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ZINC PHOSPHIDE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Zinc phosphide is an inorganic compound used as a rodenticide.

Specific Substances

    1) Trizinc diphosphide
    2) ZnP
    3) Zn3P2
    4) CAS 1314-84-7
    1.2.1) MOLECULAR FORMULA
    1) P2-Zn3

Available Forms Sources

    A) FORMS
    1) Zinc phosphide is dark gray to black in color and is available as pellets, granules, dust, and tracking powders (Gervais, et al, 2010).
    B) USES
    1) Zinc phosphide is used as a rodenticide (Sogut et al, 2011; Chugh et al, 1998; Mack, 1989).

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: Zinc phosphide (Zn3P2, ZnP) is an inorganic dark gray crystalline powder used as a rodenticide.
    B) TOXICOLOGY: Its toxicity is secondary to the release of phosphine gas on contact with moisture or moist air. Phosphine blocks cytochrome C oxidase. This document covers effects from ingestion of zinc phosphide. Information on the effects of inhalation of phosphine gas are covered in a separate management.
    C) EPIDEMIOLOGY: Human poisoning is uncommon, but occurs worldwide and can be fatal.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Nausea, vomiting, and abdominal pain are common. Tachycardia, fatigue, headache, dizziness, anxiety, restlessness, dyspnea, tachypnea, and hypoglycemia may develop.
    2) SEVERE TOXICITY: CNS excitation or depression, hypotension, dysrhythmias, metabolic and respiratory acidosis, jaundice, elevated liver enzymes, seizures, and acute lung injury may develop. Pancreatitis is a rare complication.
    0.2.3) VITAL SIGNS
    A) Hypotension, shock, and tachycardia occur commonly.
    0.2.5) CARDIOVASCULAR
    A) WITH POISONING/EXPOSURE
    1) Cardiac dysrhythmias and ECG abnormalities have ben reported following zinc phosphide ingestions.
    2) Hypotension, shock, toxic myocarditis, myocardial failure, and massive focal myocardial injury with elevated cardiac enzymes may occur.
    0.2.6) RESPIRATORY
    A) WITH POISONING/EXPOSURE
    1) Cough, dyspnea, cyanosis, chest tightness, and tachypnea may occur. Pulmonary edema has been reported following zinc phosphide ingestion.
    2) Zinc phosphide releases toxic and irritating fumes of oxides of phosphorus and zinc oxide when heated to decomposition. Inhalation exposure to such fumes would be predicted to result in respiratory tract irritation with bronchospasm, chemical pneumonitis, or noncardiogenic pulmonary edema.
    0.2.7) NEUROLOGIC
    A) WITH POISONING/EXPOSURE
    1) Acute exposure may result in headache, dizziness, fatigue, and CNS depression leading to coma, and chronic exposure may lead to neuropsychiatric manifestations. Seizures are not uncommon after acute exposure. Restlessness and anxiety may be noted following acute zinc phosphide ingestion.
    0.2.8) GASTROINTESTINAL
    A) WITH POISONING/EXPOSURE
    1) Nausea, vomiting, and abdominal pain may occur. Pancreatitis has been rarely reported.
    0.2.9) HEPATIC
    A) Acute exposure may produce jaundice with hepatomegaly. Elevations of serum transaminases may be noted.
    0.2.11) ACID-BASE
    A) WITH POISONING/EXPOSURE
    1) Metabolic acidosis may be seen in acute poisonings.
    0.2.12) FLUID-ELECTROLYTE
    A) WITH POISONING/EXPOSURE
    1) Hypokalemia may occur secondary to profuse vomiting following zinc phosphide ingestion.
    0.2.16) ENDOCRINE
    A) Severe hypoglycemia has been reported.
    0.2.20) REPRODUCTIVE
    A) At the time of this review, no data were available to assess the teratogenic potential of this agent.
    B) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.
    C) In experimental animals, zinc phosphide induced a high percentage of abnormal sperm.

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, blood glucose, renal function, and liver enzymes.
    E) Obtain a chest radiograph in patients with respiratory symptoms.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TOXICITY
    1) For mild to moderate exposures, the mainstay of treatment is good supportive care. Do not induce emesis in cases of zinc phosphide ingestion as this could cause off-gassing of phosphine and secondary contamination in enclosed areas. 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, supportive care is again the most important initial measure. Severe metabolic acidosis can be treated with sodium bicarbonate, and standard treatment for dysrhythmias may be needed. Treat seizures with benzodiazepines; add barbiturates and propofol as 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, such as dopamine or norepinephrine.
    C) DECONTAMINATION
    1) PREHOSPITAL: Move patient to fresh air as soon as possible from inhalational exposures. Prehospital gastrointestinal (GI) decontamination is not recommended because of the potential for formation of phosphine gas and the potential for abrupt deterioration.
    2) HOSPITAL: The role of GI decontamination is not clear, as contact with water has the potential to form phosphine gas. Activated charcoal could be considered for patients with recent zinc phosphide ingestion (less than one hour) who are awake, alert, and cooperative.
    D) AIRWAY MANAGEMENT
    1) Airway management is one of the primary issues with phosphine toxicity; patients may get critically ill quickly, and 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) There is no evidence for the use of dialysis, hemoperfusion, urinary alkalinization, or multiple dose charcoal, and are unlikely to be helpful for zinc phosphide exposures.
    G) PATIENT DISPOSITION
    1) HOME CRITERIA: There is no role for home management of zinc phosphide exposures.
    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 with careful instructions to return if any respiratory symptoms develop.
    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, hypotension, dysrhythmias, CNS depression), 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 and/or poison centers for any patient with significant zinc phosphide poisoning. Other helpful consultants may include critical care physicians and pulmonologists to help management of the patient's symptoms.
    H) PITFALLS
    1) One concern from off-gassing of phosphine from zinc phosphide exposure is that the characteristic odor might be masked by olfactory fatigue at higher concentrations. The minimal detectable concentration via phosphine's decaying fish odor is 1 to 3 parts per million (ppm) in air. Patients should be removed from the exposure as the first line of treatment. Severe symptoms, such as pulmonary edema, may be delayed up to 72 hours after exposure.
    I) TOXICOKINETICS
    1) Zinc phosphide reacts rapidly with water or acids to form phosphine. Phosphine is absorbed rapidly in the human body as reflected by the abrupt onset of symptoms, of which can range from immediate to within a few hours. Some toxic manifestations, such as abnormalities in liver function tests 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.
    0.4.3) INHALATION EXPOSURE
    A) Move patient to fresh air and monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as needed. Bronchospasm can be treated with B2 agonists and oral or parenteral corticosteroids.
    0.4.4) EYE EXPOSURE
    A) Irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) Remove contaminated clothing and wash exposed area thoroughly with soap and water.

Range Of Toxicity

    A) TOXICITY: Ingestion of 4 to 7 g of zinc phosphide has caused death; doses as low as 40 mg/kg may be fatal in humans. Survival has been reported after total zinc phosphide ingestions of 25 to 50 g.

Clinical Effects

Summary Of Exposure

    A) USES: Zinc phosphide (Zn3P2, ZnP) is an inorganic dark gray crystalline powder used as a rodenticide.
    B) TOXICOLOGY: Its toxicity is secondary to the release of phosphine gas on contact with moisture or moist air. Phosphine blocks cytochrome C oxidase. This document covers effects from ingestion of zinc phosphide. Information on the effects of inhalation of phosphine gas are covered in a separate management.
    C) EPIDEMIOLOGY: Human poisoning is uncommon, but occurs worldwide and can be fatal.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Nausea, vomiting, and abdominal pain are common. Tachycardia, fatigue, headache, dizziness, anxiety, restlessness, dyspnea, tachypnea, and hypoglycemia may develop.
    2) SEVERE TOXICITY: CNS excitation or depression, hypotension, dysrhythmias, metabolic and respiratory acidosis, jaundice, elevated liver enzymes, seizures, and acute lung injury may develop. Pancreatitis is a rare complication.

Vital Signs

    3.3.1) SUMMARY
    A) Hypotension, shock, and tachycardia occur commonly.
    3.3.4) BLOOD PRESSURE
    A) WITH POISONING/EXPOSURE
    1) Hypotension, cardiac dysrhythmias, and shock are common in acute poisoning (Sogut et al, 2011; Chugh et al, 1998).
    3.3.5) PULSE
    A) WITH POISONING/EXPOSURE
    1) INCIDENCE: A prospective analysis of patients with acute zinc phosphide poisoning was conducted over a 5-year-period. Palpitations and sweating were reported in 80% of patients (n=20) following ingestion of zinc phosphide. The mean amount of zinc phosphide ingested was 7.5 g (ranging from 5 to 20 g) (Chugh et al, 1998).

Cardiovascular

    3.5.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Cardiac dysrhythmias and ECG abnormalities have ben reported following zinc phosphide ingestions.
    2) Hypotension, shock, toxic myocarditis, myocardial failure, and massive focal myocardial injury with elevated cardiac enzymes may occur.
    3.5.2) CLINICAL EFFECTS
    A) CONDUCTION DISORDER OF THE HEART
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 52-year-old man ingested a diluted rodenticide solution of zinc phosphide and developed vomiting and nystagmus. He became agitated and hypotensive (78/58), and he developed respiratory depression requiring intubation. Shortly thereafter he developed ventricular fibrillation followed by asystole and could not be resuscitated. Autopsy revealed pulmonary edema (Broderick & Birnbaum, 2002).
    b) INCIDENCE: A prospective analysis of patients with acute zinc phosphide poisoning was conducted over a 5-year-period. ECG abnormalities (wide QRS interval with varied ST-T changes, supraventricular ectopy, ventricular ectopy) were reported in 4 of 20 patients following ingestion of zinc phosphide. The mean amount of zinc phosphide ingested was 7.5 g (ranging from 5 to 20 g) (Chugh et al, 1998)
    B) HYPOTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) Hypotension has been reported with zinc phosphide ingestions (Sogut et al, 2011).
    b) CASE REPORT: A 52-year-old man ingested a diluted rodenticide solution of zinc phosphide and developed vomiting and nystagmus. He became agitated and hypotensive (78/58), and he developed respiratory depression requiring intubation. Shortly thereafter he developed ventricular fibrillation followed by asystole and could not be resuscitated. Autopsy revealed pulmonary edema (Broderick & Birnbaum, 2002).
    c) INCIDENCE: A prospective analysis of patients with acute zinc phosphide poisoning was conducted over a 5-year-period. Hypotension was reported in 40% of patients (n=20) following ingestion of zinc phosphide. The mean amount of zinc phosphide ingested was 7.5 g (ranging from 5 to 20 g) (Chugh et al, 1998).
    C) HEART FAILURE
    1) WITH POISONING/EXPOSURE
    a) Zinc phosphide ingestion has resulted in primary myocardial failure as a terminal event, probably due to phosphine release (Rodenberg et al, 1989).
    b) CASE REPORT: A 22-year-old woman presented to the emergency department comatose (Glasgow Coma Scale score of 8) with tachypnea, dyspnea, cyanosis, tachycardia, and hypotension after intentionally ingesting 10% zinc phosphide powder. The estimated ingested amount was approximately 10 g . Physical examination revealed hyperventilation and rales and rhonchi in lungs bilaterally, an ECG revealed ST depression, laboratory data showed elevated cardiac enzyme concentrations (creatine phosphokinase 286 international units/L, creatine kinase MB 35 ng/mL, troponin I 2.5 ng/mL, and lactate dehydrogenase 416 international units/L), and a chest radiograph demonstrated increased radiodensity in the basal lobes of the lungs, indicating acute pulmonary edema and congestive heart failure. Despite aggressive supportive measures, the patient had a cardiac arrest and could not be successfully resuscitated, with death occurring approximately 4 hours post-admission. Autopsy revealed congested and edematous lungs with petechial hemorrhages on the cardiac surface (Sogut et al, 2011).
    D) MYOCARDITIS
    1) WITH POISONING/EXPOSURE
    a) Toxic myocarditis has been reported following zinc phosphide poisoning (Patial et al, 1990).
    E) HEART FAILURE
    1) WITH POISONING/EXPOSURE
    a) Zinc phosphide is reported to produce primary myocardial failure as a terminal event (Rodenberg et al, 1989). This phenomenon is probably due to phosphine rather than to the zinc ion itself.
    F) SHOCK
    1) WITH POISONING/EXPOSURE
    a) INCIDENCE: A prospective analysis of patients with acute zinc phosphide poisoning was conducted over a 5-year-period. Shock was reported in 8 of 20 patients following ingestion of zinc phosphide, resulting in death in 5 patients. The mean amount of zinc phosphide ingested was 7.5 g (ranging from 5 to 20 g) (Chugh et al, 1998).

Respiratory

    3.6.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Cough, dyspnea, cyanosis, chest tightness, and tachypnea may occur. Pulmonary edema has been reported following zinc phosphide ingestion.
    2) Zinc phosphide releases toxic and irritating fumes of oxides of phosphorus and zinc oxide when heated to decomposition. Inhalation exposure to such fumes would be predicted to result in respiratory tract irritation with bronchospasm, chemical pneumonitis, or noncardiogenic pulmonary edema.
    3.6.2) CLINICAL EFFECTS
    A) DYSPNEA
    1) Cough, dyspnea, cyanosis, chest tightness, and tachypnea may occur with zinc phosphide ingestion (Sogut et al, 2011; Gervais, et al, 2010; Chugh et al, 1998).
    B) ACUTE CARDIAC PULMONARY EDEMA
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 22-year-old woman presented to the emergency department comatose (Glasgow Coma Scale score of 8) with tachypnea, dyspnea, cyanosis, tachycardia, and hypotension after intentionally ingesting 10% zinc phosphide powder. The estimated ingested amount was approximately 10 g. Physical examination revealed hyperventilation and rales and rhonchi in lungs bilaterally, an ECG revealed ST depression, laboratory data showed elevated cardiac enzyme concentrations, and a chest radiograph demonstrated increased radiodensity in the basal lobes of the lungs, indicating acute pulmonary edema and congestive heart failure. Despite aggressive supportive measures, the patient had a cardiac arrest and could not be successfully resuscitated, with death occurring approximately 4 hours post-admission. Autopsy revealed congested and edematous lungs with petechial hemorrhages on the cardiac surface (Sogut et al, 2011).
    b) CASE REPORT: A 52-year-old man ingested a diluted rodenticide solution of zinc phosphide and developed vomiting and nystagmus. He became agitated and hypotensive (78/58), and he developed respiratory depression requiring intubation. Shortly thereafter he developed ventricular fibrillation followed by asystole and could not be resuscitated. Autopsy revealed pulmonary edema (Broderick & Birnbaum, 2002).
    c) INCIDENCE: A prospective analysis of patients with acute zinc phosphide poisoning was conducted over a 5-year-period. Pulmonary edema was reported in 15% of patients (n=20) following ingestion of zinc phosphide. The mean amount of zinc phosphide ingested was 7.5 g (ranging from 5 to 20 g) (Chugh et al, 1998).
    C) RESPIRATORY CONDITION DUE TO CHEMICAL FUMES AND/OR VAPORS
    1) Zinc phosphide releases toxic and irritating fumes of oxides of phosphorus and zinc oxide when heated to decomposition (Sax & Lewis, 1989) EPA, 1985; (CHRIS , 1990). Inhalation exposure to such fumes would be predicted to result in respiratory tract irritation with bronchospasm, chemical pneumonitis, or noncardiogenic pulmonary edema.

Neurologic

    3.7.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Acute exposure may result in headache, dizziness, fatigue, and CNS depression leading to coma, and chronic exposure may lead to neuropsychiatric manifestations. Seizures are not uncommon after acute exposure. Restlessness and anxiety may be noted following acute zinc phosphide ingestion.
    3.7.2) CLINICAL EFFECTS
    A) CENTRAL NERVOUS SYSTEM DEFICIT
    1) WITH POISONING/EXPOSURE
    a) Large acute exposures may result in headache, dizziness, fatigue, and CNS depression leading to coma (Gervais, et al, 2010; Mack, 1989).
    B) SEIZURE
    1) WITH POISONING/EXPOSURE
    a) Seizures may occur following zinc phosphide ingestions (Sogut et al, 2011; Gervais, et al, 2010; Mack, 1989).
    C) ANXIETY
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 52-year-old man ingested a diluted rodenticide solution of zinc phosphide and developed vomiting and nystagmus. He became agitated and hypotensive (78/58), and he developed respiratory depression requiring intubation. Shortly thereafter he developed ventricular fibrillation followed by asystole and could not be resuscitated. Autopsy revealed pulmonary edema (Broderick & Birnbaum, 2002).
    b) INCIDENCE: A prospective analysis of patients with acute zinc phosphide poisoning was conducted over a 5-year-period. Restlessness and anxiety were reported in all 20 patients following ingestion of zinc phosphide. The mean amount of zinc phosphide ingested was 7.5 g (ranging from 5 to 20 g) (Chugh et al, 1998).

Gastrointestinal

    3.8.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Nausea, vomiting, and abdominal pain may occur. Pancreatitis has been rarely reported.
    3.8.2) CLINICAL EFFECTS
    A) NAUSEA AND VOMITING
    1) WITH POISONING/EXPOSURE
    a) Nausea and vomiting is common (Gervais, et al, 2010; Orak et al, 2008; Sax & Lewis, 1989; Lewis, 1996) generally occurs early following ingestion (Mack, 1989).
    b) INCIDENCE: A prospective analysis of patients with acute zinc phosphide poisoning was conducted over a 5-year-period. Profuse vomiting was reported in all 20 patients following ingestion of zinc phosphide. The mean amount of zinc phosphide ingested was 7.5 g (ranging from 5 to 20 g). The vomitus was black in color (Chugh et al, 1998).
    B) ABDOMINAL PAIN
    1) WITH POISONING/EXPOSURE
    a) Abdominal pain has been reported (Orak et al, 2008) and generally occurs early following zinc phosphide ingestion (Mack, 1989).
    C) PANCREATITIS
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: Pancreatitis developed in one patient following zinc phosphide ingestion (Sarma & Narula, 1996).

Hepatic

    3.9.1) SUMMARY
    A) Acute exposure may produce jaundice with hepatomegaly. Elevations of serum transaminases may be noted.
    3.9.2) CLINICAL EFFECTS
    A) JAUNDICE
    1) WITH POISONING/EXPOSURE
    a) INCIDENCE: A prospective analysis of patients with acute zinc phosphide poisoning was conducted over a 5-year-period. Jaundice with hepatomegaly and elevated hepatic transaminase concentrations was reported in 15% of patients (n=20) following ingestion of zinc phosphide. The mean amount of zinc phosphide ingested was 7.5 g (ranging from 5 to 20 g) (Chugh et al, 1998).
    B) LIVER ENZYMES ABNORMAL
    1) WITH POISONING/EXPOSURE
    a) Elevated hepatic enzyme concentrations may occur with zinc phosphide ingestions (Sogut et al, 2011; Chugh et al, 1998).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) RENAL TUBULAR ACIDOSIS
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: Acute distal renal tubular acidosis (type 1) developed in a 25-year-old man after ingesting approximately 7 grams of zinc phosphide powder in a suicide attempt. Arterial blood gas analysis showed pH 6.973, PaCO2 24.2 mm Hg, PaO2 91 mm Hg, HCO3 9.3 mEq/L, lactate 2 mEq/L and urine pH 6. Despite supportive care, he developed cardio-pulmonary arrest and died 5 hours after admission (Orak et al, 2008).

Acid-Base

    3.11.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Metabolic acidosis may be seen in acute poisonings.
    3.11.2) CLINICAL EFFECTS
    A) ACIDOSIS
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: Severe metabolic acidosis developed in a 25-year-old man after ingesting approximately 7 grams of zinc phosphide powder in a suicide attempt. He presented with confusion, tachypnea, nausea, vomiting, and abdominal pain. Arterial blood gas analysis showed pH 6.973, PaCO2 24.2 mm Hg, PaO2 91 mm Hg, HCO3 9.3 mEq/L, lactate 2 mEq/L and urine pH 6. He was diagnosed with acute distal renal tubular acidosis (type 1). Despite supportive care, he developed cardio-pulmonary arrest and died 5 hours after admission (Orak et al, 2008).
    b) INCIDENCE: A prospective analysis of patients with acute zinc phosphide poisoning was conducted over a 5-year-period. Metabolic acidosis was reported in 60% of patients (n=20) following ingestion of zinc phosphide. The mean amount of zinc phosphide ingested was 7.5 g (ranging from 5 to 20 g) (Chugh et al, 1998).
    c) CASE REPORT: Mixed metabolic and respiratory acidosis (pH 6.91, PCO2 55.4 mmHg, PO2 65.5 mmHg, HCO3 9.7 mmol/L, lactate 6.8 mmol/L) was reported in a 22-year-old woman following intentional ingestion of approximately 10 g of 10% zinc phosphide powder (Sogut et al, 2011).

Endocrine

    3.16.1) SUMMARY
    A) Severe hypoglycemia has been reported.
    3.16.2) CLINICAL EFFECTS
    A) HYPOGLYCEMIA
    1) WITH POISONING/EXPOSURE
    a) Severe hypoglycemia has been reported following zinc phosphide poisoning (Patial et al, 1990).
    b) CASE REPORT: Persistent severe hypoglycemia (blood glucose 30 mg/dL by Dextrostix), lasting 11 days, was reported in 1 patient after zinc phosphide ingestion (Frangides & Pneumatikos, 2002). The patient did not develop any other manifestation of severe phosphine poisoning. It is not clear if this represents a true effect or laboratory interference.

Reproductive

    3.20.1) SUMMARY
    A) At the time of this review, no data were available to assess the teratogenic potential of this agent.
    B) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.
    C) In experimental animals, zinc phosphide induced a high percentage of abnormal sperm.
    3.20.2) TERATOGENICITY
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the teratogenic potential of this agent.
    3.20.3) EFFECTS IN PREGNANCY
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.
    3.20.4) EFFECTS DURING BREAST-FEEDING
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS1314-84-7 (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
    3.21.4) ANIMAL STUDIES
    A) LACK OF EFFECT
    1) LACK OF EFFECT
    a) Rats fed diets containing 0.337 to 0.996 mg/kg of phosphine derived from aluminum phosphide had no toxicity and no evidence of an increased incidence of neoplasms (Hackenberg, 1972).

Genotoxicity

    A) In experimental animals, zinc phosphide induced bone marrow chromosome aberrations.

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, blood glucose, renal function, and liver enzymes.
    E) Obtain a chest radiograph in patients with respiratory symptoms.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    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, hypotension, dysrhythmias, CNS depression), may require an ICU bed. Patients can be discharged once they are hemodynamically stable with clear improvement or asymptomatic from their exposure.
    6.3.1.2) HOME CRITERIA/ORAL
    A) There is no role for home management of zinc phosphide exposures.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Consult a medical toxicologist and/or poison centers for any patient with significant zinc phosphide poisoning. Other helpful consultants may include critical care physicians and pulmonologists to help management of the patient's symptoms.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    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 with careful instructions to return if any respiratory symptoms develop.

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, blood glucose, renal function, and liver enzymes.
    E) Obtain a chest radiograph in patients with respiratory symptoms.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) Prehospital gastrointestinal decontamination is not recommended because of the potential for formation of phosphine gas and the potential for abrupt deterioration.
    6.5.2) PREVENTION OF ABSORPTION
    A) SUMMARY
    1) The role of GI decontamination is not clear, as contact with water has the potential to form phosphine gas. Activated charcoal could be considered for patients with recent zinc phosphide ingestion (less than one hour) who are awake, alert, and cooperative.
    B) ACTIVATED CHARCOAL
    1) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.3) TREATMENT
    A) SUPPORT
    1) CIRCULATORY/RESPIRATORY SUPPORT: Anticipate the need to provide circulatory support and the possible development of pulmonary edema.
    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, blood glucose, 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) ACIDOSIS
    1) METABOLIC ACIDOSIS: Treat severe metabolic acidosis (pH less than 7.1) with sodium bicarbonate, 1 to 2 mEq/kg is a reasonable starting dose(Kraut & Madias, 2010). Monitor serum electrolytes and arterial or venous blood gases to guide further therapy.

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) Move patient to fresh air as soon as possible from inhalational exposures.
    6.7.2) TREATMENT
    A) SUPPORT
    1) Move patient to fresh air and monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as needed. Bronchospasm can be treated with B2 agonists and oral or parenteral corticosteroids.
    B) 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) There is no evidence for the use of dialysis, hemoperfusion, urinary alkalinization, or multiple dose charcoal, and are unlikely to be helpful for zinc phosphide exposures.

Range Of Toxicity

Summary

    A) TOXICITY: Ingestion of 4 to 7 g of zinc phosphide has caused death; doses as low as 40 mg/kg may be fatal in humans. Survival has been reported after total zinc phosphide ingestions of 25 to 50 g.

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) Ingestion of 4 to 7 grams of zinc phosphide has caused death (Orak et al, 2008; EPA, 1985). Doses as low as 40 mg/kg may cause death in humans (Dipalma, 1981).
    2) Deaths have been reported from a total dose of 4 grams of zinc phosphide (Stephenson, 1967).
    3) A prospective analysis of 20 patients with acute zinc phosphide poisoning was conducted. Clinical signs and symptoms, including vomiting, restlessness and anxiety, palpitations and sweating, dyspnea, tachypnea, metabolic acidosis, hypotension, jaundice with hepatomegaly, pulmonary edema, and shock were reported following a mean ingestion of 7.5 g (ranging from 5 to 20 g). Five of the 20 patients died due to intractable shock, unresponsive to resuscitative measures (Chugh et al, 1998).
    B) CASE REPORTS
    1) Severe metabolic acidosis (acute distal renal tubular acidosis) developed in a 25-year-old man after ingesting approximately 7 g of zinc phosphide powder in a suicide attempt. Despite supportive care, he developed cardio-pulmonary arrest and died 5 hours after admission (Orak et al, 2008).
    2) CASE REPORT: A 22-year-old woman presented to the emergency department comatose (Glasgow Coma Scale score of 8) with tachypnea, dyspnea, cyanosis, tachycardia, and hypotension after intentionally ingesting 10% zinc phosphide powder. The estimated ingested amount was approximately 10 g . Physical examination revealed hyperventilation and rales and rhonchi in lungs bilaterally, an ECG revealed depression of ST waves, laboratory data showed elevated cardiac enzyme concentrations and a chest radiograph demonstrated increased radiodensity in the basal lobes of the lungs, indicating acute pulmonary edema and congestive heart failure. Despite aggressive supportive measures, the patient had a cardiac arrest and could not be successfully resuscitated, with death occurring approximately 4 hours post-admission. Autopsy revealed congested and edematous lungs with petechial hemorrhages on the cardiac surface (Sogut et al, 2011).

Maximum Tolerated Exposure

    A) GENERAL/SUMMARY
    1) Phosphine is a highly toxic gas.
    2) The minimal detectable (decaying fish odor) concentration is 1 to 3 ppm in air. The gas dissipates rapidly in an open air environment; it is primarily a problem in confined spaces.
    3) A prospective analysis of 20 patients with acute zinc phosphide poisoning was conducted. Clinical signs and symptoms, including vomiting, restlessness and anxiety, palpitations and sweating, dyspnea, tachypnea, metabolic acidosis, hypotension, jaundice with hepatomegaly, pulmonary edema, and shock were reported following a mean ingestion of 7.5 g (ranging from 5 to 20 g). Five of the 20 patients died due to intractable shock, unresponsive to resuscitative measures (Chugh et al, 1998).
    B) CASE REPORTS
    1) A 36-year-old male psychiatric patient ingested 2 capfuls (approximately 20 grams) of ACME(R) MOLE and RAT KILLER (PBI/Gordon Corporation) containing 2% zinc phosphide (approximately 400 milligrams) in a suicide attempt 1 to 2 hours prior to admission (Rodenberg et al, 1989).
    a) This patient was given syrup of ipecac and activated charcoal/sorbitol, and remained asymptomatic during a 4-hour observation period (Rodenberg et al, 1989). It was estimated that this patient did not ingest more than 6 milligrams/kilogram of zinc phosphide.
    2) Survival has been reported after a total dose of 50 grams of zinc phosphide (Stephenson, 1967). Zinc phosphide ingestions of 25 to 50 grams have been survived (EPA, 1985).
    3) In a review of 21 zinc phosphide exposures, ingestion of one gram or less was associated with a good outcome (Lohani et al, 2000).
    C) ANIMAL DATA
    1) In rats, phosphine concentrations of 0.14 to 0.26 mg/L can be withstood without ill effects for 30 to 60 minutes (Schoof, 1970).

Workplace Standards

    A) ACGIH TLV Values for CAS1314-84-7 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    B) NIOSH REL and IDLH Values for CAS1314-84-7 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    C) Carcinogenicity Ratings for CAS1314-84-7 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Assessed under the IRIS program. ; Listed as: Zinc phosphide
    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
    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 CAS1314-84-7 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: (RTECS, 1996)
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 263 mg/kg
    2) LD50- (ORAL)MOUSE:
    a) 40 mg/kg
    3) LD50- (INTRAPERITONEAL)RAT:
    a) 450 mg/kg
    4) LD50- (ORAL)RAT:
    a) 12 mg/kg

Physicochemical

Physical Characteristics

    A) Cubic, dark-gray, tetragonal crystalline or powder solid with a faint phosphorus odor (Budavari, 1996).

Molecular Weight

    A) 258.05 (Lewis, 1996)

References

General Bibliography

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