUMMARY
    A) Nausea, vomiting, drooling, and fecal incontinence may occur following acute ingestion exposure.
    3.8.2) CLINICAL EFFECTS
    A) VOMITING
    1) Anorexia, nausea, vomiting, and cramping abdominal pain have been noted in humans exposed by inhalation (Taxay, 1966) CDC, 1987; (Lewis, 2000; HSDB , 2001).
    B) INCONTINENCE OF FECES
    1) Fecal incontinence and drooling has been reported in exposed humans. These may be parasympathetic effects (Scheuerman, 1986).

Hepatic

    3.9.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) HEPATOCELLULAR DAMAGE
    a) Chronically exposed experimental animals developed hepatic injury (ACGIH, 1991; Hathaway et al, 1996). This effect has not been reported in exposed humans.

Genitourinary

    3.10.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) NEPHROPATHY TOXIC
    a) Chronically exposed experimental animals have developed kidney injury (ACGIH, 1991; Hathaway et al, 1996; Eisenbrandt & Nitschke, 1989; Mattsson et al, 1988). This effect has not been reported in exposed humans.

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) FROSTBITE
    1) Dermal exposure to the liquefied gas can cause frostbite injury (AAR, 1998).
    B) ITCHING OF SKIN
    1) Pruritus has been noted after dermal exposure (Taxay, 1966; Lewis, 2000; HSDB , 2001).

Reproductive

    3.20.1) SUMMARY
    A) Inhalation exposure to sulfuryl fluoride was not teratogenic or embryotoxic in rats or rabbits.
    3.20.2) TERATOGENICITY
    A) LACK OF EFFECT
    1) EXPERIMENTAL ANIMAL DATA - Inhalation exposure to sulfuryl fluoride was not teratogenic in rats or rabbits exposed to airborne levels of up to 225 ppm for 6 hours/day during the period of major organogenesis (Hanley et al, 1989).
    3.20.3) EFFECTS IN PREGNANCY
    A) LACK OF EFFECT
    1) EXPERIMENTAL ANIMAL DATA - Inhalation exposure to sulfuryl fluoride was not embryotoxic or fetotoxic in rats exposed to airborne levels of up to 225 ppm for 6 hr/day during the period of major organogenesis. (Hanley et al, 1989).
    2) Inhalation exposure to sulfuryl fluoride was not embryotoxic in rabbits exposed to airborne levels of up to 225 ppm for 6 hr/day during the period of major organogenesis; fetotoxicity was observed (Hanley et al, 1989).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS2699-79-8 (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) At the time of this review, no data were available to assess the carcinogenic or mutagenic potential of this agent.

Laboratory Monitoring

Radiographic Studies

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

Methods

    A) MULTIPLE ANALYTICAL METHODS
    1) Air levels may be measured by gas liquid chromatography following collection of samples by fritted bubbler or impinger (Sittig, 1991).
    2) A Conway diffusion cell and spectrophotometric method was used by Scheuerman (1986) to measure fluoride concentrations as the sodium salt in serum or plasma.

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Serum fluoride and calcium levels may be useful following ingestion or significant inhalation exposure.
    B) 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.
    C) 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) Monitoring serum fluoride and calcium levels may be valuable in patients with significant exposure (Scheuerman, 1986).
    2) 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) MONITORING
    a) Obtain an ECG and institute continuous cardiac monitoring.
    b) If respiratory tract irritation is present, monitor arterial blood gases and chest x-ray.
    2) PULMONARY FUNCTION TESTS
    a) If respiratory tract irritation is present, it may be useful to monitor pulmonary function tests.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.3) DISPOSITION/INHALATION EXPOSURE
    6.3.3.5) OBSERVATION CRITERIA/INHALATION
    A) Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    B) Monitor liver and renal functions and serum fluoride and calcium levels in patients with significant exposure.

Monitoring

    A) Serum fluoride and calcium levels may be useful following ingestion or significant inhalation exposure.
    B) 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.
    C) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) INHALATION EXPOSURE
    1) Remove victims of inhalation exposure from the toxic environment and administer 100 percent supplemental humidified oxygen with assisted ventilation as required. Rescuers should not enter areas with suspected high air concentrations without self-contained breathing apparatus.
    B) DERMAL EXPOSURE
    1) TOPICAL: Rewarming and a variety of topical treatments have been recommended for treating frostbite injuries.

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) AIRWAY MANAGEMENT
    1) If coma or seizures occur, assure airway patency and adequacy of ventilation and oxygenation. Endotracheal intubation, supplemental oxygenation, and assisted ventilation could be required.
    B) IRRITATION SYMPTOM
    1) Respiratory tract irritation, if severe, can progress to pulmonary edema which may be delayed in onset up to 24 to 72 hours after exposure in some cases.
    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) SEIZURE
    1) In a rat model of severe sulfuryl fluoride intoxication, phenobarbital reduced the incidence of seizures and delayed death, diazepam was less effective than phenobarbital, and phenytoin was ineffective in controlling seizures (Nitschke et al, 1986).
    2) 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).
    3) 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 .
    4) 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).
    5) 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).
    6) 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).
    7) 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).
    E) HYPOTENSIVE EPISODE
    1) SUMMARY
    a) Infuse 10 to 20 milliliters/kilogram of isotonic fluid and keep the patient supine. If hypotension persists, administer dopamine or norepinephrine. Consider central venous pressure monitoring to guide further fluid therapy.
    2) DOPAMINE
    a) DOSE: Begin at 5 micrograms per kilogram per minute progressing in 5 micrograms per kilogram per minute increments as needed (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). If hypotension persists, dopamine may need to be discontinued and a more potent vasoconstrictor (eg, norepinephrine) should be considered (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    b) CAUTION: If ventricular dysrhythmias occur, decrease rate of administration (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). Extravasation may cause local tissue necrosis, administration through a central venous catheter is preferred (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    3) NOREPINEPHRINE
    a) PREPARATION: 4 milligrams (1 amp) added to 1000 milliliters of diluent provides a concentration of 4 micrograms/milliliter of norepinephrine base. Norepinephrine bitartrate should be mixed in dextrose solutions (dextrose 5% in water, dextrose 5% in saline) since dextrose-containing solutions protect against excessive oxidation and subsequent potency loss. Administration in saline alone is not recommended (Prod Info norepinephrine bitartrate injection, 2005).
    b) DOSE
    1) ADULT: Dose range: 0.1 to 0.5 microgram/kilogram/minute (eg, 70 kg adult 7 to 35 mcg/min); titrate to maintain adequate blood pressure (Peberdy et al, 2010).
    2) CHILD: Dose range: 0.1 to 2 micrograms/kilogram/minute; titrate to maintain adequate blood pressure (Kleinman et al, 2010).
    3) CAUTION: Extravasation may cause local tissue ischemia, administration by central venous catheter is advised (Peberdy et al, 2010).
    F) VENTRICULAR ARRHYTHMIA
    1) VENTRICULAR DYSRHYTHMIAS SUMMARY
    a) Obtain an ECG, institute continuous cardiac monitoring and administer oxygen. Evaluate for hypoxia, acidosis, and electrolyte disorders (particularly hypokalemia, hypocalcemia, and hypomagnesemia). Lidocaine and amiodarone are generally first line agents for stable monomorphic ventricular tachycardia, particularly in patients with underlying impaired cardiac function. Amiodarone should be used with caution if a substance that prolongs the QT interval and/or causes torsades de pointes is involved in the overdose. Unstable rhythms require immediate cardioversion.
    2) LIDOCAINE
    a) LIDOCAINE/DOSE
    1) ADULT: 1 to 1.5 milligrams/kilogram via intravenous push. For refractory VT/VF an additional bolus of 0.5 to 0.75 milligram/kilogram can be given at 5 to 10 minute intervals to a maximum dose of 3 milligrams/kilogram (Neumar et al, 2010). Only bolus therapy is recommended during cardiac arrest.
    a) Once circulation has been restored begin a maintenance infusion of 1 to 4 milligrams per minute. If dysrhythmias recur during infusion repeat 0.5 milligram/kilogram bolus and increase the infusion rate incrementally (maximal infusion rate is 4 milligrams/minute) (Neumar et al, 2010).
    2) CHILD: 1 milligram/kilogram initial bolus IV/IO; followed by a continuous infusion of 20 to 50 micrograms/kilogram/minute (de Caen et al, 2015).
    b) LIDOCAINE/MAJOR ADVERSE REACTIONS
    1) Paresthesias; muscle twitching; confusion; slurred speech; seizures; respiratory depression or arrest; bradycardia; coma. May cause significant AV block or worsen pre-existing block. Prophylactic pacemaker may be required in the face of bifascicular, second degree, or third degree heart block (Prod Info Lidocaine HCl intravenous injection solution, 2006; Neumar et al, 2010).
    c) LIDOCAINE/MONITORING PARAMETERS
    1) Monitor ECG continuously; plasma concentrations as indicated (Prod Info Lidocaine HCl intravenous injection solution, 2006).
    G) TORSADES DE POINTES
    1) SUMMARY
    a) Withdraw the causative agent. Hemodynamically unstable patients with Torsades de pointes (TdP) require electrical cardioversion. Emergent treatment with magnesium (first-line agent) or atrial overdrive pacing is indicated. Detect and correct underlying electrolyte abnormalities (ie, hypomagnesemia, hypokalemia, hypocalcemia). Correct hypoxia, if present (Drew et al, 2010; Neumar et al, 2010; Keren et al, 1981; Smith & Gallagher, 1980).
    b) Polymorphic VT associated with acquired long QT syndrome may be treated with IV magnesium. Overdrive pacing or isoproterenol may be successful in terminating TdP, particularly when accompanied by bradycardia or if TdP appears to be precipitated by pauses in rhythm (Neumar et al, 2010). In patients with polymorphic VT with a normal QT interval, magnesium is unlikely to be effective (Link et al, 2015).
    2) MAGNESIUM SULFATE
    a) Magnesium is recommended (first-line agent) for the prevention and treatment of drug-induced torsades de pointes (TdP) even if the serum magnesium concentration is normal. QTc intervals greater than 500 milliseconds after a potential drug overdose may correlate with the development of TdP (Charlton et al, 2010; Drew et al, 2010). ADULT DOSE: No clearly established guidelines exist; an optimal dosing regimen has not been established. Administer 1 to 2 grams diluted in 10 milliliters D5W IV/IO over 15 minutes (Neumar et al, 2010). Followed if needed by a second 2 gram bolus and an infusion of 0.5 to 1 gram (4 to 8 mEq) per hour in patients not responding to the initial bolus or with recurrence of dysrhythmias (American Heart Association, 2005; Perticone et al, 1997). Rate of infusion may be increased if dysrhythmias recur. For persistent refractory dysrhythmias, a continuous infusion of up to 3 to 10 milligrams/minute in adults may be given (Charlton et al, 2010).
    b) PEDIATRIC DOSE: 25 to 50 milligrams/kilogram diluted to 10 milligrams/milliliter for intravenous infusion over 5 to 15 minutes up to 2 g (Charlton et al, 2010).
    c) PRECAUTIONS: Use with caution in patients with renal insufficiency.
    d) MAJOR ADVERSE EFFECTS: High doses may cause hypotension, respiratory depression, and CNS toxicity (Neumar et al, 2010). Toxicity may be observed at magnesium levels of 3.5 to 4.0 mEq/L or greater (Charlton et al, 2010).
    e) MONITORING PARAMETERS: Monitor heart rate and rhythm, blood pressure, respiratory rate, motor strength, deep tendon reflexes, serum magnesium, phosphorus, and calcium concentrations (Prod Info magnesium sulfate heptahydrate IV, IM injection, solution, 2009).
    3) OVERDRIVE PACING
    a) Institute electrical overdrive pacing at a rate of 130 to 150 beats per minute, and decrease as tolerated. Rates of 100 to 120 beats per minute may terminate torsades (American Heart Association, 2005). Pacing can be used to suppress self-limited runs of TdP that may progress to unstable or refractory TdP, or for override refractory, persistent TdP before the potential development of ventricular fibrillation (Charlton et al, 2010). In a case series overdrive pacing was successful in terminating TdP associated with bradycardia and drug-induced QT prolongation (Neumar et al, 2010).
    4) POTASSIUM REPLETION
    a) Potassium supplementation, even if serum potassium is normal, has been recommended by many experts (Charlton et al, 2010; American Heart Association, 2005). Supplementation to supratherapeutic potassium concentrations of 4.5 to 5 mmol/L has been suggested, although there is little evidence to determine the optimal range in dysrhythmia (Drew et al, 2010; Charlton et al, 2010).
    5) ISOPROTERENOL
    a) Isoproterenol has been successful in aborting torsades de pointes that was resistant to magnesium therapy in a patient in whom transvenous overdrive pacing was not an option (Charlton et al, 2010) and has been successfully used to treat torsades de pointes associated with bradycardia and drug induced QT prolongation (Keren et al, 1981; Neumar et al, 2010). Isoproterenol may have a limited role in pharmacologic overdrive pacing in select patients with drug-induced torsades de pointes and acquired long QT syndrome (Charlton et al, 2010; Neumar et al, 2010). Isoproterenol should be avoided in patients with polymorphic VT associated with familial long QT syndrome (Neumar et al, 2010).
    b) DOSE: ADULT: 2 to 10 micrograms/minute via a continuous monitored intravenous infusion; titrate to heart rate and rhythm response (Neumar et al, 2010).
    c) PRECAUTIONS: Correct hypovolemia before using; contraindicated in patients with acute cardiac ischemia (Prod Info Isuprel(TM) intravenous injection, intramuscular injection, subcutaneous injection, intracardiac injection, 2013).
    1) Contraindicated in patients with preexisting dysrhythmias; tachycardia or heart block due to digitalis toxicity; ventricular dysrhythmias that require inotropic therapy; and angina. Use with caution in patients with coronary insufficiency (Prod Info Isuprel(TM) intravenous injection, intramuscular injection, subcutaneous injection, intracardiac injection, 2013).
    d) MAJOR ADVERSE EFFECTS: Tachycardia, cardiac dysrhythmias, palpitations, hypotension or hypertension, nervousness, headache, dizziness, and dyspnea (Prod Info Isuprel(TM) intravenous injection, intramuscular injection, subcutaneous injection, intracardiac injection, 2013).
    e) MONITORING PARAMETERS: Monitor heart rate and rhythm, blood pressure, respirations and central venous pressure to guide volume replacement (Prod Info Isuprel(TM) intravenous injection, intramuscular injection, subcutaneous injection, intracardiac injection, 2013).
    6) OTHER DRUGS
    a) Mexiletine, verapamil, propranolol, and labetalol have also been used to treat TdP, but results have been inconsistent (Khan & Gowda, 2004).
    7) AVOID
    a) Avoid class Ia antidysrhythmics (eg, quinidine, disopyramide, procainamide, aprindine), class Ic (eg, flecainide, encainide, propafenone) and most class III antidysrhythmics (eg, N-acetylprocainamide, sotalol) since they may further prolong the QT interval and have been associated with TdP.
    H) HYPOCALCEMIA
    1) If seriously elevated levels of fluoride are present together with symptoms of systemic fluorosis, ECG changes or hypocalcemia, administer intravenous calcium.
    2) In a rat model of severe sulfuryl fluoride toxicity, pretreatment with calcium gluconate improved survival in the group exposed to 4,000 ppm for 45 minutes to 4 of 5 rats, compared with 0 of 5 rats surviving without calcium gluconate treatment, and 0 of 5 rats surviving receiving calcium gluconate after sulfuryl fluoride exposure (Nitschke et al, 1986).

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).

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) FROSTBITE
    1) PREHOSPITAL
    a) Rewarming of a localized area should only be considered if the risk of refreezing is unlikely. Avoid rubbing the frozen area which may cause further damage to the area (Grieve et al, 2011; Hallam et al, 2010).
    2) REWARMING
    a) Do not institute rewarming unless complete rewarming can be assured; refreezing thawed tissue increases tissue damage. Place affected area in a water bath with a temperature of 40 to 42 degrees Celsius for 15 to 30 minutes until thawing is complete. The bath should be large enough to permit complete immersion of the injured part, avoiding contact with the sides of the bath. A whirlpool bath would be ideal. Some authors suggest a mild antibacterial (ie, chlorhexidine, hexachlorophene or povidone-iodine) be added to the bath water. Tissues should be thoroughly rewarmed and pliable; the skin will appear a red-purple color (Grieve et al, 2011; Hallam et al, 2010; Murphy et al, 2000).
    b) Correct systemic hypothermia which can cause cold diuresis due to suppression of antidiuretic hormone; consider IV fluids (Grieve et al, 2011).
    c) Rewarming may be associated with increasing acute pain, requiring narcotic analgesics.
    d) For severe frostbite, clinical trials have shown that pentoxifylline, a phosphodiesterase inhibitor, can enhance tissue viability by increasing blood flow and reducing platelet activity (Hallam et al, 2010).
    3) WOUND CARE
    a) Digits should be separated by sterile absorbent cotton; no constrictive dressings should be used. Protective dressings should be changed twice per day.
    b) Perform twice daily hydrotherapy for 30 to 45 minutes in warm water at 40 degrees Celsius. This helps debride devitalized tissue and maintain range of motion. Keep the area warm and dry between treatments (Hallam et al, 2010; Murphy et al, 2000).
    c) The injured extremities should be elevated and should not be allowed to bear weight.
    d) In patients at risk for infection of necrotic tissue, prophylactic antibiotics and tetanus toxoid have been recommended by some authors (Hallam et al, 2010; Murphy et al, 2000).
    e) Non-tense clear blisters should be left intact due to the risk of infection; tense or hemorrhagic blisters may be carefully aspirated in a setting where aseptic technique is provided (Hallam et al, 2010).
    f) Further surgical debridement should be delayed until mummification demarcation has occurred (60 to 90 days). Spontaneous amputation may occur.
    g) Analgesics may be required during the rewarming phase; however, patients with severe pain should be evaluated for vasospasm.
    h) IMAGING: Arteriography and noninvasive vascular techniques (e.g., plain radiography, laser Doppler studies, digital plethysmography, infrared thermography, isotope scanning), have been useful in evaluating the extent of vasospasm after thawing and assessing whether debridement is needed (Hallam et al, 2010). In cases of severe frostbite, Technetium 99 (triple phase scanning) and MRI angiography have been shown to be the most useful to assess injury and determine the extent or need for surgical debridement (Hallam et al, 2010).
    i) TOPICAL THERAPY: Topical aloe vera may decrease tissue destruction and should be applied every 6 hours (Murphy et al, 2000).
    j) IBUPROFEN THERAPY: Ibuprofen, a thromboxane inhibitor, may help limit inflammatory damage and reduce tissue loss (Grieve et al, 2011; Murphy et al, 2000). DOSE: 400 mg orally every 12 hours is recommended (Hallam et al, 2010).
    k) THROMBOLYTIC THERAPY: Thrombolysis (intra-arterial or intravenous thrombolytic agents) may be beneficial in those patients at risk to lose a digit or a limb, if done within the first 24 hours of exposure. The use of tissue plasminogen activator (t-PA) to clear microvascular thromboses can restore arterial blood flow, but should be accompanied by close monitoring including angiography or technetium scanning to evaluate the injury and to evaluate the effects of t-PA administration. Potential risk of the procedure includes significant tissue edema that can lead to a rise in interstitial pressures resulting in compartment syndrome (Grieve et al, 2011).
    l) CONTROVERSIAL: Adjunct pharmacological agents (ie, heparin, vasodilators, prostacyclins, prostaglandin synthetase inhibitors, dextran) are controversial and not routinely recommended. The role of hyperbaric oxygen therapy, sympathectomy remains unclear (Grieve et al, 2011).
    m) CHRONIC PAIN: Vasomotor dysfunction can produce chronic pain. Amitriptyline has been used in some patients; some patients may need a referral for pain management. Inability to tolerate the cold (in the affected area) has been observed following a single episode of frostbite (Hallam et al, 2010).
    n) MORBIDITIES: Frostbite can produce localized osteoporosis and possible bone loss following a severe case. These events may take a year or more to develop. Children may be at greater risk to develop more severe events (ie, early arthritis) (Hallam et al, 2010).
    B) GENERAL TREATMENT
    1) Treatment should include recommendations listed in the INHALATION EXPOSURE section when appropriate.

Abstracts

Case Reports

    A) ADULT
    1) Taxay (1966) reported a worker who inhaled a mixture of sulfuryl fluoride and chloropicrin for 4 hours in a confined space. Nausea, vomiting, cramping abdominal pain, pruritus, diffuse rhonchi, and paresthesias of the right leg developed, which rapidly subsided.
    2) An elderly couple died when their house was fumigated with sulfuryl fluoride; about 250 pounds of sulfuryl were used (MMWR, 1987).
    a) The homeowners developed weakness, nausea, vomiting, chills, dyspnea, restlessness, anorexia, cough, generalized seizures, cardiopulmonary arrest, hypoxemia, and pulmonary infiltrates. At autopsy, both had acute pulmonary edema which was the likely cause of death
    b) One had an elevated serum fluoride level postmortem (0.5 mg/L; normals: 0.01 mg/L).
    3) Scheuerman (1986) described three fatal cases of sulfuryl fluoride exposure.
    a) A 29-year-old male apparently committed suicide by entering an apartment that had been tent-fumigated with 50 pounds (22.5 kg) of sulfuryl fluoride. Postmortem examination revealed pulmonary edema and postmortem blood fluoride level was 50.42 mg/L.
    b) A 22-year-old male was found dead next to an empty tank in a warehouse which normally held 70 pounds (31.5 kg) of sulfuryl fluoride. Pulmonary and cerebral edema were found at autopsy.
    c) A 19-year-old female entered a building which had been tent-fumigated with sulfuryl fluoride. The patient was initially alert, coughing, and complaining of chest discomfort. Shortly after arriving at an emergency department, hypotension and rales were noted. By six hours after exposure, hyperexcitability, hyperventilation, supraventricular tachycardia, and productive cough with drooling developed as well as pulmonary edema, carpal-pedal tetany, cardiac dysrhythmias, and the patient eventually died. Pulmonary edema was found at postmortem examination and a pre-mortem blood fluoride level was 20 mg/L.
    d) Eight construction workers entered a tarped house which had been fumigated with sulfuryl fluoride. Three workers reported dizziness and exposures were estimated to be from 10 to 20 minutes at airborne levels subsequently measured at 0 to 5 ppm (Maddy & Edmiston, 1988).
    e) Two fatal incidents in California in 1986 occurred when persons entered tarped buildings earlier fumigated with sulfuryl fluoride (Maddy & Edmiston, 1988).

Range Of Toxicity

Summary

    A) Two fatalities occurred in a couple who lived in an 80,000 cubic foot house fumigated with 250 pounds of sulfuryl fluoride. Following fumigation, no one should enter the area without a self-contained breathing apparatus until measured air concentrations are below 5 ppm.

Minimum Lethal Exposure

    A) CASE REPORTS
    1) Two fatalities occurred in an elderly couple who lived in an 80,000 cubic foot house fumigated with 250 pounds of sulfuryl fluoride (MMWR, 1987).
    2) Two fatal incidents in California in 1986 occurred when persons entered tarped buildings which had been earlier fumigated with sulfuryl fluoride (Maddy & Edmiston, 1988).

Maximum Tolerated Exposure

    A) CONCENTRATION LEVEL
    1) Following fumigation with sulfuryl fluoride, no one should enter the area until measured air concentrations are below 5 parts per million (MMWR, 1987). If the measured air levels are greater than 5 parts per million, a self-contained breathing apparatus should be worn if entry into the area is required (MMWR, 1987).
    B) OCCUPATIONAL
    1) CASE REPORT - Eight construction workers entered a tarped house which had been fumigated with sulfuryl fluoride; three of them reported dizziness; exposures were estimated to be from 10 to 20 minutes at levels subsequently measured at 0 to 5 parts per million (Maddy & Edmiston, 1988).
    C) ANIMAL DATA
    1) Experimental animals exposed to airborne concentrations of 1000 parts per million for 3 hours or 15,000 parts per million for six minutes had less than 5 percent fatalities (Hathaway et al, 1996).

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) CONCENTRATION LEVEL
    a) One of two victims who died from pulmonary edema following inhalation exposure to sulfuryl fluoride had an elevated serum fluoride level postmortem (0.5 milligram/liter; normals: 0.01 milligram/liter) (MMWR, 1987).
    b) Blood fluoride levels were 50.42 milligrams/liter (postmortem) and 20 milligrams/liter (premortem) in two fatal cases (Scheuerman, 1986).

Workplace Standards

    A) ACGIH TLV Values for CAS2699-79-8 (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) Sulfuryl fluoride
    a) TLV:
    1) TLV-TWA: 5 ppm
    2) TLV-STEL: 10 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): CNS impair
    d) Molecular Weight: 102.07
    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 CAS2699-79-8 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Sulfuryl fluoride
    2) REL:
    a) TWA: 5 ppm (20 mg/m(3))
    b) STEL: 10 ppm (40 mg/m(3))
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s):
    3) IDLH:
    a) IDLH: 200 ppm
    b) Note(s): Not Listed

    C) Carcinogenicity Ratings for CAS2699-79-8 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Sulfuryl fluoride
    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: Sulfuryl fluoride
    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 CAS2699-79-8 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Sulfuryl fluoride
    2) Table Z-1 for Sulfuryl fluoride:
    a) 8-hour TWA:
    1) ppm: 5
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3: 20
    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) Reference: RTECS, 2002
    1) LD50- (ORAL)RAT:
    a) 100 mg/kg

Pharmacology Toxicology

Toxicologic Mechanism

    A) Sulfuryl fluoride is a direct irritant of eyes and mucous membranes of the respiratory tract (HSDB , 2001; Sittig, 1991). Systemic absorption and systemic fluorosis with possible hypocalcemia can occur following inhalation exposure (MMWR, 1987; Scheuerman, 1986).
    B) The gas is shipped in a liquefied form, and frostbite injury can occur with dermal exposure (AAR, 1998).
    C) Sulfuryl fluoride may cause a parasympathetic stimulation. Release of free fluoride ion binds to calcium and may result in tetany, seizures and cardiac dysrhythmias. High airborne concentrations may evoke narcotic properties. Cardiovascular collapse may result from direct cellular toxic responses (Scheuerman, 1986; Mattsson et al, 1988; Nitschke et al, 1986).

Physicochemical

Physical Characteristics

    A) Sulfuryl fluoride is a colorless, odorless, nonflammable gas which is not very reactive and is not hydrolyzed by water (Budavari, 1996; ITI, 1995; ACGIH, 1991; Lewis, 2000).
    1) This material may be shipped as a liquefied gas under its own vapor pressure. The gas is heavier than air (AAR, 1998).

Molecular Weight

    A) 102.06 (RTECS , 2002)

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 Material in Surface Transportation, Bureau of Explosives, Association of American Railroads, Washington, DC, 1987, pp 661-662.
    14) ACGIH: Documentation of the Threshold Limit Values and Biological Exposure Indices, 6th ed, Am Conference of Govt Ind Hyg, Inc, Cincinnati, OH, 1991.
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