Contact Us    Contact Us     |     Feedback
MOBILE VIEW  | 

PHOSPHINE

Export To Excel

Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Phosphine is a colorless, flammable, poisonous gas.

Specific Substances

    A) PHOSPHINE
    1) Hydrogen Phosphide
    2) Phosphorus Hydride
    3) Phosphoretted Hydrogen
    4) Phosphorated Hydrogen
    5) Phosphorus Trihydride
    6) Molecular Formula: PH3
    7) CAS 7803-51-2
    ALUMINUM PHOSPHIDE
    1) Celphos
    2) Detia
    3) Delicia
    4) Detia Gas EX-B
    5) Gas EX-B
    6) Molecular Formula: AlP
    7) CAS 20859-73-8
    8) CAS 7803-51-2
    CALCIUM PHOSPHIDE
    1) Molecular Formula: Ca3P2
    2) Photophor
    3) CAS 1305-99-3
    ZINC PHOSPHIDE
    1) Molecular Formula: P2Zn3
    2) CAS 1314-84-7
    OTHER
    1) Aluminum Fosfide (Dutch)
    2) Fosforowodor (Polish)
    3) Phosphorwasserstoff (German)

    1.2.1) MOLECULAR FORMULA
    1) H3-P

Available Forms Sources

    A) FORMS
    1) Phosphine is a colorless, flammable, potentially poisonous gas (Windholz et al, 1983).
    2) ALUMINUM PHOSPHIDE
    a) Aluminum phosphide is available over-the-counter in India and human poisonings are common (Gupta & Ahlawat, 1995). Indian products are found as 3 gram pellets containing 57% aluminum phosphide. Trade names include Celphos, Quickphos, Synfume, and Phosfume (Chopra et al, 1986).
    b) A single 3 gram pellet of aluminum phosphide gives off 1 gram of phosphine (Jayaraman, 1991).
    c) Pellets are composed of aluminum phosphide, urea, and ammonium carbamate. Phosphine gas, ammonia, and carbon dioxide are the products of the reaction of the pellet, in air or in grain, and moisture (Zaebst et al, 1988).
    B) SOURCES
    1) Phosphine is produced by the action of water on calcium phosphide, by the quenching of metal alloys with water, and by the accidental wetting of zinc phosphide rodenticides and aluminum phosphide or magnesium phosphide grain fumigants (Finkel, 1983).
    2) Waste treatment can generate phosphine (Garry et al, 1989).
    3) Phosphine can be generated in illicit methamphetamine labs. One method of producing methamphetamine involves red phosphorus, hydriodic acid and ephedrine or pseudoephedrine. Phosphine can be produced when red phosphorus is heated in the presence of acids. A forensic specialist investigating a methamphetamine lab was exposed to 2.7 ppm phosphine for 20 to 30 minutes without respiratory protection. She developed dizziness, cough, headache and diarrhea and has rhonchi on physical exam (Burgess, 2001).
    C) USES
    1) Phosphine is used in organic preparations; preparations of phosphonium halides; as a doping agent for n-type semiconductors; a polymerization initiator; a condensation catalyst; and, as an insecticide used for fumigation. NOTE: A synthetic dye, crystalline yellow, is sometimes called phosphine (Sax & Lewis, 1987; Proctor et al, 1988; Garry et al, 1989).
    2) Outside the US, aluminum phosphide and zinc phosphide are used as household rodenticides. Phosphine gas is released on contact with water or if these substances are ingested (Lohani et al, 2000; Broderick & Birnbaum, 2002) Ragone et al, 2002.

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) USES: Phosphine (PH3) is a colorless, flammable toxic gas used in the semiconductor industry. It is also used as a fumigant, polymerization initiator, and as an intermediate for the preparation flame retardants. When pure, it is odorless, but technical grade samples have an unpleasant odor similar to garlic or rotting fish. Phosphine can also be generated in illicit methamphetamine labs, especially production involving red phosphorus, hydriodic acid, and ephedrine or pseudoephedrine. Phosphine is produced when red phosphorus is heated in the presence of acids. The vast majority of exposures are inhalational; when used as a fumigant, pellets of aluminum phosphide, calcium phosphide, or zinc phosphide release phosphine upon contact with atmospheric water or an organism's stomach acid. Phosphine is a gas at room temperature, so ingestion is unlikely. Toxicity from ingestion of aluminum phosphide or zinc phosphide are covered in separate managements.
    B) TOXICOLOGY: Phosphine exerts its toxic effects via inhibition of cytochrome oxidase and generation of free radical damage. Injury occurs primarily after inhalation exposure, though toxicity can occur from ingestion or transdermal contamination. Phosphine gas may form explosive mixtures with air and self ignite. When phosphine burns, a dense white cloud of phosphorus pentoxide, a severe respiratory irritant, is formed. Phosphine breaks down in water.
    C) EPIDEMIOLOGY: Human poisoning is uncommon, but occurs worldwide and can be fatal.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Exposure to phosphine gas may cause nausea and vomiting, abdominal pain, diarrhea, thirst, chest tightness, dyspnea, cough productive of sputum, jaundice, elevated liver enzymes, muscle pains, dizziness, headache, fatigue, ataxia, paresthesias, irritation of mucous membranes, acute renal failure with proteinuria, and hematopoietic cancers.
    2) SEVERE TOXICITY: More severe exposures may cause tachycardia and hypotension, metabolic acidosis, ventricular dysrhythmias, seizures, coma, acute lung injury (which may be delayed), and death. Direct contact with phosphine liquid may cause frostbite, but phosphine gas is not known to produce adverse effects on the skin. Phosphine gas produces no known adverse effects on the eyes. Contact with the skin or eyes to phosphine gas does not normally result in systemic toxicity.
    0.2.21) CARCINOGENICITY
    A) Hematopoietic system cancers have been seen in grain workers and fumigators.

Laboratory Monitoring

    A) Monitor vital signs and mental status.
    B) Monitor continuous pulse oximetry.
    C) Institute continuous cardiac monitoring and obtain an ECG.
    D) Monitor serum electrolytes, renal function, and liver enzymes.
    E) Obtain a chest radiograph in patients with respiratory symptoms.
    F) Echocardiogram may be useful to assess left ventricular function in patients with hypotension or pulmonary edema.

Treatment Overview

    0.4.3) INHALATION EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) For mild to moderate exposures, the mainstay of treatment is removal from phosphine exposure and supportive care. Monitoring of cardiac, hepatic, and renal functions should occur. Fluid and electrolytes should also be measured, and circulatory and respiratory support given as needed for symptoms.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) For severe overdoses, removal from phosphine exposure and supportive care are the most important initial measures. Severe metabolic acidosis can be treated with sodium bicarbonate and standard treatment for dysrhythmias may be needed. Respiratory distress with pulmonary edema and/or acute lung injury may be treated with supplementary oxygen and mechanical ventilation. Hypotension can be treated initially with fluids and then pressors (ie, dopamine, norepinephrine).
    C) DECONTAMINATION
    1) PREHOSPITAL: Move patient to fresh air as soon as possible.
    2) HOSPITAL: Administer oxygen. Wash exposed skin and irrigate exposed eyes.
    D) AIRWAY MANAGEMENT
    1) Airway management is one of the primary issues with phosphine toxicity and patients may get critically ill quickly; early intubation may be needed. Patients should be moved to fresh air as soon as possible, and treated with supplemental oxygen and assisted ventilation as needed. Bronchospasm can be treated with B2 agonists and oral or parenteral corticosteroids.
    E) ANTIDOTE
    1) None
    F) ENHANCED ELIMINATION
    1) Dialysis or hemoperfusion are unlikely to be helpful for phosphine exposures.
    G) PATIENT DISPOSITION
    1) HOME CRITERIA: There is no data to support home management.
    2) OBSERVATION CRITERIA: All patients with exposures should be sent to a healthcare facility for observation for at least a period of 6 to 8 hours of observation. Patients may be discharged home if they are asymptomatic or clearly improving and stable for discharge. Patients should be instructed to return immediately if any respiratory symptoms develop, as onset of acute lung injury may be delayed.
    3) ADMISSION CRITERIA: Patients with worsening or severe symptoms should be admitted to the hospital and, depending on the severity of their symptoms (eg, respiratory distress requiring intubation), may require an ICU bed. Patients can be discharged once they are hemodynamically stable with clear improvement or asymptomatic from their exposure.
    4) CONSULT CRITERIA: Consult a medical toxicologist or poison center for any patient with suspected phosphine exposure. An occupational physician and industrial hygienist should be involved if the exposure is work-related. Other helpful consultants may include critical care physicians and pulmonologists to help management of the patient's symptoms.
    H) PITFALLS
    1) One concern from phosphine exposure is that the characteristic odor might be masked by olfactory fatigue at higher concentrations. Patients should be removed from the exposure as the first line treatment. Severe symptoms, such as pulmonary edema, may be delayed for up to 72 hours after exposure.
    I) TOXICOKINETICS
    1) Onset of symptoms may range from immediate to within a few hours. Some toxic manifestations, such as abnormalities in liver enzymes or pulmonary edema, may be delayed for up to 1 to 3 days.
    J) PREDISPOSING CONDITIONS
    1) Patients at extremes of age or underlying morbidities, such as chronic lung disease, may be more susceptible to phosphine exposure.
    K) DIFFERENTIAL DIAGNOSIS
    1) Includes other irritant or toxic gases such as chlorine or cyanide gases.
    0.4.4) EYE EXPOSURE
    A) Eye exposures can be treated with simple decontamination and removal from the exposure area. Irrigate exposed eyes.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) Dermal exposures can be treated with simple decontamination and removal from the exposure area. Wash exposed skin.

Range Of Toxicity

    A) TOXICITY: Occupational exposure limits established by various agencies include NIOSH REL of a 10-hour TWA of 0.3 parts per million (ppm) and 15 minute STEL of 1 ppm, OSHA PEL of an 8-hour TWA of 0.3 ppm, ACGIH TLV 8-hour TWA of 0.3 ppm and 15 minute STEL of 1 ppm, and NIOSH has designated 50 ppm as immediately dangerous to life and health. There have been case reports of a physician being symptomatic after exposure to phosphine released from the excised stomach of a patient who died from aluminum phosphide poisoning. A forensic specialist, investigating a methamphetamine lab, who was exposed to 2.7 ppm phosphine for 20 to 30 minutes without respiratory protection, and subsequently developed dizziness, cough, headache, and diarrhea, and had rhonchi on physical exam. Occupational exposure to phosphine at airborne concentrations of 0.17 to 2.11 ppm during aluminum phosphide grain fumigation resulted in the development of cough, dyspnea, chest tightness, headache, giddiness, numbness, lethargy, anorexia, and epigastric pain.

Clinical Effects

Summary Of Exposure

    A) USES: Phosphine (PH3) is a colorless, flammable toxic gas used in the semiconductor industry. It is also used as a fumigant, polymerization initiator, and as an intermediate for the preparation flame retardants. When pure, it is odorless, but technical grade samples have an unpleasant odor similar to garlic or rotting fish. Phosphine can also be generated in illicit methamphetamine labs, especially production involving red phosphorus, hydriodic acid, and ephedrine or pseudoephedrine. Phosphine is produced when red phosphorus is heated in the presence of acids. The vast majority of exposures are inhalational; when used as a fumigant, pellets of aluminum phosphide, calcium phosphide, or zinc phosphide release phosphine upon contact with atmospheric water or an organism's stomach acid. Phosphine is a gas at room temperature, so ingestion is unlikely. Toxicity from ingestion of aluminum phosphide or zinc phosphide are covered in separate managements.
    B) TOXICOLOGY: Phosphine exerts its toxic effects via inhibition of cytochrome oxidase and generation of free radical damage. Injury occurs primarily after inhalation exposure, though toxicity can occur from ingestion or transdermal contamination. Phosphine gas may form explosive mixtures with air and self ignite. When phosphine burns, a dense white cloud of phosphorus pentoxide, a severe respiratory irritant, is formed. Phosphine breaks down in water.
    C) EPIDEMIOLOGY: Human poisoning is uncommon, but occurs worldwide and can be fatal.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Exposure to phosphine gas may cause nausea and vomiting, abdominal pain, diarrhea, thirst, chest tightness, dyspnea, cough productive of sputum, jaundice, elevated liver enzymes, muscle pains, dizziness, headache, fatigue, ataxia, paresthesias, irritation of mucous membranes, acute renal failure with proteinuria, and hematopoietic cancers.
    2) SEVERE TOXICITY: More severe exposures may cause tachycardia and hypotension, metabolic acidosis, ventricular dysrhythmias, seizures, coma, acute lung injury (which may be delayed), and death. Direct contact with phosphine liquid may cause frostbite, but phosphine gas is not known to produce adverse effects on the skin. Phosphine gas produces no known adverse effects on the eyes. Contact with the skin or eyes to phosphine gas does not normally result in systemic toxicity.

Vital Signs

    3.3.4) BLOOD PRESSURE
    A) WITH POISONING/EXPOSURE
    1) HYPOTENSION was reported in 3 patients from the same family following several hours of exposure to phosphine gas released from aluminum phosphide tablets stored in rice bags (Shadnia et al, 2008).
    3.3.5) PULSE
    A) WITH POISONING/EXPOSURE
    1) TACHYCARDIA has been reported following exposure to phosphine gas released from aluminum phosphide tablets stored in rice bags (Shadnia et al, 2008).

Heent

    3.4.6) THROAT
    A) WITH POISONING/EXPOSURE
    1) Phosphine has an irritant effect on the mucous membranes of the mouth, throat, and respiratory tract (Brautbar & Howard, 2002).
    2) Thirst has been reported following inhalational exposure to phosphine (Willers-Russo, 1999).

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) CONDUCTION DISORDER OF THE HEART
    1) WITH POISONING/EXPOSURE
    a) In a study of 30 patients with severe aluminum phosphide poisoning who underwent continuous Holter monitoring, all patients had supraventricular and ventricular ectopy. Ventricular tachycardia developed in 40% and ventricular fibrillation developed in 23.3%. Supraventricular tachycardia developed in 46.7% and atrial fibrillation or flutter developed in 20%. ST-T changes were universal, with 90% developing S-T depression and 10% developing S-T elevation (Siwach et al, 1998).
    b) CASE REPORT: A 23-year-old man developed frequent PVCs (greater than 600 per hour) with periods of bigeminy after acute inhalational exposure to phosphine. Magnesium sulfate was given with no immediate benefit. An echocardiogram performed the following day was normal. The patient received trimetazidine 20 mg twice daily without further dysrhythmias. The authors suggested a possible cardioprotective effect of trimetazidine via an antiischemic mechanism (Duenas et al, 1999). Trimetazidine is not a pharmacological agent available in the United States.
    c) CASE REPORTS: Sinus tachycardia was reported in a 35-year-old woman (100 bpm) and her 18-year-old daughter (125 bpm) following several hours of exposure to phosphine gas released from 15 bags of rice that contained 20 tablets of aluminum phosphide. Both patients recovered with supportive care (Shadnia et al, 2008).
    d) CASE REPORT: A 42-year-old man, working at an aluminum phosphide fumigant manufacturing facility, developed chest pain, dyspnea, weakness, dizziness, disorientation, nausea. vomiting, and hypotension following inhalational exposure of phosphine gas. A rhythm strip indicated junctional bradycardia and an ECG demonstrated normal sinus rhythm with non-specific ST and T-wave abnormalities. With supportive care, the patient recovered without developing dysrhythmias or other specific indicators of cardiac injury (Sudakin, 2005).
    e) CASE REPORT: A 15-month-old child experienced abdominal pain, vomiting, and diarrhea approximately 24 hours following inhalational exposure to phosphine gas resulting from fumigation using aluminum phosphide pellets. Following supportive treatment, the patient was discharged home. However, 36 hours post-exposure, the patient developed respiratory distress, lethargy, tachycardia, and tachypnea. An echocardiogram indicated decreased systolic function with a left ventricle (LV) ejection fraction of 50% and dyskinetic LV motion. An ECG revealed sinus tachycardia (175 bpm) with diffuse ST segment abnormalities and a short PR interval. She became hypotensive (62/39 mmHg) that continued to persist despite IV fluids and pressor administration. Approximately 50 hours post-exposure, the patient's hemodynamic status deteriorated, subsequently progressing to cardiac arrest that did not respond to resuscitation. She was placed on cardiopulmonary bypass; however, the patient's neurologic functioning was minimal and the decision was made to remove her from life support (Lemoine et al, 2011).
    f) CASE REPORTS: A family of 6, including the parents and 4 children (19 months, 4 years, 5 years, and 6 years of age) presented to the emergency department (ED) a day after initial evaluation at a local clinic for nausea and vomiting secondary to suspected food poisoning. At arrival to the ED the next day, the 19-month-old child was pronounced dead. The 4-year-old developed hemodynamic collapse, with an echocardiogram demonstrating severe biventricular failure. Cardiac arrest occurred and the patient died 2 hours later following unsuccessful resuscitation. The 6-year-old developed ventricular fibrillation requiring cardioversion and cardiopulmonary bypass for complete hemodynamic support. The 5-year-old became unresponsive and hypoxic with tachycardia (170 beats/min). An echocardiogram demonstrated left ventricular dysfunction, requiring inotropic support. Extracorporeal mechanical oxygenation (ECMO) was initiated in both children; however, cardiac deterioration continued to occur, with development of severe ventricular systolic dysfunction and multiple episodes of polymorphic ventricular tachycardia and prolonged ventricular fibrillation. With maintenance of the magnesium and potassium levels at approximately 2 mEq/L and greater than 3.5 mEq/L, respectively, the children gradually recovered with improving systolic function and normalizing ECGs. They were weaned from ECMO in 7 to 10 days, and were discharged 3 weeks later, with normal cardiac systolic function. There was no evidence of sequelae at their 2-month follow-up. Interview of the parents revealed that 2 days prior to presentation, fumigation occurred in the home with a pesticide suspected to be aluminum phosphide (Merin et al, 2015).
    B) HYPOTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) Hypotension develops with severe poisoning (Lemoine et al, 2011; Sudakin, 2005; Nocera et al, 2000).
    b) Of 25 adult patients with acute aluminum phosphide poisoning, 23 developed peripheral circulatory failure (Khosla et al, 1988).
    c) CASE REPORTS: Hypotension was reported in 2 patients, a 35-year-old woman (85/60 mmHg) and her 18-year-old daughter (80/60 mmHg) following several hours of exposure to phosphine gas released from 15 bags of rice that contained 20 tablets of aluminum phosphide. Both patients recovered with supportive care (Shadnia et al, 2008). A 6-year-old boy from the same family also developed hypotension, as well as severe vomiting, abdominal pain, and respiratory distress following the same exposure to phosphine gas. En route to the hospital, he developed cardiopulmonary arrest and died before hospital admission.

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) DYSPNEA
    1) WITH POISONING/EXPOSURE
    a) Cough, sputum production, and dyspnea have been noted following inhalational exposure of phosphine gas (Brautbar & Howard, 2002; Wilson et al, 1980).
    b) Phosphine can be generated in illicit methamphetamine labs. One method of producing methamphetamine involves red phosphorus, hydriodic acid and ephedrine or pseudoephedrine. Phosphine can be produced when red phosphorus is heated in the presence of acids. A forensic specialist investigating a methamphetamine lab was exposed to 2.7 ppm phosphine for 20 to 30 minutes without respiratory protection. She developed dizziness, cough, headache and diarrhea and had rhonchi on physical exam (Burgess, 2001).
    c) OCCUPATIONAL EXPOSURE: Workers (n=22), who were involved in grain fumigation using aluminum phosphide tablets, developed cough (18.2%), dyspnea (31.8%), chest tightness (27.3%), headache (31.8%), giddiness, numbness, and lethargy (31.8% each), and anorexia and epigastric pain (18.2% each) following the fumigation. The phosphine airborne concentration ranged from 0.17 to 2.11 ppm (Misra et al, 1988b).
    B) ACUTE LUNG INJURY
    1) WITH POISONING/EXPOSURE
    a) ONSET: Delayed onset of pulmonary edema may be noted from inhalation exposure to phosphine gas.
    b) INCIDENCE: Pulmonary edema was observed in 2 patients in a study of 25 adult patients with acute aluminum phosphide poisoning (Khosla et al, 1988).
    c) Pulmonary edema was reported on autopsy (Abder-Rahman et al, 2000).
    d) Three individuals were found dead from apparent exposure to phosphine gas during methamphetamine manufacturing. Autopsy of one of the deceased revealed the presence of pulmonary edema (Willers-Russo, 1999).
    C) RESPIRATORY CONDITION DUE TO CHEMICAL FUMES AND/OR VAPORS
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 6-year-old boy developed respiratory distress, severe vomiting, epigastric pain, hypotension, and cyanosis following several hours of exposure (over the course of 2 nights) to phosphine gas released from 15 bags of rice that contained 20 aluminum phosphide tablets. Following the second night of exposure, the patient developed cardiopulmonary arrest and died en route to the hospital (Shadnia et al, 2008).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) CENTRAL NERVOUS SYSTEM FINDING
    1) WITH POISONING/EXPOSURE
    a) Large acute exposures produce signs and symptoms including fatigue, headache, drowsiness, dizziness, paresthesias, ataxia, and CNS depression leading to coma (Burgess, 2001; Nocera et al, 2000; Willers-Russo, 1999; Wilson et al, 1980) .
    b) OCCUPATIONAL EXPOSURE: Workers (n=22), who were involved in grain fumigation using aluminum phosphide tablets, developed cough (18.2%), dyspnea (31.8%), chest tightness (27.3%), headache (31.8%), giddiness, numbness, and lethargy (31.8% each), and anorexia and epigastric pain (18.2% each) following the fumigation. The phosphine airborne concentration ranged from 0.17 to 2.11 ppm (Misra et al, 1988b).
    B) SEIZURE
    1) WITH POISONING/EXPOSURE
    a) Seizures may occur after acute exposures (Willers-Russo, 1999).
    C) COMA
    1) WITH POISONING/EXPOSURE
    a) Coma may occur with inhalational exposure to phosphine gas (Willers-Russo, 1999).
    D) NEUROPATHY
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 52-year-old woman, exposed to aluminum phos-toxin and ammonium carbamate for approximately 30 minutes in a closed truck without protective equipment, developed an itching and burning sensation of her skin, severe headaches, weakness, dyspnea, nausea, and vomiting 30 to 60 minutes after exposure. She also experienced neuromuscular weakness of her left leg. The patient received supportive treatment and was discharged 4 days later. Investigation of phosphine levels within the truck determined a maximum phosphine exposure level of 242 ppm. Following hospital discharge, the patient continued to have headaches and decreased sensation of her left side. At the 6-month follow-up, the patient was diagnosed with peripheral neuropathy secondary to phosphine exposure (Brautbar & Howard, 2002).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) NAUSEA AND VOMITING
    1) WITH POISONING/EXPOSURE
    a) Nausea and vomiting may occur following inhalational exposure to phosphine gas (Lemoine et al, 2011; Sudakin, 2005; Brautbar & Howard, 2002; Centers for Disease Control and Prevention, 1994).
    b) Nausea and vomiting has been reported following exposure to phosphine gas released from aluminum phosphide tablets stored in rice bags (Shadnia et al, 2008).
    c) Nausea and vomiting were reported in 72% and 45% of patients (n=31), respectively, who were exposed to phosphine gas while working aboard a grain freighter (Wilson et al, 1980).
    B) DIARRHEA
    1) WITH POISONING/EXPOSURE
    a) Phosphine can be generated in illicit methamphetamine labs. One method of producing methamphetamine involves red phosphorus, hydriodic acid and ephedrine or pseudoephedrine. Phosphine can be produced when red phosphorus is heated in the presence of acids. A forensic specialist investigating a methamphetamine lab was exposed to 2.7 ppm phosphine for 20 to 30 minutes without respiratory protection. She developed dizziness, cough, headache and diarrhea and had rhonchi on physical exam (Burgess, 2001).
    b) Diarrhea was reported in 21% of patients (n=31) who were exposed to phosphine gas while working aboard a grain freighter (Wilson et al, 1980).
    c) CASE REPORT: Abdominal pain, vomiting, and diarrhea was reported in a 15-month-old child approximately 24 hours following inhalational exposure to phosphine gas resulting from fumigation using aluminum phosphide pellets (Lemoine et al, 2011).
    C) ABDOMINAL PAIN
    1) WITH POISONING/EXPOSURE
    a) Abdominal pain has been reported following exposure to phosphine gas released from aluminum phosphide tablets stored in rice bags (Shadnia et al, 2008).
    b) OCCUPATIONAL EXPOSURE: Workers (n=22), who were involved in grain fumigation using aluminum phosphide tablets, developed cough (18.2%), dyspnea (31.8%), chest tightness (27.3%), headache (31.8%), giddiness, numbness, and lethargy (31.8% each), and anorexia and epigastric pain (18.2% each) following the fumigation. The phosphine airborne concentration ranged from 0.17 to 2.11 ppm (Misra et al, 1988b).
    c) CASE REPORT: Abdominal pain, vomiting, and diarrhea was reported in a 15-month-old child approximately 24 hours following inhalational exposure to phosphine gas resulting from fumigation using aluminum phosphide pellets (Lemoine et al, 2011).

Hepatic

    3.9.2) CLINICAL EFFECTS
    A) INJURY OF LIVER
    1) WITH POISONING/EXPOSURE
    a) CASE SERIES: In a study of 25 adult patients with acute aluminum phosphide poisoning, 5 had mild to moderate elevation of serum transaminases (Khosla et al, 1988).
    B) JAUNDICE
    1) WITH POISONING/EXPOSURE
    a) Jaundice was reported in 52% of patients (n=31) who were exposed to phosphine gas while working aboard a grain freighter (Wilson et al, 1980).
    b) CASE SERIES: In a study of 25 adult patients with acute aluminum phosphide poisoning, of 5 patients with elevated serum transaminases, 2 also had hyperbilirubinemia (Khosla et al, 1988).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) ABNORMAL RENAL FUNCTION
    1) WITH POISONING/EXPOSURE
    a) CASE SERIES: In a study of 25 adult patients with acute aluminum phosphide poisoning, 1 developed acute renal failure and another had mild proteinuria (Khosla et al, 1988).

Acid-Base

    3.11.2) CLINICAL EFFECTS
    A) ACIDOSIS
    1) WITH POISONING/EXPOSURE
    a) CASE SERIES: In a study of 25 adult patients with acute aluminum phosphide poisoning, 8 patients studied for acid-base disturbances were found to have metabolic acidosis (Khosla et al, 1988). Metabolic acidosis is likely secondary to hypotension.
    b) CASE REPORTS: Metabolic acidosis was reported in 2 patients, a 35-year-old woman and her 18-year-old daughter, following several hours of exposure to phosphine gas released from 15 bags of rice containing 20 tablets of aluminum phosphide. The arterial blood gas results of the mother and daughter were pH 7.30, PaCO2 17.8 mmHg, HCO3 11.4 mEq/L, and pH 7.29, PaCO2 16.9 mmHg, HCO3 10 mEq/L, respectively. Both patients recovered following supportive care (Shadnia et al, 2008).
    c) CASE REPORTS: Four children (ages ranging from 19 months to 6 years) developed severe lactic acidosis (ranges: pH less than 6.8 to 7.3; HCO3 incalculable to 15.9, lactate 10 to greater than 15) following exposure to fumigation involving a pesticide suspected to be aluminum phosphide. The two youngest children died a short time after admission of hemodynamic collapse (Merin et al, 2015).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) FROSTBITE
    1) WITH POISONING/EXPOSURE
    a) Direct contact with phosphine liquid or compressed phosphine gas may cause frostbite (National Institute for Occupational Safety and Health (NIOSH), 2008).

Musculoskeletal

    3.15.2) CLINICAL EFFECTS
    A) MUSCLE PAIN
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 53-year-old man experienced generalized weakness with myalgia following inhalational exposure to phosphine produced from application of a rodenticide, containing 28% calcium phosphide, to the wet ground (Schoonbroodt et al, 1992).

Endocrine

    3.16.2) CLINICAL EFFECTS
    A) HYPERGLYCEMIA
    1) WITH POISONING/EXPOSURE
    a) CASE REPORTS: Hyperglycemia was reported in a 35-year-old woman (blood glucose 212 mg/dL) and her 18-year-old daughter (blood glucose 206 mg/dL) following several hours of exposure to phosphine gas released from aluminum phosphide tablets stored in rice bags. The hyperglycemia spontaneously resolved within 24 hours (Shadnia et al, 2008).

Reproductive

    3.20.2) TERATOGENICITY
    A) ANIMAL STUDIES
    1) Teratogenic effects were not noted in rats exposed to an airborne phosphine concentration of 5 ppm during days 6 to 15 of pregnancy (Schroeder et al, 1992).
    3.20.3) EFFECTS IN PREGNANCY
    A) LACK OF EFFECT
    1) No significant increased risk of spontaneous abortion was found in a study of female electronics workers with potential phosphine exposure (Shusterman et al, 1993).
    B) ANIMAL STUDIES
    1) Rats exposed to an airborne phosphine concentration of 5 ppm during days 6 to 15 of pregnancy did NOT develop maternal toxicity, fetotoxicity, embryotoxicity, or teratogenicity (Schroeder et al, 1992).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS7803-51-2 (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
    3.21.2) SUMMARY/HUMAN
    A) Hematopoietic system cancers have been seen in grain workers and fumigators.
    3.21.3) HUMAN STUDIES
    A) CARCINOMA
    1) Grain millers exposed to phosphine (as well as fungicides and other fumigants) had a slight increase of lymphatic tumors (Alavanja et al, 1987).

Genotoxicity

    A) In some studies, phosphine exposure has been associated with a significant increase in the frequency of chromosome aberrations in peripheral blood lymphocytes.
    B) A study of fumigant applicators exposed to phosphine alone or together with other pesticides found significantly increased stable chromosome rearrangements (primarily translocations in G- banded lymphocytes).
    C) In rats and mice, phosphine was only a weak genotoxic agent causing only simple chromatid or chromosome deletions at near-toxic exposure levels.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor vital signs and mental status.
    B) Monitor continuous pulse oximetry.
    C) Institute continuous cardiac monitoring and obtain an ECG.
    D) Monitor serum electrolytes, renal function, and liver enzymes.
    E) Obtain a chest radiograph in patients with respiratory symptoms.
    F) Echocardiogram may be useful to assess left ventricular function in patients with hypotension or pulmonary edema.

Methods

    A) OTHER
    1) The diagnosis of acute phosphine poisoning is based on history of exposure to the agent and abnormal physical examination findings consistent with the substance.
    2) Chronic low level exposure to phosphine may be identified by evaluation of blood and urine phosphorous levels; however, this procedure has not often been used, and is not specific.
    3) Measurement of aluminum in tissue and body fluids by atomic absorption spectroscopy was used to establish the cause of death in a non-occupational exposure to aluminum phosphide (Garry et al, 1993). Aluminum-containing antacids may potentially confound these results.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.3) DISPOSITION/INHALATION EXPOSURE
    6.3.3.1) ADMISSION CRITERIA/INHALATION
    A) Patients with worsening or severe symptoms should be admitted to the hospital and, depending on the severity of their symptoms (eg, respiratory distress requiring intubation), may require an ICU bed. Patients can be discharged once they are hemodynamically stable with clear improvement or asymptomatic from their exposure.
    6.3.3.2) HOME CRITERIA/INHALATION
    A) There is no data to support home management.
    6.3.3.3) CONSULT CRITERIA/INHALATION
    A) Consult a medical toxicologist or poison center for any patient with suspected phosphine exposure. An occupational physician and industrial hygienist should be involved if the exposure is work-related. Other helpful consultants may include critical care physicians and pulmonologists to help management of the patient's symptoms.
    6.3.3.5) OBSERVATION CRITERIA/INHALATION
    A) All patients with exposures should be sent to a healthcare facility for observation for at least a period of 6 to 8 hours of observation. Patients may be discharged home if they are asymptomatic or clearly improving and stable for discharge. Patients should be instructed to return immediately if any respiratory symptoms develop, as onset of acute lung injury may be delayed.

Monitoring

    A) Monitor vital signs and mental status.
    B) Monitor continuous pulse oximetry.
    C) Institute continuous cardiac monitoring and obtain an ECG.
    D) Monitor serum electrolytes, renal function, and liver enzymes.
    E) Obtain a chest radiograph in patients with respiratory symptoms.
    F) Echocardiogram may be useful to assess left ventricular function in patients with hypotension or pulmonary edema.

Oral Exposure

    6.5.3) TREATMENT
    A) SUPPORT
    1) Refer to INHALATION EXPOSURE section for treatment recommendations.

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) SUPPORT
    1) Removal from phosphine exposure and supportive care are the most important initial measures
    B) MONITORING OF PATIENT
    1) Monitor vital signs and mental status.
    2) Monitor continuous pulse oximetry.
    3) Institute continuous cardiac monitoring and obtain an ECG.
    4) Monitor serum electrolytes, renal function, and liver enzymes.
    5) Obtain a chest radiograph in patients with respiratory symptoms.
    C) SEIZURE
    1) SUMMARY
    a) Attempt initial control with a benzodiazepine (eg, diazepam, lorazepam). If seizures persist or recur, administer phenobarbital or propofol.
    b) Monitor for respiratory depression, hypotension, and dysrhythmias. Endotracheal intubation should be performed in patients with persistent seizures.
    c) Evaluate for hypoxia, electrolyte disturbances, and hypoglycemia (or, if immediate bedside glucose testing is not available, treat with intravenous dextrose).
    2) DIAZEPAM
    a) ADULT DOSE: Initially 5 to 10 mg IV, OR 0.15 mg/kg IV up to 10 mg per dose up to a rate of 5 mg/minute; may be repeated every 5 to 20 minutes as needed (Brophy et al, 2012; Prod Info diazepam IM, IV injection, 2008; Manno, 2003).
    b) PEDIATRIC DOSE: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed (Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
    c) Monitor for hypotension, respiratory depression, and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after repeated doses of diazepam .
    3) NO INTRAVENOUS ACCESS
    a) DIAZEPAM may be given rectally or intramuscularly (Manno, 2003). RECTAL DOSE: CHILD: Greater than 12 years: 0.2 mg/kg; 6 to 11 years: 0.3 mg/kg; 2 to 5 years: 0.5 mg/kg (Brophy et al, 2012).
    b) MIDAZOLAM has been used intramuscularly and intranasally, particularly in children when intravenous access has not been established. ADULT DOSE: 0.2 mg/kg IM, up to a maximum dose of 10 mg (Brophy et al, 2012). PEDIATRIC DOSE: INTRAMUSCULAR: 0.2 mg/kg IM, up to a maximum dose of 7 mg (Chamberlain et al, 1997) OR 10 mg IM (weight greater than 40 kg); 5 mg IM (weight 13 to 40 kg); INTRANASAL: 0.2 to 0.5 mg/kg up to a maximum of 10 mg/dose (Loddenkemper & Goodkin, 2011; Brophy et al, 2012). BUCCAL midazolam, 10 mg, has been used in adolescents and older children (5-years-old or more) to control seizures when intravenous access was not established (Scott et al, 1999).
    4) LORAZEPAM
    a) MAXIMUM RATE: The rate of intravenous administration of lorazepam should not exceed 2 mg/min (Brophy et al, 2012; Prod Info lorazepam IM, IV injection, 2008).
    b) ADULT DOSE: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist (Manno, 2003; Brophy et al, 2012).
    c) PEDIATRIC DOSE: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue (Brophy et al, 2012; Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008; Sreenath et al, 2009; Chin et al, 2008).
    5) PHENOBARBITAL
    a) ADULT LOADING DOSE: 20 mg/kg IV at an infusion rate of 50 to 100 mg/minute IV. An additional 5 to 10 mg/kg dose may be given 10 minutes after loading infusion if seizures persist or recur (Brophy et al, 2012).
    b) Patients receiving high doses will require endotracheal intubation and may require vasopressor support (Brophy et al, 2012).
    c) PEDIATRIC LOADING DOSE: 20 mg/kg may be given as single or divided application (2 mg/kg/minute in children weighing less than 40 kg up to 100 mg/min in children weighing greater than 40 kg). A plasma concentration of about 20 mg/L will be achieved by this dose (Loddenkemper & Goodkin, 2011).
    d) REPEAT PEDIATRIC DOSE: Repeat doses of 5 to 20 mg/kg may be given every 15 to 20 minutes if seizures persist, with cardiorespiratory monitoring (Loddenkemper & Goodkin, 2011).
    e) MONITOR: For hypotension, respiratory depression, and the need for endotracheal intubation (Loddenkemper & Goodkin, 2011; Manno, 2003).
    f) SERUM CONCENTRATION MONITORING: Monitor serum concentrations over the next 12 to 24 hours. Therapeutic serum concentrations of phenobarbital range from 10 to 40 mcg/mL, although the optimal plasma concentration for some individuals may vary outside this range (Hvidberg & Dam, 1976; Choonara & Rane, 1990; AMA Department of Drugs, 1992).
    6) OTHER AGENTS
    a) If seizures persist after phenobarbital, propofol or pentobarbital infusion, or neuromuscular paralysis with general anesthesia (isoflurane) and continuous EEG monitoring should be considered (Manno, 2003). Other anticonvulsants can be considered (eg, valproate sodium, levetiracetam, lacosamide, topiramate) if seizures persist or recur; however, there is very little data regarding their use in toxin induced seizures, controlled trials are not available to define the optimal dosage ranges for these agents in status epilepticus (Brophy et al, 2012):
    1) VALPROATE SODIUM: ADULT DOSE: An initial dose of 20 to 40 mg/kg IV, at a rate of 3 to 6 mg/kg/minute; may give an additional dose of 20 mg/kg 10 minutes after loading infusion. PEDIATRIC DOSE: 1.5 to 3 mg/kg/minute (Brophy et al, 2012).
    2) LEVETIRACETAM: ADULT DOSE: 1000 to 3000 mg IV, at a rate of 2 to 5 mg/kg/min IV. PEDIATRIC DOSE: 20 to 60 mg/kg IV (Brophy et al, 2012; Loddenkemper & Goodkin, 2011).
    3) LACOSAMIDE: ADULT DOSE: 200 to 400 mg IV; 200 mg IV over 15 minutes (Brophy et al, 2012). PEDIATRIC DOSE: In one study, median starting doses of 1.3 mg/kg/day and maintenance doses of 4.7 mg/kg/day were used in children 8 years and older (Loddenkemper & Goodkin, 2011).
    4) TOPIRAMATE: ADULT DOSE: 200 to 400 mg nasogastric/orally OR 300 to 1600 mg/day orally divided in 2 to 4 times daily (Brophy et al, 2012).
    D) 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).
    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/INDICATIONS
    1) Ventricular tachycardia or ventricular fibrillation (Prod Info Lidocaine HCl intravenous injection solution, 2006; Neumar et al, 2010; Vanden Hoek et al, 2010).
    b) 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).
    c) 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).
    d) LIDOCAINE/MONITORING PARAMETERS
    1) Monitor ECG continuously; plasma concentrations as indicated (Prod Info Lidocaine HCl intravenous injection solution, 2006).
    3) AMIODARONE
    a) AMIODARONE/INDICATIONS
    1) Effective for the control of hemodynamically stable monomorphic ventricular tachycardia. Also recommended for pulseless ventricular tachycardia or ventricular fibrillation in cardiac arrest unresponsive to CPR, defibrillation and vasopressor therapy (Link et al, 2015; Neumar et al, 2010). It should be used with caution when the ingestion involves agents known to cause QTc prolongation, such as fluoroquinolones, macrolide antibiotics or azoles, and when ECG reveals QT prolongation suspected to be secondary to overdose (Prod Info Cordarone(R) oral tablets, 2015).
    b) AMIODARONE/ADULT DOSE
    1) For ventricular fibrillation or pulseless VT unresponsive to CPR, defibrillation, and a vasopressor therapy give an initial dose of 300 mg IV followed by 1 dose of 150 mg IV. For stable ventricular tachycardias: Infuse 150 milligrams over 10 minutes, and repeat if necessary. Follow by a 1 milligram/minute infusion for 6 hours, then a 0.5 milligram/minute. Maximum total dose over 24 hours is 2.2 grams (Neumar et al, 2010).
    c) AMIODARONE/PEDIATRIC DOSE
    1) Infuse 5 milligrams/kilogram as a bolus for pulseless ventricular tachycardia or ventricular fibrillation; may repeat twice up to 15 mg/kg. Infuse 5 milligrams/kilogram over 20 to 60 minutes for perfusing tachycardias. Maximum single dose is 300 mg. Routine use with other drugs that prolong the QT interval is NOT recommended (Kleinman et al, 2010).
    d) ADVERSE EFFECTS
    1) Hypotension and bradycardia are the most common adverse effects (Neumar et al, 2010).
    G) CORTICOSTEROID
    1) Corticosteroids have not been shown to be efficacious (Banjaj & Wasir, 1988).
    H) EXTRACORPOREAL MEMBRANE OXYGENATION
    1) CASE REPORTS: Extracorporeal membrane oxygenation (ECMO) was initiated in 2 patients (ages 5 and 6 years) who developed severe ventricular dysfunction following inhalation exposure to a pesticide suspected to be aluminum phosphide. Prior to ECMO initiation, the 6-year-old had been placed on cardiopulmonary bypass as a bridge to ECMO. Despite a smooth run of ECMO, cardiac deterioration continued to occur in both patients, with development of severe ventricular systolic dysfunction and multiple episodes of polymorphic ventricular tachycardia and prolonged ventricular fibrillation. With maintenance of the magnesium and potassium levels at approximately 2 mEq/L and greater than 3.5 mEq/L, respectively, the patients gradually recovered with improving systolic function and normalizing ECGs. They were weaned from ECMO in 7 to 10 days, and were discharged 3 weeks later, with normal cardiac systolic function. There was no evidence of sequelae at their 2-month follow-up (Merin et al, 2015).
    I) 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).

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) 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).

Enhanced Elimination

    A) SUMMARY
    1) Dialysis or hemoperfusion are unlikely to be helpful for phosphine exposures.

Abstracts

Case Reports

    A) ROUTE OF EXPOSURE
    1) INHALATION
    a) Three federal grain inspectors developed symptoms of facial numbness and tingling, dizziness, nausea, and shortness of breath approximately 1 hour following inhalation exposure to phosphine while inspecting wheat on a railroad train. Only 1 worker was asymptomatic after 4 days of follow-up. Concentrations of phosphine, after at least 20 minutes of aeration of the railroad cars, were 159 ppm, 298 ppm, and 2029 ppm (Feldstein et al, 1991).
    B) A physician required medical treatment following exposure to phosphine released from the excised stomach of a patient who died from aluminum phosphide poisoning (Jayaraman, 1991).

Range Of Toxicity

Summary

    A) TOXICITY: Occupational exposure limits established by various agencies include NIOSH REL of a 10-hour TWA of 0.3 parts per million (ppm) and 15 minute STEL of 1 ppm, OSHA PEL of an 8-hour TWA of 0.3 ppm, ACGIH TLV 8-hour TWA of 0.3 ppm and 15 minute STEL of 1 ppm, and NIOSH has designated 50 ppm as immediately dangerous to life and health. There have been case reports of a physician being symptomatic after exposure to phosphine released from the excised stomach of a patient who died from aluminum phosphide poisoning. A forensic specialist, investigating a methamphetamine lab, who was exposed to 2.7 ppm phosphine for 20 to 30 minutes without respiratory protection, and subsequently developed dizziness, cough, headache, and diarrhea, and had rhonchi on physical exam. Occupational exposure to phosphine at airborne concentrations of 0.17 to 2.11 ppm during aluminum phosphide grain fumigation resulted in the development of cough, dyspnea, chest tightness, headache, giddiness, numbness, lethargy, anorexia, and epigastric pain.

Minimum Lethal Exposure

    A) Inhalation of phosphine released after fumigation using aluminum phosphide on a grain freighter resulted in acute poisoning of 29 of 31 crew members and two children, one of whom died. Air concentrations measured 2 days after onset of illness ranged from 0.5 ppm in some of the living quarters to 12 ppm at an air intake (Proctor et al, 1988).

Maximum Tolerated Exposure

    A) Phosphine is a highly toxic gas, especially to organs with high oxygen demand.
    B) The minimal detectable (decaying fish odor) concentration is 0.01 to 5 ppm in air (AIHA, 1989). The gas dissipates rapidly in an open air environment; it is primarily a problem in confined spaces.
    C) Three federal grain inspectors developed facial numbness and tingling, dizziness, nausea, and shortness of breath approximately one hour following inhalation exposure to phosphine while inspecting wheat on a railroad train. Only one worker was asymptomatic after 4 days of follow-up (Feldstein et al, 1991).
    1) Concentrations of phosphine after at least 20 minutes of aeration of the railroad cars were 159 ppm, 298 ppm, and 2029 ppm.
    D) Workers exposed intermittently to concentrations up to 35 ppm, but averaging below 10 ppm, complained of nausea, vomiting, diarrhea, chest tightness and cough, headache, and dizziness; no evidence of cumulative effects was noted (Proctor et al, 1988).
    E) Exposure to 50 ppm is considered immediately dangerous to life and health (NIOSH , 1996).
    F) Phosphine can be generated in illicit methamphetamine labs. One method of producing methamphetamine involves red phosphorus, hydriodic acid and ephedrine or pseudoephedrine. Phosphine can be produced when red phosphorus is heated in the presence of acids. A forensic specialist investigating a methamphetamine lab was exposed to 2.7 ppm phosphine for 20 to 30 minutes without respiratory protection. She developed dizziness, cough, headache and diarrhea and had rhonchi on physical exam (Burgess, 2001).
    G) A physician required medical treatment following exposure to phosphine released from the excised stomach of a patient who died from aluminum phosphide poisoning (Jayaraman, 1991).
    H) OCCUPATIONAL EXPOSURE: Workers (n=22), who were involved in grain fumigation using aluminum phosphide tablets, developed cough (18.2%), dyspnea (31.8%), chest tightness (27.3%), headache (31.8%), giddiness, numbness, and lethargy (31.8% each), and anorexia and epigastric pain (18.2% each) following the fumigation. The phosphine airborne concentration ranged from 0.17 to 2.11 ppm (Misra et al, 1988b).
    I) CASE REPORT: A 52-year-old woman exposed to aluminum phos-toxin and ammonium carbamate for approximately 30 minutes in a closed truck without protective equipment, developed an itching and burning sensation of her skin, severe headaches, weakness, dyspnea, nausea, and vomiting 30 to 60 minutes post-exposure. She also experienced neuromuscular weakness of her left leg. The patient received supportive treatment and was discharged 4 days later. Investigation of phosphine levels within the truck determined a maximum phosphine exposure level of 242 ppm. Following hospital discharge, the patient continued to have headaches and decreased sensation of her left side. At the 6-month follow-up, the patient was diagnosed with peripheral neuropathy secondary to phosphine exposure (Brautbar & Howard, 2002).

Workplace Standards

    A) ACGIH TLV Values for CAS7803-51-2 (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) Phosphine
    a) TLV:
    1) TLV-TWA: 0.3 ppm
    2) TLV-STEL: 1 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): URT and GI irr; headache; CNS impair
    d) Molecular Weight: 34
    1) For gases and vapors, to convert the TLV from ppm to mg/m(3):
    a) [(TLV in ppm)(gram molecular weight of substance)]/24.45
    2) For gases and vapors, to convert the TLV from mg/m(3) to ppm:
    a) [(TLV in mg/m(3))(24.45)]/gram molecular weight of substance
    e) Additional information:

    B) NIOSH REL and IDLH Values for CAS7803-51-2 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Phosphine
    2) REL:
    a) TWA: 0.3 ppm (0.4 mg/m(3))
    b) STEL: 1 ppm (1 mg/m(3))
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s):
    3) IDLH:
    a) IDLH: 50 ppm
    b) Note(s): Not Listed

    C) Carcinogenicity Ratings for CAS7803-51-2 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Phosphine
    2) EPA (U.S. Environmental Protection Agency, 2011): D ; Listed as: Phosphine
    a) D : Not classifiable as to human carcinogenicity.
    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: Phosphine
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS7803-51-2 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Phosphine
    2) Table Z-1 for Phosphine:
    a) 8-hour TWA:
    1) ppm: 0.3
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3: 0.4
    a) Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.
    3) Ceiling Value:
    4) Skin Designation: No
    5) Notation(s): Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: RTECS, 1991 Budavari, 1989
    1) LD50- (ORAL)RAT:
    a) 12 mg/kg (RTECS, 1989)

Pharmacology Toxicology

Toxicologic Mechanism

    A) Phosphine blocks cytochrome c oxidase (Chefurka et al, 1976).
    B) Phosphine is a highly toxic gas, especially to organs with high oxygen demand. Signs and symptoms are rapid in onset and initially characterized by respiratory, cardiac, circulatory, and cerebral adverse effects and extreme gastrointestinal irritation followed later by renal and hepatic toxicity.
    C) Mechanisms of toxicity may include free radical generation and lipid peroxidation (Chugh et al, 1996).

Physicochemical

Physical Characteristics

    A) PHOSPHINE is a colorless, flammable, heavier than air, gas with a fish- or garlic-like odor. It is shipped as a liquefied compressed gas. The pure compound is odorless (NIOSH , 1990).
    B) ALUMINUM PHOSPHIDE: dark gray or yellow crystals
    C) CALCIUM PHOSPHIDE: brown-red crystalline powder
    D) ZINC PHOSPHIDE: faint odor of phosphorus, dark gray tetragonal crystals or powder

Ph

    A) Phosphine solutions are neutral (HSDB , 1991).

Molecular Weight

    A) PHOSPHINE: 34
    B) ALUMINUM PHOSHIDE: 57.96
    C) CALCIUM PHOSPHIDE: 182.2
    D) ZINC PHOSPHIDE: 258.09

Other

    A) ODOR THRESHOLD
    1) 0.03 PPM (HSDB , 2002)
    2) Air: 0.51 ul/l; Water: 0.0002 mg/l; Odor Safety Class: D; D= 10-50% of attentive persons can detect TLV concn in the air. (HSDB , 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 Materials in Surface Transportation, Bureau of Explosives, Association of American Railroads, Washington, DC, 1987, pp 547-548.
    14) ACGIH: Documentation of the Threshold Limit Values and Biological Exposure Indices, 5th ed, Am Conference of Govt Ind Hyg, Inc, Cincinnati, OH, 1986.
    15) ACGIH: Documentation of the Threshold Limit Values and Biological Exposure Indices, 6th ed, Am Conference of Govt Ind Hyg, Inc, Cincinnati, OH, 1991, pp 1248-1249.
    16) AIHA: 2006 Emergency Response Planning Guidelines and Workplace Environmental Exposure Level Guides Handbook, American Industrial Hygiene Association, Fairfax, VA, 2006.
    17) AIHA: Odor Thresholds for Chemicals with Established Occupational Health Standards, American Industrial Hygeine Association, Fairfax, VA, 1989.
    18) AMA Department of DrugsAMA Department of Drugs: AMA Evaluations Subscription, American Medical Association, Chicago, IL, 1992.
    19) Abder-Rahman AH, Battah AH, & Ibraheem YM: Aluminum phosphide fatalities, new local experience. Med Sci Law 2000; 40:164-168.
    20) Alavanja MCR, Rush GA, & Steward P: J Natl Cancer Inst 1987; 78:247.
    21) American Conference of Governmental Industrial Hygienists : ACGIH 2010 Threshold Limit Values (TLVs(R)) for Chemical Substances and Physical Agents and Biological Exposure Indices (BEIs(R)), American Conference of Governmental Industrial Hygienists, Cincinnati, OH, 2010.
    22) Ansell-Edmont: SpecWare Chemical Application and Recommendation Guide. Ansell-Edmont. Coshocton, OH. 2001. Available from URL: http://www.ansellpro.com/specware. As accessed 10/31/2001.
    23) Artigas A, Bernard GR, Carlet J, et al: The American-European consensus conference on ARDS, part 2: ventilatory, pharmacologic, supportive therapy, study design strategies, and issues related to recovery and remodeling.. Am J Respir Crit Care Med 1998; 157:1332-1347.
    24) Banjaj R & Wasir HS: Epidemic aluminum phosphide poisoning in northern India. Lancet 1988; 1:820-821.
    25) Barbosa A & Bonin AM: Evaluation of phosphine genotoxicity at occupational levels of exposure in New South Wales, Australia. Occup Environ Med 1994; 51:700-705.
    26) Bata Shoe Company: Industrial Footwear Catalog, Bata Shoe Company, Belcamp, MD, 1995.
    27) Bell CH: Time, concentration and temperature relationships for phosphine activity in tests on diapausing larvae of Ephestia elutella (Hubner) (Ledidoptera, Pyralidae). Pest Sci 1992; 35:255-264.
    28) Best Manufacturing: ChemRest Chemical Resistance Guide. Best Manufacturing. Menlo, GA. 2002. Available from URL: http://www.chemrest.com. As accessed 10/8/2002.
    29) Best Manufacturing: Degradation and Permeation Data. Best Manufacturing. Menlo, GA. 2004. Available from URL: http://www.chemrest.com/DomesticPrep2/. As accessed 04/09/2004.
    30) Boss Manufacturing Company: Work Gloves, Boss Manufacturing Company, Kewanee, IL, 1998.
    31) Brautbar N & Howard J: Phosphine toxicity: report of two cases and review of the literature. Toxicol Ind Health 2002; 18(2):71-75.
    32) Bretherick L: Bretherick's Handbook of Reactive Chemical Hazards, 4th ed, Butterworths, London, England, 1990, pp 1237-1239.
    33) Broderick M & Birnbaum K: Fatal ingestion of zinc phosphide rodenticide (abstract). J Toxicol Clin Toxicol 2002; 40:684.
    34) Brophy GM, Bell R, Claassen J, et al: Guidelines for the evaluation and management of status epilepticus. Neurocrit Care 2012; 17(1):3-23.
    35) Brower RG, Matthay AM, & Morris A: Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Eng J Med 2000; 342:1301-1308.
    36) Budavari S: The Merck Index, 11th ed, Merck & Co, Inc, Rahway, New Jersey, 1989, pp 1058.
    37) Burgess JL, Kirk M, Borron SW, et al: Emergency department hazardous materials protocol for contaminated patients. Ann Emerg Med 1999; 34(2):205-212.
    38) Burgess JL: Phosphine exposure from a methamphetamine laboratory investigation. Clin Toxicol 2001; 39:165-168.
    39) Cataletto M: Respiratory Distress Syndrome, Acute(ARDS). In: Domino FJ, ed. The 5-Minute Clinical Consult 2012, 20th ed. Lippincott Williams & Wilkins, Philadelphia, PA, 2012.
    40) Centers for Disease Control and Prevention: Deaths associated with exposure to fumigants in railroad cars--United States. MMWR Morb Mortal Wkly Rep 1994; 43(27):489-491.
    41) Chamberlain JM, Altieri MA, & Futterman C: A prospective, randomized study comparing intramuscular midazolam with intravenous diazepam for the treatment of seizures in children. Ped Emerg Care 1997; 13:92-94.
    42) Chefurka W, Kashi KP, & Bond EJ: The effect of phosphine on electron transport of mitochondria. Pesticide Biochem Physiol 1976; 6:65-84.
    43) ChemFab Corporation: Chemical Permeation Guide Challenge Protective Clothing Fabrics, ChemFab Corporation, Merrimack, NH, 1993.
    44) Chin RF , Neville BG , Peckham C , et al: Treatment of community-onset, childhood convulsive status epilepticus: a prospective, population-based study. Lancet Neurol 2008; 7(8):696-703.
    45) Choonara IA & Rane A: Therapeutic drug monitoring of anticonvulsants state of the art. Clin Pharmacokinet 1990; 18:318-328.
    46) Chopra JS, Kalra OP, & Malik R: Aluminum phosphide poisoning: a prospective study of 16 cases in one year. Postgrad Med J 1986; 62:1113-1115.
    47) Chugh SN, Arora V, & Sharma A: Free radical scavengers & lipid peroxidation in acute aluminum phosphide poisoning. Indian J Med Res 1996; 104:190-193.
    48) Clayton GD & Clayton GE: Pattys Industrial Hygiene and Toxicology, 4th ed, Vol 2A, Toxicology, John Wiley & Sons, New York, NY, 1993, pp 785791-793.
    49) Comasec Safety, Inc.: Chemical Resistance to Permeation Chart. Comasec Safety, Inc.. Enfield, CT. 2003. Available from URL: http://www.comasec.com/webcomasec/english/catalogue/mtabgb.html. As accessed 4/28/2003.
    50) Comasec Safety, Inc.: Product Literature, Comasec Safety, Inc., Enfield, CT, 2003a.
    51) DFG: List of MAK and BAT Values 2002, Report No. 38, Deutsche Forschungsgemeinschaft, Commission for the Investigation of Health Hazards of Chemical Compounds in the Work Area, Wiley-VCH, Weinheim, Federal Republic of Germany, 2002.
    52) DuPont: DuPont Suit Smart: Interactive Tool for the Selection of Protective Apparel. DuPont. Wilmington, DE. 2002. Available from URL: http://personalprotection.dupont.com/protectiveapparel/suitsmart/smartsuit2/na_english.asp. As accessed 10/31/2002.
    53) DuPont: Permeation Guide for DuPont Tychem Protective Fabrics. DuPont. Wilmington, DE. 2003. Available from URL: http://personalprotection.dupont.com/en/pdf/tyvektychem/pgcomplete20030128.pdf. As accessed 4/26/2004.
    54) DuPont: Permeation Test Results. DuPont. Wilmington, DE. 2002a. Available from URL: http://www.tyvekprotectiveapprl.com/databases/default.htm. As accessed 7/31/2002.
    55) Duenas A, Perez-Castrillon JL, & Cobos MA: Treatment of the cardiovascular manifestations of phosphine with trimetazidine, a new antiischemic drug (letter). Am J Emerg Med 1999; 17:219-220.
    56) EPA: Search results for Toxic Substances Control Act (TSCA) Inventory Chemicals. US Environmental Protection Agency, Substance Registry System, U.S. EPA's Office of Pollution Prevention and Toxics. Washington, DC. 2005. Available from URL: http://www.epa.gov/srs/.
    57) ERG: Emergency Response Guidebook. A Guidebook for First Responders During the Initial Phase of a Dangerous Goods/Hazardous Materials Incident, U.S. Department of Transportation, Research and Special Programs Administration, Washington, DC, 2004.
    58) Feldstein A, Heumann M, & Barnett M: Fumigant intoxication during transport of grain by railroad. J Occup Med 1991; 33:64-65.
    59) Finkel AJ: Hamilton and Hardy's Industrial Toxicology, 4th Ed, John Wright, PSG Inc, Boston, MA, 1983, pp 117-118.
    60) Garry VF, Good PF, & Manivel C: Investigation of a fatality from nonoccupational aluminum phosphide exposure: Measurement of aluminum in tissue and body fluids as a marker of exposure. J Lab Clin Med 1993; 122:739-747.
    61) Garry VF, Griffith J, & Danzl TJ: Human genotoxicity: pesticide applicators and phosphine. Science 1989; 246:251-255.
    62) Guardian Manufacturing Group: Guardian Gloves Test Results. Guardian Manufacturing Group. Willard, OH. 2001. Available from URL: http://www.guardian-mfg.com/guardianmfg.html. As accessed 12/11/2001.
    63) Gupta S & Ahlawat SK: Aluminum phosphide poisoning -- a review. J Toxicol - Clin Toxicol 1995; 33:19-24.
    64) HSDB : Hazardous Substances Data Bank. National Library of Medicine. Bethesda, MD (Internet Version). Edition expires 1991; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    65) HSDB : Hazardous Substances Data Bank. National Library of Medicine. Bethesda, MD (Internet Version). Edition expires July/31/2002; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    66) Haas CF: Mechanical ventilation with lung protective strategies: what works?. Crit Care Clin 2011; 27(3):469-486.
    67) Hathaway GJ, Proctor NH, & Hughes JP: Chemical Hazards of the Workplace, 3rd ed, Van Nostrand Reinhold Company, New York, NY, 1991, pp 477-478.
    68) Hayes WJ Jr & Laws ER Jr: Handbook of Pesticide Toxicology, Vol 1-3, Academic Press, Inc, San Diego, CA, 1991, pp 657-661.
    69) Hegenbarth MA & American Academy of Pediatrics Committee on Drugs: Preparing for pediatric emergencies: drugs to consider. Pediatrics 2008; 121(2):433-443.
    70) Hvidberg EF & Dam M: Clinical pharmacokinetics of anticonvulsants. Clin Pharmacokinet 1976; 1:161.
    71) IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: 1,3-Butadiene, Ethylene Oxide and Vinyl Halides (Vinyl Fluoride, Vinyl Chloride and Vinyl Bromide), 97, International Agency for Research on Cancer, Lyon, France, 2008.
    72) IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Formaldehyde, 2-Butoxyethanol and 1-tert-Butoxypropan-2-ol, 88, International Agency for Research on Cancer, Lyon, France, 2006.
    73) IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Household Use of Solid Fuels and High-temperature Frying, 95, International Agency for Research on Cancer, Lyon, France, 2010a.
    74) IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Smokeless Tobacco and Some Tobacco-specific N-Nitrosamines, 89, International Agency for Research on Cancer, Lyon, France, 2007.
    75) IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Some Non-heterocyclic Polycyclic Aromatic Hydrocarbons and Some Related Exposures, 92, International Agency for Research on Cancer, Lyon, France, 2010.
    76) IARC: List of all agents, mixtures and exposures evaluated to date - IARC Monographs: Overall Evaluations of Carcinogenicity to Humans, Volumes 1-88, 1972-PRESENT. World Health Organization, International Agency for Research on Cancer. Lyon, FranceAvailable from URL: http://monographs.iarc.fr/monoeval/crthall.html. As accessed Oct 07, 2004.
    77) ICAO: Technical Instructions for the Safe Transport of Dangerous Goods by Air, 2003-2004. International Civil Aviation Organization, Montreal, Quebec, Canada, 2002.
    78) ILC Dover, Inc.: Ready 1 The Chemturion Limited Use Chemical Protective Suit, ILC Dover, Inc., Frederica, DE, 1998.
    79) International Agency for Research on Cancer (IARC): IARC monographs on the evaluation of carcinogenic risks to humans: list of classifications, volumes 1-116. International Agency for Research on Cancer (IARC). Lyon, France. 2016. Available from URL: http://monographs.iarc.fr/ENG/Classification/latest_classif.php. As accessed 2016-08-24.
    80) International Agency for Research on Cancer: IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. World Health Organization. Geneva, Switzerland. 2015. Available from URL: http://monographs.iarc.fr/ENG/Classification/. As accessed 2015-08-06.
    81) Jayaraman KS: Death pills from pesticide. Nature 1991; 353:377.
    82) Kappler, Inc.: Suit Smart. Kappler, Inc.. Guntersville, AL. 2001. Available from URL: http://www.kappler.com/suitsmart/smartsuit2/na_english.asp?select=1. As accessed 7/10/2001.
    83) Khosla SN, Nand N, & Kumar P: Cardiovascular complications of aluminum phosphide poisoning. Angiology 1988; 39:355-359.
    84) Kimberly-Clark, Inc.: Chemical Test Results. Kimberly-Clark, Inc.. Atlanta, GA. 2002. Available from URL: http://www.kc-safety.com/tech_cres.html. As accessed 10/4/2002.
    85) Kleinman ME, Chameides L, Schexnayder SM, et al: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Part 14: pediatric advanced life support. Circulation 2010; 122(18 Suppl.3):S876-S908.
    86) Kligerman AD, Bishop JB, & Erexson GL: Cytogenetic and germ cell effects of phosphine inhalation by rodents: II. Subacute exposures to rats and mice. Environ Mol Mutagen 1994; 24:301-306.
    87) Kollef MH & Schuster DP: The acute respiratory distress syndrome. N Engl J Med 1995; 332:27-37.
    88) LaCrosse-Rainfair: Safety Products, LaCrosse-Rainfair, Racine, WI, 1997.
    89) Lemoine TJ, Schoolman K, Jackman G, et al: Unintentional fatal phosphine gas poisoning of a family. Pediatr Emerg Care 2011; 27(9):869-871.
    90) Link MS, Berkow LC, Kudenchuk PJ, et al: Part 7: Adult Advanced Cardiovascular Life Support: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2015; 132(18 Suppl 2):S444-S464.
    91) Loddenkemper T & Goodkin HP: Treatment of Pediatric Status Epilepticus. Curr Treat Options Neurol 2011; Epub:Epub.
    92) Lohani SP, Casavant MJ, & Ekins BR: Zinc phosphide poisoing: a retrospective case series (Abstract). J Toxicol Clin Toxicol 2000; 38:515.
    93) MAPA Professional: Chemical Resistance Guide. MAPA North America. Columbia, TN. 2003. Available from URL: http://www.mapaglove.com/pro/ChemicalSearch.asp. As accessed 4/21/2003.
    94) MAPA Professional: Chemical Resistance Guide. MAPA North America. Columbia, TN. 2004. Available from URL: http://www.mapaglove.com/ProductSearch.cfm?id=1. As accessed 6/10/2004.
    95) Manno EM: New management strategies in the treatment of status epilepticus. Mayo Clin Proc 2003; 78(4):508-518.
    96) Mar-Mac Manufacturing, Inc: Product Literature, Protective Apparel, Mar-Mac Manufacturing, Inc., McBee, SC, 1995.
    97) Marigold Industrial: US Chemical Resistance Chart, on-line version. Marigold Industrial. Norcross, GA. 2003. Available from URL: www.marigoldindustrial.com/charts/uschart/uschart.html. As accessed 4/14/2003.
    98) Memphis Glove Company: Permeation Guide. Memphis Glove Company. Memphis, TN. 2001. Available from URL: http://www.memphisglove.com/permeation.html. As accessed 7/2/2001.
    99) Merin O, Fink D, Fink DL, et al: Salvage ECMO deployment for fatal aluminum phosphide poisoning. Am J Emerg Med 2015; 33(11):1718.e1-1718.e3.
    100) Misra UK, Bhargava SK, & Nag D: Occupational phosphine exposure in Indian workers. Toxicol Lett 1988b; 42:257-263.
    101) Montgomery Safety Products: Montgomery Safety Products Chemical Resistant Glove Guide, Montgomery Safety Products, Canton, OH, 1995.
    102) NFPA: Fire Protection Guide to Hazardous Materials, 13th ed., National Fire Protection Association, Quincy, MA, 2002.
    103) NHLBI ARDS Network: Mechanical ventilation protocol summary. Massachusetts General Hospital. Boston, MA. 2008. Available from URL: http://www.ardsnet.org/system/files/6mlcardsmall_2008update_final_JULY2008.pdf. As accessed 2013-08-07.
    104) NIOSH : Pocket Guide to Chemical Hazards. National Institute for Occupational Safety and Health. Cincinnati, OH (Internet Version). Edition expires 1996; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    105) NIOSH : Pocket Guide to Chemical Hazards. National Institute for Occupational Safety and Health. Cincinnati, OH. 1990.
    106) NRC: Acute Exposure Guideline Levels for Selected Airborne Chemicals - Volume 1, Subcommittee on Acute Exposure Guideline Levels, Committee on Toxicology, Board on Environmental Studies and Toxicology, Commission of Life Sciences, National Research Council. National Academy Press, Washington, DC, 2001.
    107) NRC: Acute Exposure Guideline Levels for Selected Airborne Chemicals - Volume 2, Subcommittee on Acute Exposure Guideline Levels, Committee on Toxicology, Board on Environmental Studies and Toxicology, Commission of Life Sciences, National Research Council. National Academy Press, Washington, DC, 2002.
    108) NRC: Acute Exposure Guideline Levels for Selected Airborne Chemicals - Volume 3, Subcommittee on Acute Exposure Guideline Levels, Committee on Toxicology, Board on Environmental Studies and Toxicology, Commission of Life Sciences, National Research Council. National Academy Press, Washington, DC, 2003.
    109) NRC: Acute Exposure Guideline Levels for Selected Airborne Chemicals - Volume 4, Subcommittee on Acute Exposure Guideline Levels, Committee on Toxicology, Board on Environmental Studies and Toxicology, Commission of Life Sciences, National Research Council. National Academy Press, Washington, DC, 2004.
    110) Naradzay J & Barish RA: Approach to ophthalmologic emergencies. Med Clin North Am 2006; 90(2):305-328.
    111) Nat-Wear: Protective Clothing, Hazards Chart. Nat-Wear. Miora, NY. 2001. Available from URL: http://www.natwear.com/hazchart1.htm. As accessed 7/12/2001.
    112) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,2,3-Trimethylbenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2006k. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d68a&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    113) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,2,4-Trimethylbenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2006m. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d68a&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    114) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,2-Butylene Oxide (Proposed). United States Environmental Protection Agency. Washington, DC. 2008d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648083cdbb&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    115) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,2-Dibromoethane (Proposed). United States Environmental Protection Agency. Washington, DC. 2007g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064802796db&disposition=attachment&contentType=pdf. As accessed 2010-08-18.
    116) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,3,5-Trimethylbenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2006l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d68a&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    117) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 2-Ethylhexyl Chloroformate (Proposed). United States Environmental Protection Agency. Washington, DC. 2007b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648037904e&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    118) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Acrylonitrile (Proposed). United States Environmental Protection Agency. Washington, DC. 2007c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648028e6a3&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    119) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Adamsite (Proposed). United States Environmental Protection Agency. Washington, DC. 2007h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    120) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Agent BZ (3-quinuclidinyl benzilate) (Proposed). United States Environmental Protection Agency. Washington, DC. 2007f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803ad507&disposition=attachment&contentType=pdf. As accessed 2010-08-18.
    121) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Allyl Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2008. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648039d9ee&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    122) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Aluminum Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    123) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Arsenic Trioxide (Proposed). United States Environmental Protection Agency. Washington, DC. 2007m. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480220305&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    124) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Automotive Gasoline Unleaded (Proposed). United States Environmental Protection Agency. Washington, DC. 2009a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7cc17&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    125) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Biphenyl (Proposed). United States Environmental Protection Agency. Washington, DC. 2005j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064801ea1b7&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    126) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Bis-Chloromethyl Ether (BCME) (Proposed). United States Environmental Protection Agency. Washington, DC. 2006n. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648022db11&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    127) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Boron Tribromide (Proposed). United States Environmental Protection Agency. Washington, DC. 2008a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803ae1d3&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    128) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Bromine Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2007d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648039732a&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    129) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Bromoacetone (Proposed). United States Environmental Protection Agency. Washington, DC. 2008e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809187bf&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    130) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Calcium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    131) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Carbonyl Fluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2008b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803ae328&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    132) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Carbonyl Sulfide (Proposed). United States Environmental Protection Agency. Washington, DC. 2007e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648037ff26&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    133) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Chlorobenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2008c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803a52bb&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    134) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Cyanogen (Proposed). United States Environmental Protection Agency. Washington, DC. 2008f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809187fe&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    135) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Dimethyl Phosphite (Proposed). United States Environmental Protection Agency. Washington, DC. 2009. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7cbf3&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    136) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Diphenylchloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    137) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethyl Isocyanate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648091884e&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    138) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethyl Phosphorodichloridate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480920347&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    139) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethylbenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2008g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809203e7&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    140) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethyldichloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    141) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Germane (Proposed). United States Environmental Protection Agency. Washington, DC. 2008j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963906&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    142) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Hexafluoropropylene (Proposed). United States Environmental Protection Agency. Washington, DC. 2006. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064801ea1f5&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    143) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ketene (Proposed). United States Environmental Protection Agency. Washington, DC. 2007. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ee7c&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    144) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Magnesium Aluminum Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    145) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Magnesium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    146) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Malathion (Proposed). United States Environmental Protection Agency. Washington, DC. 2009k. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809639df&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    147) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Mercury Vapor (Proposed). United States Environmental Protection Agency. Washington, DC. 2009b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a8a087&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    148) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyl Isothiocyanate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008k. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963a03&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    149) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyl Parathion (Proposed). United States Environmental Protection Agency. Washington, DC. 2008l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963a57&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    150) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyl tertiary-butyl ether (Proposed). United States Environmental Protection Agency. Washington, DC. 2007a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064802a4985&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    151) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methylchlorosilane (Proposed). United States Environmental Protection Agency. Washington, DC. 2005. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5f4&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    152) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyldichloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    153) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyldichlorosilane (Proposed). United States Environmental Protection Agency. Washington, DC. 2005a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c646&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    154) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Mustard (HN1 CAS Reg. No. 538-07-8) (Proposed). United States Environmental Protection Agency. Washington, DC. 2006a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d6cb&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    155) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Mustard (HN2 CAS Reg. No. 51-75-2) (Proposed). United States Environmental Protection Agency. Washington, DC. 2006b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d6cb&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    156) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Mustard (HN3 CAS Reg. No. 555-77-1) (Proposed). United States Environmental Protection Agency. Washington, DC. 2006c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d6cb&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    157) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Tetroxide (Proposed). United States Environmental Protection Agency. Washington, DC. 2008n. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648091855b&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    158) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Trifluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2009l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963e0c&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    159) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Parathion (Proposed). United States Environmental Protection Agency. Washington, DC. 2008o. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963e32&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    160) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Perchloryl Fluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2009c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7e268&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    161) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Perfluoroisobutylene (Proposed). United States Environmental Protection Agency. Washington, DC. 2009d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7e26a&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    162) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phenyl Isocyanate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008p. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096dd58&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    163) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phenyl Mercaptan (Proposed). United States Environmental Protection Agency. Washington, DC. 2006d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020cc0c&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    164) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phenyldichloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007k. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    165) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phorate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008q. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096dcc8&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    166) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phosgene (Draft-Revised). United States Environmental Protection Agency. Washington, DC. 2009e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a8a08a&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    167) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phosgene Oxime (Proposed). United States Environmental Protection Agency. Washington, DC. 2009f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7e26d&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    168) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Potassium Cyanide (Proposed). United States Environmental Protection Agency. Washington, DC. 2009g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7cbb9&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    169) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Potassium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    170) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Propargyl Alcohol (Proposed). United States Environmental Protection Agency. Washington, DC. 2006e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ec91&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    171) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Selenium Hexafluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2006f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ec55&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    172) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Silane (Proposed). United States Environmental Protection Agency. Washington, DC. 2006g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d523&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    173) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Sodium Cyanide (Proposed). United States Environmental Protection Agency. Washington, DC. 2009h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7cbb9&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    174) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Sodium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    175) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Strontium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    176) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Sulfuryl Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2006h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ec7a&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    177) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Tear Gas (Proposed). United States Environmental Protection Agency. Washington, DC. 2008s. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096e551&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    178) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Tellurium Hexafluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2009i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7e2a1&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    179) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Tert-Octyl Mercaptan (Proposed). United States Environmental Protection Agency. Washington, DC. 2008r. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096e5c7&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    180) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Tetramethoxysilane (Proposed). United States Environmental Protection Agency. Washington, DC. 2006j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d632&disposition=attachment&contentType=pdf. As accessed 2010-08-17.
    181) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Trimethoxysilane (Proposed). United States Environmental Protection Agency. Washington, DC. 2006i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d632&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    182) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Trimethyl Phosphite (Proposed). United States Environmental Protection Agency. Washington, DC. 2009j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7d608&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    183) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Trimethylacetyl Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2008t. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096e5cc&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    184) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Zinc Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    185) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for n-Butyl Isocyanate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008m. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064808f9591&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    186) National Heart,Lung,and Blood Institute: Expert panel report 3: guidelines for the diagnosis and management of asthma. National Heart,Lung,and Blood Institute. Bethesda, MD. 2007. Available from URL: http://www.nhlbi.nih.gov/guidelines/asthma/asthgdln.pdf.
    187) National Institute for Occupational Safety and Health (NIOSH): Phosphine: Lung Damaging Agent. Centers for Disease Control and Prevention (CDC). Atlanta, GA. 2008. Available from URL: http://www.cdc.gov/niosh/ershdb/PrintableERC_29750035.html. As accessed 2012-07-03.
    188) National Institute for Occupational Safety and Health: NIOSH Pocket Guide to Chemical Hazards, U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, Cincinnati, OH, 2007.
    189) National Research Council : Acute exposure guideline levels for selected airborne chemicals, 5, National Academies Press, Washington, DC, 2007.
    190) National Research Council: Acute exposure guideline levels for selected airborne chemicals, 6, National Academies Press, Washington, DC, 2008.
    191) National Research Council: Acute exposure guideline levels for selected airborne chemicals, 7, National Academies Press, Washington, DC, 2009.
    192) National Research Council: Acute exposure guideline levels for selected airborne chemicals, 8, National Academies Press, Washington, DC, 2010.
    193) Neese Industries, Inc.: Fabric Properties Rating Chart. Neese Industries, Inc.. Gonzales, LA. 2003. Available from URL: http://www.neeseind.com/new/TechGroup.asp?Group=Fabric+Properties&Family=Technical. As accessed 4/15/2003.
    194) Neumar RW , Otto CW , Link MS , et al: Part 8: adult advanced cardiovascular life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2010; 122(18 Suppl 3):S729-S767.
    195) Nocera A, Levitin HW, & Hilton JMN: Dangerous bodies: a case of fatal aluminium phosphide poisoning. MJA 2000; 173:133-135.
    196) North: Chemical Resistance Comparison Chart - Protective Footwear . North Safety. Cranston, RI. 2002. Available from URL: http://www.linkpath.com/index2gisufrm.php?t=N-USA1. As accessed April 30, 2004.
    197) North: eZ Guide Interactive Software. North Safety. Cranston, RI. 2002a. Available from URL: http://www.northsafety.com/feature1.htm. As accessed 8/31/2002.
    198) Peate WF: Work-related eye injuries and illnesses. Am Fam Physician 2007; 75(7):1017-1022.
    199) Peberdy MA , Callaway CW , Neumar RW , et al: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care science. Part 9: post–cardiac arrest care. Circulation 2010; 122(18 Suppl 3):S768-S786.
    200) Playtex: Fits Tough Jobs Like a Glove, Playtex, Westport, CT, 1995.
    201) Proctor NH, Hughes JP, & Fischman ML: Chemical Hazards of the Workplace, 2nd ed, JB Lippincott Co, Philadelphia, PA, 1988, pp 410-411.
    202) Product Information: Cordarone(R) oral tablets, amiodarone HCl oral tablets. Wyeth Pharmaceuticals Inc (per FDA), Philadelphia, PA, 2015.
    203) Product Information: Lidocaine HCl intravenous injection solution, lidocaine HCl intravenous injection solution. Hospira (per manufacturer), Lake Forest, IL, 2006.
    204) Product Information: diazepam IM, IV injection, diazepam IM, IV injection. Hospira, Inc (per Manufacturer), Lake Forest, IL, 2008.
    205) Product Information: dopamine hcl, 5% dextrose IV injection, dopamine hcl, 5% dextrose IV injection. Hospira,Inc, Lake Forest, IL, 2004.
    206) Product Information: lorazepam IM, IV injection, lorazepam IM, IV injection. Akorn, Inc, Lake Forest, IL, 2008.
    207) Product Information: norepinephrine bitartrate injection, norepinephrine bitartrate injection. Sicor Pharmaceuticals,Inc, Irvine, CA, 2005.
    208) RTECS : Registry of Toxic Effects of Chemical Substances. National Institute for Occupational Safety and Health. Cincinnati, OH (Internet Version). Edition expires 1991; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    209) River City: Protective Wear Product Literature, River City, Memphis, TN, 1995.
    210) Safety 4: North Safety Products: Chemical Protection Guide. North Safety. Cranston, RI. 2002. Available from URL: http://www.safety4.com/guide/set_guide.htm. As accessed 8/14/2002.
    211) Sax NI & Lewis RJ: Dangerous Properties of Industrial Materials, 7th ed, Van Nostrand Reinhold Company, New York, NY, 1989, pp 2768-2769.
    212) Sax NI & Lewis RJ: Hawley's Condensed Chemical Dictionary, 11th ed, Van Nostrand Reinhold Company, New York, NY, 1987, pp 909.
    213) Schoonbroodt D, Guffens P, Jousten P, et al: Acute phosphine poisoning? A case report and review. Acta Clin Belg 1992; 47(4):280-284.
    214) Schroeder RE, Newton PE, & Sullivan JB: An inhalation developmental toxicity study of phosphine in rats. Toxicologist 1992; 12:122.
    215) Scott R, Besag FMC, & Neville BGR: Buccal midazolam and rectal diazepam for treatment of prolonged seizures in childhood and adolescence: a randomized trial. Lancet 1999; 353:623-626.
    216) Servus: Norcross Safety Products, Servus Rubber, Servus, Rock Island, IL, 1995.
    217) Shadnia S, Mehrpour O, & Abdollahi M: Unintentional poisoning by phosphine released from aluminum phosphide. Hum Exp Toxicol 2008; 27(1):87-89.
    218) Shusterman D, Windham GC, & Fenster L: Employment in electronics manufacturing and risk of spontaneous abortion. J Occup Med 1993; 35:381-386.
    219) Siwach SB, Singh H, & Jagdish: Cardiac arrhythmias in aluminum phosphide poisoning studies by on continuous holter and cardioscopic monitoring. J Assoc Physicians India 1998; 46:598-601.
    220) Sreenath TG, Gupta P, Sharma KK, et al: Lorazepam versus diazepam-phenytoin combination in the treatment of convulsive status epilepticus in children: A randomized controlled trial. Eur J Paediatr Neurol 2009; Epub:Epub.
    221) Standard Safety Equipment: Product Literature, Standard Safety Equipment, McHenry, IL, 1995.
    222) Stolbach A & Hoffman RS: Respiratory Principles. In: Nelson LS, Hoffman RS, Lewin NA, et al, eds. Goldfrank's Toxicologic Emergencies, 9th ed. McGraw Hill Medical, New York, NY, 2011.
    223) Sudakin DL: Occupational exposure to aluminium phosphide and phosphine gas? A suspected case report and review of the literature. Hum Exp Toxicol 2005; 24(1):27-33.
    224) Tingley: Chemical Degradation for Footwear and Clothing. Tingley. South Plainfield, NJ. 2002. Available from URL: http://www.tingleyrubber.com/tingley/Guide_ChemDeg.pdf. As accessed 10/16/2002.
    225) Trelleborg-Viking, Inc.: Chemical and Biological Tests (database). Trelleborg-Viking, Inc.. Portsmouth, NH. 2002. Available from URL: http://www.trelleborg.com/protective/. As accessed 10/18/2002.
    226) Trelleborg-Viking, Inc.: Trellchem Chemical Protective Suits, Interactive manual & Chemical Database. Trelleborg-Viking, Inc.. Portsmouth, NH. 2001.
    227) U.S. Department of Energy, Office of Emergency Management: Protective Action Criteria (PAC) with AEGLs, ERPGs, & TEELs: Rev. 26 for chemicals of concern. U.S. Department of Energy, Office of Emergency Management. Washington, DC. 2010. Available from URL: http://www.hss.doe.gov/HealthSafety/WSHP/Chem_Safety/teel.html. As accessed 2011-06-27.
    228) U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project : 11th Report on Carcinogens. U.S. Department of Health and Human Services, Public Health Service, National Toxicology Program. Washington, DC. 2005. Available from URL: http://ntp.niehs.nih.gov/INDEXA5E1.HTM?objectid=32BA9724-F1F6-975E-7FCE50709CB4C932. As accessed 2011-06-27.
    229) U.S. Environmental Protection Agency: Discarded commercial chemical products, off-specification species, container residues, and spill residues thereof. Environmental Protection Agency's (EPA) Resource Conservation and Recovery Act (RCRA); List of hazardous substances and reportable quantities 2010b; 40CFR(261.33, e-f):77-.
    230) U.S. Environmental Protection Agency: Integrated Risk Information System (IRIS). U.S. Environmental Protection Agency. Washington, DC. 2011. Available from URL: http://cfpub.epa.gov/ncea/iris/index.cfm?fuseaction=iris.showSubstanceList&list_type=date. As accessed 2011-06-21.
    231) U.S. Environmental Protection Agency: List of Radionuclides. U.S. Environmental Protection Agency. Washington, DC. 2010a. Available from URL: http://www.gpo.gov/fdsys/pkg/CFR-2010-title40-vol27/pdf/CFR-2010-title40-vol27-sec302-4.pdf. As accessed 2011-06-17.
    232) U.S. Environmental Protection Agency: List of hazardous substances and reportable quantities. U.S. Environmental Protection Agency. Washington, DC. 2010. Available from URL: http://www.gpo.gov/fdsys/pkg/CFR-2010-title40-vol27/pdf/CFR-2010-title40-vol27-sec302-4.pdf. As accessed 2011-06-17.
    233) U.S. Environmental Protection Agency: The list of extremely hazardous substances and their threshold planning quantities (CAS Number Order). U.S. Environmental Protection Agency. Washington, DC. 2010c. Available from URL: http://www.gpo.gov/fdsys/pkg/CFR-2010-title40-vol27/pdf/CFR-2010-title40-vol27-part355.pdf. As accessed 2011-06-17.
    234) U.S. Occupational Safety and Health Administration: Part 1910 - Occupational safety and health standards (continued) Occupational Safety, and Health Administration's (OSHA) list of highly hazardous chemicals, toxics and reactives. Subpart Z - toxic and hazardous substances. CFR 2010 2010; Vol6(SEC1910):7-.
    235) U.S. Occupational Safety, and Health Administration (OSHA): Process safety management of highly hazardous chemicals. 29 CFR 2010 2010; 29(1910.119):348-.
    236) United States Environmental Protection Agency Office of Pollution Prevention and Toxics: Acute Exposure Guideline Levels (AEGLs) for Vinyl Acetate (Proposed). United States Environmental Protection Agency. Washington, DC. 2006. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d6af&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    237) Vanden Hoek TL, Morrison LJ, Shuster M, et al: Part 12: cardiac arrest in special situations: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2010; 122(18 Suppl 3):S829-S861.
    238) Wells Lamont Industrial: Chemical Resistant Glove Application Chart. Wells Lamont Industrial. Morton Grove, IL. 2002. Available from URL: http://www.wellslamontindustry.com. As accessed 10/31/2002.
    239) Willers-Russo LJ: Three fatalities involving phosphine gas, produced as a result of methamphetamine manufacturing. J Forensic Sci 1999; 44(3):647-652.
    240) Willson DF, Truwit JD, Conaway MR, et al: The adult calfactant in acute respiratory distress syndrome (CARDS) trial. Chest 2015; 148(2):356-364.
    241) Wilson DF, Thomas NJ, Markovitz BP, et al: Effect of exogenous surfactant (calfactant) in pediatric acute lung injury. A randomized controlled trial. JAMA 2005; 293:470-476.
    242) Wilson R, Lovejoy FH, Jaeger RJ, et al: Acute phosphine poisoning aboard a grain freighter. Epidemiologic, clinical, and pathological findings. JAMA 1980; 244(2):148-150.
    243) Windholz M, Budavari S, & Blumetti RF: The Merck Index, 10th ed, Merck & Co, Inc, Rahway, NJ, 1983.
    244) Workrite: Chemical Splash Protection Garments, Technical Data and Application Guide, W.L. Gore Material Chemical Resistance Guide, Workrite, Oxnard, CA, 1997.
    245) Zaebst DD, Blade LM, & Burroughs GE: Phosphine exposures in grain elevators during fumigation with aluminum phosphide. Appl Ind Hyg 1988; 3:146-154.
    246) de Caen AR, Berg MD, Chameides L, et al: Part 12: Pediatric Advanced Life Support: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2015; 132(18 Suppl 2):S526-S542.