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CHLORATES

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Sodium chlorate is a strong oxidizing agent.

Specific Substances

    A) SODIUM CHLORATE
    1) B-herbtox
    2) Chlorate of soda
    3) Chloric acid, sodium salt
    4) Desolat
    5) Natriumchlorat
    6) Natrium chloraat (Dutch)
    7) Natrium chlorat (German)
    8) Sodium chlorate, aqueous solution
    9) CAS 7775-09-9
    POTASSIUM CHLORATE
    1) Chlorate of potash
    2) Potash chlorate
    3) Potassium oxymuriate
    4) Potcrate
    5) Berthollet salt
    6) Chloric acid, potassium salt
    7) Kaliumchlorat
    8) Pearl ash (potassium chlorate)
    9) CAS 3811-04-9
    BARIUM CHLORATE
    1) Chloric acid, barium salt
    2) CAS 13477-00-4
    GENERAL TERMS
    1) CHLORATES, INORGANIC, AQUEOUS SOLUTION, N.O.S.
    2) CHLORATE AND MAGNESIUM CHLORIDE MIXTURE
    3) CHLORATE AND BORATE MIXTURE

Available Forms Sources

    A) FORMS
    1) Chlorate, n.o.s. is a crystalline compound. Chlorate, n.o.s., wet, is a slurry or sludge of white crystalline compounds (AAR, 1987).
    B) USES
    1) Chlorates are a combination of a metal or hydrogen and the chlorate monovalent radical. Chlorates are strong oxidizers used in the manufacture of dyes, explosives, matches, printing fabrics, weed killers, and as a weak antiseptic. 2 to 3% solutions have been used as a mouthwash (Budavari, 1996).
    2) POTASSIUM PERCHLORATE is used in the treatment of hyperthyroidism.
    3) SODIUM AND POTASSIUM CHLORATE were former frequent ingredients in mouthwashes, gargles, toothpaste, and medicinal lotions. Chlorate salts are currently obsolete as local antiseptics (Budavari, 1996).
    4) BARIUM CHLORATE is a common oxidizer in explosives and fireworks (Budavari, 1996). A few fatalities have been described due to taking sodium chlorate in error for table salt or epsom salts which the salt resembles physically.
    5) Chlorates are also used as herbicides (Smith & Oehme, 1991).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) WITH POISONING/EXPOSURE
    1) Chlorates are principally toxic by ingestion and inhalation. They are very potent oxidizing agents; exposure may result in hemolysis with methemoglobin formation and secondary DIC. Chlorates are nephrotoxic; acute renal failure may occur.
    2) Chlorate poisoning is characterized by a latent period of a few hours, followed initially with nausea, vomiting and diarrhea, followed by arterial hypotension, cyanosis, hemolysis and subsequent renal failure.
    a) Death in the early stage of chlorate poisoning is due to anoxia from methemoglobinemia or to DIC. Later death is generally due to renal failure.
    0.2.3) VITAL SIGNS
    A) WITH POISONING/EXPOSURE
    1) Blood pressure may be decreased.
    2) Pulse may be irregular.
    0.2.5) CARDIOVASCULAR
    A) WITH POISONING/EXPOSURE
    1) Chlorates may cause hypotension and damage to cardiac muscle.
    0.2.6) RESPIRATORY
    A) WITH POISONING/EXPOSURE
    1) Severe hypoxia with cyanosis, resistant to oxygen therapy, may be noted within several hours following exposure.
    2) Dyspnea and respiratory failure secondary to methemoglobinemia may occur.
    0.2.7) NEUROLOGIC
    A) WITH POISONING/EXPOSURE
    1) Lethargy, coma, and seizures have been reported.
    0.2.8) GASTROINTESTINAL
    A) WITH POISONING/EXPOSURE
    1) Nausea, vomiting, diarrhea and abdominal pain may be a common occurrence early in chlorate toxicity.
    0.2.9) HEPATIC
    A) WITH POISONING/EXPOSURE
    1) Elevated liver function tests, hepatomegaly and jaundice may occur.
    0.2.10) GENITOURINARY
    A) WITH POISONING/EXPOSURE
    1) Acute renal failure marked by oliguria and/or anuria is common in patients who develop significant hemolysis.
    0.2.12) FLUID-ELECTROLYTE
    A) WITH POISONING/EXPOSURE
    1) Hyperkalemia may occur secondary to hemolysis.
    0.2.13) HEMATOLOGIC
    A) WITH POISONING/EXPOSURE
    1) Hemolysis and methemoglobinemia may be noted following severe exposure and may progress to disseminated intravascular coagulation.
    2) Leukocytosis, cyanosis, and thrombocytopenia may occur.
    0.2.14) DERMATOLOGIC
    A) WITH POISONING/EXPOSURE
    1) Pallor may be noted.

Laboratory Monitoring

    A) Obtain baseline hemoglobin, hematocrit and methemoglobin level. Monitor BUN and creatinine.
    B) Type and cross match blood in symptomatic patients.
    C) Obtain urinalysis and monitor for hemoglobinuria.
    D) Monitor liver function tests.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) GASTRIC LAVAGE: Consider after ingestion of a potentially life-threatening amount of poison if it can be performed soon after ingestion (generally within 1 hour). Protect airway by placement in the head down left lateral decubitus position or by endotracheal intubation. Control any seizures first.
    1) CONTRAINDICATIONS: Loss of airway protective reflexes or decreased level of consciousness in unintubated patients; following ingestion of corrosives; hydrocarbons (high aspiration potential); patients at risk of hemorrhage or gastrointestinal perforation; and trivial or non-toxic ingestion.
    B) ACTIVATED CHARCOAL: Administer charcoal as a slurry (240 mL water/30 g charcoal). Usual dose: 25 to 100 g in adults/adolescents, 25 to 50 g in children (1 to 12 years), and 1 g/kg in infants less than 1 year old.
    C) SODIUM THIOSULFATE: Consider administering sodium thiosulfate to symptomatic patients to inactivate the chlorate ion. Administer 2 to 5 g orally or IV in 200 mL of 5% sodium bicarbonate.
    D) HEMOLYSIS: Transfuse as needed. Administer sufficient 0.9% saline to maintain urine output of 2 to 3 mL/kg/hr. Monitor input and output, serum electrolytes, CBC, and renal function. Diuretics may be necessary to maintain urine output.
    E) METHEMOGLOBINEMIA: Determine the methemoglobin concentration and evaluate the patient for clinical effects of methemoglobinemia (ie, dyspnea, headache, fatigue, CNS depression, tachycardia, metabolic acidosis). Treat patients with symptomatic methemoglobinemia with methylene blue (this usually occurs at methemoglobin concentrations above 20% to 30%, but may occur at lower methemoglobin concentrations in patients with anemia, or underlying pulmonary or cardiovascular disorders). Administer oxygen while preparing for methylene blue therapy.
    F) METHYLENE BLUE: INITIAL DOSE/ADULT OR CHILD: 1 mg/kg IV over 5 to 30 minutes; a repeat dose of up to 1 mg/kg may be given 1 hour after the first dose if methemoglobin levels remain greater than 30% or if signs and symptoms persist. NOTE: Methylene blue is available as follows: 50 mg/10 mL (5 mg/mL or 0.5% solution) single-dose ampules and 10 mg/1 mL (1% solution) vials. Additional doses may sometimes be required. Improvement is usually noted shortly after administration if diagnosis is correct. Consider other diagnoses or treatment options if no improvement has been observed after several doses. If intravenous access cannot be established, methylene blue may also be given by intraosseous infusion. Methylene blue should not be given by subcutaneous or intrathecal injection. NEONATES: DOSE: 0.3 to 1 mg/kg.
    G) Concomitant use of methylene blue with serotonergic drugs, including serotonin reuptake inhibitors (SRIs), selective serotonin reuptake inhibitors (SSRIs), serotonin and norepinephrine reuptake inhibitors (SNRIs), tricyclic antidepressants (TCAs), norepinephrine-dopamine reuptake inhibitors (NDRIs), triptans, and ergot alkaloids may increase the risk of potentially fatal serotonin syndrome.
    H) Exchange transfusion combined with hemodialysis should be considered in severely intoxicated patients.
    I) Monitor renal function carefully, especially following ingestion of 20 to 30 g or more as renal insufficiency occurs in 80% of cases.
    J) MONITOR FLUIDS AND ELECTROLYTES in symptomatic patients.
    0.4.3) INHALATION EXPOSURE
    A) INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
    0.4.4) EYE EXPOSURE
    A) DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Range Of Toxicity

    A) Chlorates are principally toxic by ingestion and inhalation. An acute or cumulative dose of 7.5 to 35 grams has been lethal in adults, however doses of 150 g or greater have been survived.
    B) Less than 20 wooden (330 mg) or 2 books of paper matches (220 mg) do not contain enough potassium chlorate to be harmful to a child.

Clinical Effects

Summary Of Exposure

    A) WITH POISONING/EXPOSURE
    1) Chlorates are principally toxic by ingestion and inhalation. They are very potent oxidizing agents; exposure may result in hemolysis with methemoglobin formation and secondary DIC. Chlorates are nephrotoxic; acute renal failure may occur.
    2) Chlorate poisoning is characterized by a latent period of a few hours, followed initially with nausea, vomiting and diarrhea, followed by arterial hypotension, cyanosis, hemolysis and subsequent renal failure.
    a) Death in the early stage of chlorate poisoning is due to anoxia from methemoglobinemia or to DIC. Later death is generally due to renal failure.

Vital Signs

    3.3.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Blood pressure may be decreased.
    2) Pulse may be irregular.
    3.3.4) BLOOD PRESSURE
    A) WITH POISONING/EXPOSURE
    1) HYPOTENSION - Decreased blood pressure occurs with progression of red blood cell lysis (Smith & Oehme, 1991).
    3.3.5) PULSE
    A) WITH POISONING/EXPOSURE
    1) IRREGULAR PULSE - may result from red blood cell lysis (Smith & Oehme, 1991).

Heent

    3.4.3) EYES
    A) No adverse ocular effects have been noted.
    1) POTASSIUM CHLORATE - Powdered or 3% to 5% aqueous solutions appear to be well tolerated in animal studies (Grant & Schuman, 1993).

Cardiovascular

    3.5.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Chlorates may cause hypotension and damage to cardiac muscle.
    3.5.2) CLINICAL EFFECTS
    A) HYPOTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) A consequence of progression of red blood cell lysis may include hypotension (Smith & Oehme, 1991). Eysseric et al (2000) reported severe arterial hypotension and refractory metabolic acidosis treated with vasoactive amines following a massive chlorate ingestion in a 49-year-old male. He experienced several cardiac arrests and died 12 hours after hospital admission (Eysseric et al, 2000).
    b) CASE REPORT - A 42-year-old man developed mild hypotension (100/60 mmHg), methemoglobinemia, hemolysis, acute renal failure, and DIC after ingesting approximately 50 mL of an herbicide containing sodium chlorate. The total amount of sodium chlorate ingested was 27 grams. The patient gradually recovered following daily intermittent hemodialysis sessions and supportive care (Ranghino et al, 2006).
    B) CARDIOMYOPATHY
    1) WITH POISONING/EXPOSURE
    a) Chlorates may cause damage to the heart muscle (Lewis, 1996).

Respiratory

    3.6.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Severe hypoxia with cyanosis, resistant to oxygen therapy, may be noted within several hours following exposure.
    2) Dyspnea and respiratory failure secondary to methemoglobinemia may occur.
    3.6.2) CLINICAL EFFECTS
    A) CYANOSIS
    1) WITH POISONING/EXPOSURE
    a) Significant hypoxia with cyanosis as a result of methemoglobinemia may occur, which also may be resistant to oxygen therapy. Cyanosis is a common feature in chlorate poisonings (Eysseric et al, 2000; Spence et al, 2006; Ranghino et al, 2006).
    b) CASE REPORT - Knight et al (1967) report a case of sodium chlorate overdose in a 35-year-old female who presented to the ED approximately 2 hours after the ingestion. She appeared cyanotic and her blood showed significant methemoglobin concentration. Oxygen saturation was measured at 82% (Knight et al, 1967).
    c) CASE REPORT - A 48-year-old gardener sprayed a concentrated solution of sodium chlorate with resultant inhalation. Nausea and vomiting occurred, followed by cyanosis (Jackson et al, 1961).
    d) CASE REPORT - Following a 24 hour history of severe respiratory distress and cyanosis with methemoglobinemia, a 49-year-old male was admitted to the hospital where he died 12 hours later. It was discovered that he had ingested a large quantity of chlorates (Eysseric et al, 2000).
    e) CASE REPORT - A 42-year-old man developed a methemoglobinemia of 48.9%, acute renal failure, and DIC after ingesting 27 grams of sodium chlorate. The patient gradually recovered following daily intermittent hemodialysis sessions and supportive care (Ranghino et al, 2006).
    B) DYSPNEA
    1) WITH POISONING/EXPOSURE
    a) Dyspnea may occur secondary to methemoglobinemia (Helliwell & Nunn, 1979; Eysseric et al, 2000).

Neurologic

    3.7.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Lethargy, coma, and seizures have been reported.
    3.7.2) CLINICAL EFFECTS
    A) COMA
    1) WITH POISONING/EXPOSURE
    a) Lethargy progressing to coma was reported in 2 of 14 cases and shortly preceded death (Helliwell & Nunn, 1979). Eysseric et al (2000) reported a 24-hour history of stupor in a 49-year-old male following chlorate salt ingestion. He subsequently died (Eysseric et al, 2000).
    b) CASE REPORT - A 21-year-old male intentionally ingested 3 boxes of matches (approximately 40 matchsticks within a box), which contained 55% potassium chlorate, and became obtunded. Neurologic exam also showed evidence of bilateral abducens palsy and hypoactive deep tendon reflexes. Supportive care included decontamination and exchange transfusion with hemodialysis. Magnetic resonance imaging revealed symmetric abnormal signal intensity within the deep gray matter and medial temporal lobes on T2-weighted and FLAIR images. Hyperbaric oxygen therapy was initiated. The patient responded well to therapy, and made a complete recovery (Mutlu et al, 2003).
    B) SEIZURE
    1) WITH POISONING/EXPOSURE
    a) Seizures have been reported in fatal cases (Timperman & Maes, 1966).

Gastrointestinal

    3.8.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Nausea, vomiting, diarrhea and abdominal pain may be a common occurrence early in chlorate toxicity.
    3.8.2) CLINICAL EFFECTS
    A) GASTROENTERITIS
    1) WITH POISONING/EXPOSURE
    a) Nausea, vomiting, abdominal cramping, diarrhea or colic proceed from the onset of pallor, with severity depending upon the amount ingested (Helliwell & Nunn, 1979; Lee et al, 1970; Eysseric et al, 2000; Ranghino et al, 2006). This is a common occurrence in chlorate poisonings.

Hepatic

    3.9.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Elevated liver function tests, hepatomegaly and jaundice may occur.
    3.9.2) CLINICAL EFFECTS
    A) ABNORMAL LIVER FUNCTION
    1) WITH POISONING/EXPOSURE
    a) Moderate elevations in SGOT and SGPT were reported for 10 days following ingestion of 150 to 200 g of sodium chlorate (Steffen & Seitz, 1981).
    b) CASE REPORT - Jaundice, enlarged liver, and elevated liver enzymes were reported in a 13-year-old boy who ingested a small amount of sodium chlorate (Stavrou et al, 1978).
    c) CASE REPORT - Davies & Lond (1956) report jaundice, hepatomegaly and elevated liver function tests in a 54-year-old male following ingestion of 13 g potassium chlorate (Davies & Lond, 1956).
    d) CASE REPORT - Inhalation of a concentrated sprayed solution of sodium chlorate resulted in jaundice and hepatomegaly on the fifth day in a 48-year-old gardener (Jackson et al, 1961).

Genitourinary

    3.10.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Acute renal failure marked by oliguria and/or anuria is common in patients who develop significant hemolysis.
    3.10.2) CLINICAL EFFECTS
    A) ACUTE RENAL FAILURE SYNDROME
    1) WITH POISONING/EXPOSURE
    a) Renal tubular necrosis and oliguria or anuria may occur secondary to hemolysis (Ranghino et al, 2006; Steffen & Seitz, 1981; Lee et al, 1970; Davies & Lond, 1956; Eysseric et al, 2000).
    b) INCIDENCE - Anuria was reported in 7 of 14 cases in one series (Helliwell & Nunn, 1979).
    c) COMPLICATIONS - Death is normally a result of both the hematological and renal complications which follow extensive hemolysis (Steffen & Seitz, 1981; Steffen & Wetzel, 1993; Vakili, 1977).
    d) CASE REPORT - Extensive hemolysis followed by port-colored urine then anuria and elevated creatinine and BUN (15.5 mmol/L) were reported in a 49-year-old male following the ingestion of chlorate salts. Twelve hours after hospital admission, the patient died. Autopsy revealed an acute tubular necrosis (Eysseric et al, 2000).
    B) ABNORMAL URINE
    1) WITH POISONING/EXPOSURE
    a) Urine may become brown or black due to hemoglobinuria and contain casts, RBCs, free hemoglobin, and methemoglobin (Smith & Oehme, 1991; Klendshoj et al, 1962; Bloxham et al, 1979; Eysseric et al, 2000; Ranghino et al, 2006).

Hematologic

    3.13.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Hemolysis and methemoglobinemia may be noted following severe exposure and may progress to disseminated intravascular coagulation.
    2) Leukocytosis, cyanosis, and thrombocytopenia may occur.
    3.13.2) CLINICAL EFFECTS
    A) METHEMOGLOBINEMIA
    1) WITH POISONING/EXPOSURE
    a) Chlorate toxicity results in oxidation of hemoglobin and increased red blood cell membrane rigidity with ensuing methemoglobinemia and hemolytic anemia. The hematological abnormalities may progress from hemolysis and methemoglobinemia to subacute intravascular coagulation (Ranghino et al, 2006; Steffen & Seitz, 1981; Lee et al, 1970; Eysseric et al, 2000).
    1) Within several hours generalized cyanosis, irreversible and resistant to oxygen therapy occurs (Steffen & Seitz, 1981; Lee et al, 1970; Jackson et al, 1961).
    b) INCIDENCE - Methemoglobinemia was present in 13 of 14 cases in one series (Helliwell & Nunn, 1979).
    c) CASE REPORT - Inhalation of a concentrated solution of sodium chlorate used as an herbicidal spray resulted in methemoglobinemia (57%) on the following day in a 48-year-old gardener (Jackson et al, 1961).
    d) CASE REPORT - A 49-year-old male was admitted to the hospital with acute hemolysis (3.9 g/L plasma hemoglobin concentration) and 30% methemoglobinemia after ingesting a chlorate salt about one day earlier. He died 12 hours after admission (Eysseric et al, 2000).
    e) CASE REPORT - A 42-year-old man developed hypotension, acute renal failure with anuria, DIC, and methemoglobinemia after ingesting approximately 50 mL of an herbicide containing sodium chlorate. The total amount of sodium chlorate ingested was 27 grams. The patient was cyanotic and an arterial blood gas revealed a methemoglobin level of 48.9%. The patient gradually recovered following daily intermittent hemodialysis sessions and supportive care (Ranghino et al, 2006).
    B) HEMOLYTIC ANEMIA
    1) WITH POISONING/EXPOSURE
    a) In severe cases of chlorate poisoning, hemolysis is followed by methemoglobinemia, hemolytic anemia and resultant hemoglobinuria (Knight et al, 1967; Cunningham, 1982; Steffen & Seitz, 1981; Vakili, 1977).
    1) CASE REPORT - Heinz-body hemolytic anemia was reported in a patient following the ingestion of potassium chlorate (Davies & Lond, 1956).
    2) CASE REPORT - A 42-year-old man ingested approximately 50 mL of an herbicide containing sodium chlorate (equivalent to a total sodium chlorate dose of 27 grams) and subsequently developed cyanosis, hypotension, acute renal failure with anuria, hemolytic anemia, methemoglobinemia, and DIC. Laboratory analysis revealed a hemoglobin level of 11 g/dL (decreasing to 3.9 g/dL at its lowest point), a platelet count of 74 x 10(3)/mcL, an LDH level of 3583 units/L (normal 240 to 480 units/L), and his blood samples were brown in color. The patient gradually recovered following daily intermittent hemodialysis sessions and supportive treatment with darbepoetin alfa and iron, folic acid and vitamin B12 supplementation (Ranghino et al, 2006).
    C) DISSEMINATED INTRAVASCULAR COAGULATION
    1) WITH POISONING/EXPOSURE
    a) Disseminated intravascular coagulation (DIC) is preceded by hemolysis of red blood cells and methemoglobinemia. Death is normally a result of both the hematological and renal complications which follow extensive hemolysis (Steffen & Seitz, 1981; Steffen & Wetzel, 1993; Vakili, 1977; Eysseric et al, 2000).
    b) CASE REPORT - A 42-year-old man developed hypotension, methemoglobinemia, DIC, and acute renal failure with anuria after ingesting approximately 50 mL of an herbicide containing sodium chlorate. The total amount of sodium chlorate ingested was 27 grams. Laboratory analysis revealed a platelet count of 74 x 10(3)/mcL, and antithrombin III of 65% (normal 80% to 125%), a D-dimer of 18.8 mcg/mL (normal <0.5), and an INR of 1.81. The patient refused treatment with exchange transfusion and fresh plasma for personal reasons. He gradually recovered following daily intermittent hemodialysis sessions and supportive care (Ranghino et al, 2006).
    D) THROMBOCYTOPENIC DISORDER
    1) WITH POISONING/EXPOSURE
    a) Significant DIC will result in decreased platelet counts.
    b) CASE REPORT - Steffen & Seitz (1981) describe a patient with a significant decrease of the thrombocyte count following ingestion of 150 to 200 g of a chlorate-containing herbicide (Steffen & Seitz, 1981).
    c) CASE REPORT - Knight et al (1967) report a case of ingestion of 40 g sodium chlorate in a 35-year-old female who subsequently developed a platelet count of 40,000/cu mm (Knight et al, 1967).
    d) CASE REPORT - A 42-year-old man developed a platelet count of 74 x 10(3)/mcL after ingesting 50 mL of an herbicide containing sodium chlorate (equivalent to a total sodium chlorate dose of 27 grams) (Ranghino et al, 2006).
    E) LEUKOCYTOSIS
    1) WITH POISONING/EXPOSURE
    a) Leukocytosis has been described, which persisted for 40 to 70 days (Steffen & Seitz, 1981; Knight et al, 1967). A significant leukocytosis of 40.0 x 10(9)/liter was reported in a 29-year-old male following ingestion of approximately 20 g sodium chlorate (Bloxham et al, 1979). This may be a common finding in chlorate poisonings.

Dermatologic

    3.14.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Pallor may be noted.
    3.14.2) CLINICAL EFFECTS
    A) PALE COMPLEXION
    1) WITH POISONING/EXPOSURE
    a) There may be a latent period after acute ingestion in which the only sign is pallor. No specific discomfort may occur at this time (Timperman & Maes, 1966).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Obtain baseline hemoglobin, hematocrit and methemoglobin level. Monitor BUN and creatinine.
    B) Type and cross match blood in symptomatic patients.
    C) Obtain urinalysis and monitor for hemoglobinuria.
    D) Monitor liver function tests.
    4.1.2) SERUM/BLOOD
    A) HEMATOLOGIC
    1) Baseline values should be taken for total hemoglobin, hematocrit, platelets, and red cell morphology. Free plasma hemoglobin and hemoglobin in the urine should be followed.
    B) COAGULATION STUDIES
    1) A workup for disseminated intravascular coagulation, such as fibrin split products, may prove helpful in determining possible occurrence of DIC. Early type and crossmatch should be made available.
    C) BLOOD/SERUM CHEMISTRY
    1) Serum electrolytes, especially potassium, should be followed. Monitor fluid status.
    2) Monitor liver function tests. Follow blood urea nitrogen and serum creatinine
    D) OTHER
    1) GENERAL-METHEMOGLOBINEMIA - If patient is cyanotic, obtain CBC, electrolytes, ABG's, and methemoglobin level.
    a) Methemoglobinemia may not develop for several hours (eg, 1 to 10) after exposure.
    b) The methemoglobin level, expressed as a percentage of total hemoglobin, is essential both in making the diagnosis and grading the severity.
    c) Diagnostic - levels >15% usually produce symptoms; cyanosis may be present with level of 15%. Methemoglobin levels will be reduced by endogenous methemoglobin reductase if blood is not analyzed rapidly (ie, within a few hours).
    2) BEDSIDE METHOD - If a rapid methemoglobin determination cannot be done, a simple test can help to confirm the diagnosis. Both sample and control blood are placed on filter paper and exposed to room air; the control blood will be red, while the blood containing large amounts of methemoglobin (>15%) will be dry and deep chocolate brown.
    a) In an asymptomatic but cyanotic patient in whom methemoglobinemia is suspected, none of the bedside techniques commonly recommended are completely reliable; diagnosis should be pursued with a spectrophotometric analysis.
    4.1.3) URINE
    A) URINARY LEVELS
    1) Urine is probably the fluid of choice from which to make determinations, but blood containing chlorate can also be used (Oliver et al, 1972).
    B) URINALYSIS
    1) Urinalysis and urine output monitoring is recommended.
    4.1.4) OTHER
    A) OTHER
    1) MAGNETIC RESONANCE IMAGING
    a) An adult male presented with obtundation, bilateral abducens palsy, and hypoactive deep tendon reflexes after ingesting 3 boxes of matches (40 matchsticks/box) which contained 55% potassium chlorate. On MRI T2-weighted and FLAIR (fluid-attenuated inversion recovery) images revealed symmetric abnormal signal intensity within the deep gray matter and medial temporal lobes (Mutlu et al, 2003).

Methods

    A) CHROMATOGRAPHY
    1) Eysseric et al (2000) described an ion chromatography method for the quantitative determination of chlorates in body fluids. The method is simple and rapid and determines both chlorate and chlorite ions in various body fluids such as blood, urine and gastric contents.
    B) SPECTROSCOPY/SPECTROMETRY
    1) Various other methods are available to distinguish between chlorates and other oxidizers and to make quantitative determinations, spectrophotometry being most recommended.
    C) OTHER
    1) A qualitative technique exists to determine the presence of an oxidizing agent. When 1 mL of a 1% (w/v) solution of diphenylamine in concentrated sulphuric acid is added to two drops of material containing chlorate, a blue color is produced immediately. Other oxidizing agents may interfere (Oliver et al, 1972).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) Obtain baseline hemoglobin, hematocrit and methemoglobin level. Monitor BUN and creatinine.
    B) Type and cross match blood in symptomatic patients.
    C) Obtain urinalysis and monitor for hemoglobinuria.
    D) Monitor liver function tests.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) ACTIVATED CHARCOAL
    1) Although activated charcoal is reported not to adsorb chlorate in vitro (Steffen & Wetzel, 1985), its use is recommended until definitive quantitative data are available.
    2) PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION
    a) Consider prehospital administration of activated charcoal as an aqueous slurry in patients with a potentially toxic ingestion who are awake and able to protect their airway. Activated charcoal is most effective when administered within one hour of ingestion. Administration in the prehospital setting has the potential to significantly decrease the time from toxin ingestion to activated charcoal administration, although it has not been shown to affect outcome (Alaspaa et al, 2005; Thakore & Murphy, 2002; Spiller & Rogers, 2002).
    1) In patients who are at risk for the abrupt onset of seizures or mental status depression, activated charcoal should not be administered in the prehospital setting, due to the risk of aspiration in the event of spontaneous emesis.
    2) The addition of flavoring agents (cola drinks, chocolate milk, cherry syrup) to activated charcoal improves the palatability for children and may facilitate successful administration (Guenther Skokan et al, 2001; Dagnone et al, 2002).
    3) 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).
    6.5.2) PREVENTION OF ABSORPTION
    A) GASTRIC LAVAGE
    1) INDICATIONS: Consider gastric lavage with a large-bore orogastric tube (ADULT: 36 to 40 French or 30 English gauge tube {external diameter 12 to 13.3 mm}; CHILD: 24 to 28 French {diameter 7.8 to 9.3 mm}) after a potentially life threatening ingestion if it can be performed soon after ingestion (generally within 60 minutes).
    a) Consider lavage more than 60 minutes after ingestion of sustained-release formulations and substances known to form bezoars or concretions.
    2) PRECAUTIONS:
    a) SEIZURE CONTROL: Is mandatory prior to gastric lavage.
    b) AIRWAY PROTECTION: Place patients in the head down left lateral decubitus position, with suction available. Patients with depressed mental status should be intubated with a cuffed endotracheal tube prior to lavage.
    3) LAVAGE FLUID:
    a) Use small aliquots of liquid. Lavage with 200 to 300 milliliters warm tap water (preferably 38 degrees Celsius) or saline per wash (in older children or adults) and 10 milliliters/kilogram body weight of normal saline in young children(Vale et al, 2004) and repeat until lavage return is clear.
    b) The volume of lavage return should approximate amount of fluid given to avoid fluid-electrolyte imbalance.
    c) CAUTION: Water should be avoided in young children because of the risk of electrolyte imbalance and water intoxication. Warm fluids avoid the risk of hypothermia in very young children and the elderly.
    4) COMPLICATIONS:
    a) Complications of gastric lavage have included: aspiration pneumonia, hypoxia, hypercapnia, mechanical injury to the throat, esophagus, or stomach, fluid and electrolyte imbalance (Vale, 1997). Combative patients may be at greater risk for complications (Caravati et al, 2001).
    b) Gastric lavage can cause significant morbidity; it should NOT be performed routinely in all poisoned patients (Vale, 1997).
    5) CONTRAINDICATIONS:
    a) Loss of airway protective reflexes or decreased level of consciousness if patient is not intubated, following ingestion of corrosive substances, hydrocarbons (high aspiration potential), patients at risk of hemorrhage or gastrointestinal perforation, or trivial or non-toxic ingestion.
    B) ACTIVATED CHARCOAL
    1) Activated charcoal is reported not to adsorb chlorate in vitro (Steffen & Wetzel, 1985).
    2) 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.
    3) 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) SODIUM THIOSULFATE
    1) Sodium thiosulfate was reported to inactivate the chlorate ion to form less toxic chloride and was used orally or intravenously, 2 to 5 grams sodium thiosulfate in 200 milliliters of 5 percent sodium bicarbonate (Helliwell & Nunn, 1979).
    2) An in vitro study showed that chlorate did not react with sodium thiosulfate nor did thiosulfate prevent methemoglobin formation (Steffen & Wetzel, 1985).
    B) MONITORING OF PATIENT
    1) FLUIDS AND ELECTROLYTES should be monitored appropriately.
    2) MONITOR RENAL FUNCTION, especially following an ingestion of 20 to 30 grams or more. Renal shutdown occurs in 80 percent of these cases.
    C) METHEMOGLOBINEMIA
    1) Ascorbic acid and methylene blue have been used to combat formation of methemoglobin, although it has been theorized that methylene blue catalyzes chlorate to chlorite, which might increase the methemoglobinemic action of the chlorate. Chlorate poisoning may be unresponsive to both methylene blue and ascorbic acid (Singelmann & Steffen, 1983).
    2) In vitro studies demonstrated the irreversibility of methemoglobinemia by methylene blue, which was postulated to be related to increased red cell rigidity. Ascorbic acid is nonenzymic, and the rate of reduction of methemoglobin will progress more slowly (Singelmann & Steffen, 1983).
    3) SUMMARY
    a) Determine the methemoglobin concentration and evaluate the patient for clinical effects of methemoglobinemia (ie, dyspnea, headache, fatigue, CNS depression, tachycardia, metabolic acidosis). Treat patients with symptomatic methemoglobinemia with methylene blue (this usually occurs at methemoglobin concentrations above 20% to 30%, but may occur at lower methemoglobin concentrations in patients with anemia, or underlying pulmonary or cardiovascular disorders). Administer oxygen while preparing for methylene blue therapy.
    4) METHYLENE BLUE
    a) INITIAL DOSE/ADULT OR CHILD: 1 mg/kg IV over 5 to 30 minutes; a repeat dose of up to 1 mg/kg may be given 1 hour after the first dose if methemoglobin levels remain greater than 30% or if signs and symptoms persist. NOTE: Methylene blue is available as follows: 50 mg/10 mL (5 mg/mL or 0.5% solution) single-dose ampules (Prod Info PROVAYBLUE(TM) intravenous injection, 2016) and 10 mg/1 mL (1% solution) vials (Prod Info methylene blue 1% intravenous injection, 2011). REPEAT DOSES: Additional doses may be required, especially for substances with prolonged absorption, slow elimination, or those that form metabolites that produce methemoglobin. NOTE: Large doses of methylene blue may cause methemoglobinemia or hemolysis (Howland, 2006). Improvement is usually noted shortly after administration if diagnosis is correct. Consider other diagnoses or treatment options if no improvement has been observed after several doses. If intravenous access cannot be established, methylene blue may also be given by intraosseous infusion. Methylene blue should not be given by subcutaneous or intrathecal injection (Prod Info methylene blue 1% intravenous injection, 2011; Herman et al, 1999). NEONATES: DOSE: 0.3 to 1 mg/kg (Hjelt et al, 1995).
    b) CONTRAINDICATIONS: G-6-PD deficiency (methylene blue may cause hemolysis), known hypersensitivity to methylene blue, methemoglobin reductase deficiency (Shepherd & Keyes, 2004)
    c) FAILURE: Failure of methylene blue therapy suggests: inadequate dose of methylene blue, inadequate decontamination, NADPH dependent methemoglobin reductase deficiency, hemoglobin M disease, sulfhemoglobinemia, or G-6-PD deficiency. Methylene blue is reduced by methemoglobin reductase and nicotinamide adenosine dinucleotide phosphate (NADPH) to leukomethylene blue. This in turn reduces methemoglobin. Red blood cells of patients with G-6-PD deficiency do not produce enough NADPH to convert methylene blue to leukomethylene blue (do Nascimento et al, 2008).
    d) DRUG INTERACTION: Concomitant use of methylene blue with serotonergic drugs, including serotonin reuptake inhibitors (SRIs), selective serotonin reuptake inhibitors (SSRIs), serotonin and norepinephrine reuptake inhibitors (SNRIs), tricyclic antidepressants (TCAs), norepinephrine-dopamine reuptake inhibitors (NDRIs), triptans, and ergot alkaloids may increase the risk of potentially fatal serotonin syndrome (U.S. Food and Drug Administration, 2011; Stanford et al, 2010; Prod Info methylene blue 1% IV injection, 2011).
    5) TOLUIDINE BLUE OR TOLONIUM CHLORIDE (GERMANY)
    a) DOSE: 2 to 4 mg/kg intravenously over 5 minutes. Dose may be repeated in 30 minutes (Nemec, 2011; Lindenmann et al, 2006; Kiese et al, 1972).
    b) SIDE EFFECTS: Hypotension with rapid intravenous administration. Vomiting, diarrhea, excessive sweating, hypotension, dysrhythmias, hemolysis, agranulocytosis and acute renal insufficiency after overdose (Dunipace et al, 1992; Hix & Wilson, 1987; Winek et al, 1969; Teunis et al, 1970; Marquez & Todd, 1959).
    c) CONTRAINDICATIONS: G-6-PD deficiency; may cause hemolysis.
    6) ASCORBIC ACID 500 milligrams to 1 gram slowly intravenously or orally every 4 hours as needed.
    D) DISSEMINATED INTRAVASCULAR COAGULATION
    1) Onset of DIC should be treated with fresh frozen plasma and exchange transfusion as needed (Steffen & Seitz, 1981).
    E) HEMOLYSIS
    1) SUMMARY: Early aggressive fluid replacement may help prevent renal insufficiency. Diuretics such as mannitol or furosemide may be needed to maintain urine output. Urinary alkalinization is NOT routinely recommended.
    2) Vigorous fluid replacement with 0.9% saline is necessary even if there is no evidence of dehydration. Hypovolemia, increased insensible losses, and third spacing of fluid may increase fluid requirements. Strive to maintain a urine output of at least 2 to 3 milliliters/kilogram per hour. Monitor fluid input and urine output, plus insensible losses. Monitor for evidence of fluid overload; monitor serum electrolytes, CBC with peripheral smear, LDH, bilirubin, and renal function tests.
    3) DARBEPOIETIN ALFA: To improve hematopoiesis in a 42-year-old man who ingested 27 grams of sodium chlorate and subsequently developed severe hemolysis (lowest hemoglobin 3.9 mg/dl) and refused transfusion. He was treated with darbepoietin alfa at a dose of 0.75 mcg/kg once a week, along with iron, folic acid, and vitamin B12 supplementation, and recovered (Ranghino et al, 2006).
    F) HYPERBARIC OXYGEN THERAPY
    1) CASE REPORT - A 21-year-old male intentionally ingested 3 boxes of matches (approximately 40 matchsticks within a box), which contained 55% potassium chlorate, and developed obtundation, bilateral abducens palsy, hypoactive deep tendon reflexes, and hyperkalemia (7.5 mmol/L). Supportive care included decontamination and exchange transfusion with hemodialysis. Magnetic resonance imaging revealed abnormal signal intensity on T2-weighted and FLAIR images in the deep gray matter and medial temporal lobes. He was treated with hyperbaric oxygen therapy at 2.2 absolute atmosphere pressures in three sessions (90 minutes/session). The patient was discharged with complete recovery one week after admission. Upon follow-up, MR imaging was normal 2 months after exposure (Mutlu et al, 2003).

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.

Eye Exposure

    6.8.1) DECONTAMINATION
    A) EYE IRRIGATION, ROUTINE: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, an ophthalmologic examination should be performed (Peate, 2007; Naradzay & Barish, 2006).

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL DECONTAMINATION
    1) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Enhanced Elimination

    A) EXTRACORPOREAL ELIMINATION
    1) Exchange transfusion combined with hemodialysis has been the most successful treatment in severe poisoning. Early exchange transfusion has been recommended in all cases of chlorate poisoning (Singelmann & Steffen, 1983) .
    2) The presence of methemoglobin in red blood cells, but not in serum, 2 hours postingestion suggests that early exchange transfusion may be beneficial (O'Grady & Jarecsni, 1971).

Abstracts

Case Reports

    A) ADULT
    1) A 26-year-old woman ingested 150 to 200 grams of sodium chlorate. Cyanosis and methemoglobinemia (50%) were present 5 hours postingestion. Hemolysis and intravascular coagulation developed over the next 14 hours, followed by anuric renal failure. Renal function recovered slowly and incompletely. Peritoneal dialysis was required for 40 days (Steffen & Seitz, 1981).
    2) A 48-year-old gardener sprayed a concentrated solution of sodium chlorate with resultant inhalation. Nausea and vomiting occurred, followed by cyanosis, anuria, and methemoglobinemia (57%) on the following day. On the fifth day, icterus, hepatomegaly, and epistaxis were present. Renal function returned gradually over 67 days (Jackson et al, 1961).

Range Of Toxicity

Summary

    A) Chlorates are principally toxic by ingestion and inhalation. An acute or cumulative dose of 7.5 to 35 grams has been lethal in adults, however doses of 150 g or greater have been survived.
    B) Less than 20 wooden (330 mg) or 2 books of paper matches (220 mg) do not contain enough potassium chlorate to be harmful to a child.

Minimum Lethal Exposure

    A) CASE REPORTS
    1) Amounts ingested ranged from 15 to 300 grams of sodium chlorate in 7 fatal adult cases (Helliwell & Nunn, 1979), however, doses of up to 150 to 200 grams have been survived (Steffen & Seitz, 1981; O'Grady & Jarecsni, 1971).
    2) Ingestion of 90 grams of sodium chlorate was fatal in a 78-year-old man (O'Grady & Jarecsni, 1971).
    3) Ingestion of 7.5 grams of potassium chlorate in a toothpaste formulation was fatal in an adult (Bernstein, 1930).
    4) Ingestion of 10 grams/day of potassium chlorate for 3 days resulted in death in a 43-year-old man (total dose 30 to 35 grams) (Cochrane & Smith, 1940).
    5) An acute or cumulative dose of 7.5 to 35 grams has been lethal in adults; however, doses of 150 grams or greater have been survived.

Maximum Tolerated Exposure

    A) ROUTE OF EXPOSURE
    1) INHALATION
    a) The smallest recorded dose was inhaled by a gardener after using a concentrated solution in an atomizer; he developed renal failure but subsequently recovered (Jackson et al, 1961).
    b) Chlorates are principally toxic by ingestion and inhalation with no known reports of skin absorption.
    2) INGESTION
    a) Less than 20 wooden (330 milligrams) or 2 books of paper matches (220 milligrams) do not contain enough potassium chlorate to be harmful to a child.
    b) Acute ingestion of 150 to 200 grams of sodium chlorate resulted in serious toxicity and survival in adults (Steffen & Seitz, 1981).
    c) In 5 adults who recovered from sodium chlorate poisoning, the amount ingested was 1-2, 5, 30, 45, and 100 grams (Helliwell & Nunn, 1979).
    d) A 28-year-old male recovered over 32 days after ingesting 40 grams of sodium chlorate. He developed extensive hemolysis, progressive kidney failure, liver dysfunction and hyperkalemia (Klendshoj et al, 1962).
    e) Acute ingestion of 20 grams of sodium chlorate by a 15-year-old boy resulted in cyanosis, anuria, and DIC (Lee et al, 1970).
    f) Severe toxicity (renal failure, jaundice, methemoglobinemia) was described in a 13-year-old boy who dipped his finger into sodium chlorate crystals and licked the finger (Stavrou et al, 1978).
    g) A 42-year-old man developed hypotension, methemoglobinemia, acute renal failure, hemolytic anemia, and DIC after ingesting approximately 50 mL of an herbicide containing sodium chlorate. The total amount of sodium chlorate ingested was 27 grams. The patient gradually recovered following daily intermittent hemodialysis sessions and supportive care (Ranghino et al, 2006).

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) CASE REPORTS
    a) In a woman who died within 75 minutes of ingestion of a chlorate weed killer, the blood concentration was 152.4 milligrams/deciliter and gastric content 362 milligrams/deciliter. In a case where death was delayed, the urine level was 700 milligrams/deciliter, with no detectable levels in the blood (Cunningham, 1982).
    b) Eysseric et al (2000) reported blood chlorate ion level of 78 and 29 milligrams/liter, respectively, before and after exchange transfusion. The patient presented to the hospital over 24 hours after ingestion of an unknown amount of chlorate salts, and subsequently died 12 hours after admission. An ion chromatography method was used to quantitate chlorate ions.

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) POTASSIUM CHLORATE
    1) LD50- (ORAL)RAT:
    a) 1870 mg/kg (RTECS, 2000)
    B) SODIUM CHLORATE
    1) LD50- (ORAL)MOUSE:
    a) 596 mg/kg (Smith & Oehme, 1991)
    2) LD50- (ORAL)RAT:
    a) 1200 mg/kg (Smith & Oehme, 1991)

Pharmacology Toxicology

Toxicologic Mechanism

    A) OXIDATION - Chlorate compounds are a local irritant, especially on the gastrointestinal mucosa, and are very potent oxidizing agents, causing intense hemolysis with methemoglobin formation. Acute hemolytic anemia occurs with varying degrees of bilirubinemia. Chlorate induced hemolysis may account for destruction of 50% of the circulating red blood cells. A recorded fatality had demonstrated 91.9% methemoglobin (Gettler & St George, 1935). Death during early phases of chlorate toxicity is due to anoxia from methemoglobinemia or to disseminated intravascular coagulation (Lee et al, 1970; Steffen & Seitz, 1981).
    B) RENAL TOXICITY
    1) Chlorates are toxic to renal tubules. The direct toxic effects are on the proximal tubules and the resultant anuria blocks the main route of elimination of the drug. This action prolongs exposure of the red cells to the oxidant effects. The direct action on tubules produces necrosis, and an intense renal vasoconstriction causes tubular damage. The resulting lesion is acute tubular necrosis (Lee et al, 1970) Oliver et al, 1951; (Jackson et al, 1961).
    2) Steffen & Wetzel (1993) have demonstrated in rabbit studies the nephrotoxicity of chlorate to be mediated by methemoglobin catalysis. Bing (1944) postulated the renal effects of chlorate toxicity to be secondary to hemolysis. Degree of renal insufficiency is generally the determining factor in fatalities in later stages of toxicity.
    C) The toxic effects of chlorates involve many organ systems. Hepatic failure with hepatomegaly has occurred, but the rapid destruction of blood cells and the progressive kidney failure are the focal points for treatment. Elimination is exclusively by the kidneys. The chlorate ion is excreted slowly, therefore intermittent administration can have a cumulative effect. Hemolysis, formation of methemoglobinemia and pigment nephrosis are the chief manifestations.

Physicochemical

Physical Characteristics

    A) POTASSIUM CHLORATE: odorless; cooling saline taste
    B) Chlorates are generally white in color (AAR, 1987).
    C) Chlorates can be a crystalline solid, slurry or sludge of crystalline material (AAR, 1987).

Molecular Weight

    A) POTASSIUM CHLORATE: 122.55 (Budavari, 1996)
    B) SODIUM CHLORATE: 106.44 (Budavari, 1996)

Animal Toxicology

Clinical Effects

    11.1.3) CANINE/DOG
    A) Vomiting, tachycardia, leukocytosis, hemolysis, hyperkalemia, methemoglobinemia, and nephropathy were seen in experimental animals given sodium chlorate (Sheahan et al, 1971).

Treatment

    11.2.1) SUMMARY
    A) GENERAL TREATMENT
    1) Treatment consists of removing the animal from the toxic environment, administering sodium thiosulfate to inactivate the chlorate ion, demulcents to relieve gastric irritation, and methylene blue to combat formation of methemoglobin (Smith & Oehme, 1991).
    11.2.2) LIFE SUPPORT
    A) GENERAL
    1) MAINTAIN VITAL FUNCTIONS: Secure airway, supply oxygen, and begin supportive fluid therapy if necessary.
    11.2.4) DECONTAMINATION
    A) GASTRIC DECONTAMINATION
    1) GENERAL TREATMENT
    a) GASTRIC LAVAGE -
    1) Mineral oil with 1% sodium thiosulfate is recommended via gastric lavage for monogastric animals. Mineral oil may prevent further GI absorption of chlorates and help speed unabsorbed chlorate through the intestinal tract (Smith & Oehme, 1991).
    11.2.5) TREATMENT
    A) GENERAL TREATMENT
    1) DEMULCENTS - Milk or demulcents may be administered to relieve gastric irritation (Smith & Oehme, 1991).
    2) METHYLENE BLUE - 10 mg/kg intravenously, as a 2 or 4% solution, is recommended to convert high levels of methemoglobin to hemoglobin (Smith & Oehme, 1991).
    3) OXYGEN - Cyanosis or a methemoglobin level above 40% may require oxygen therapy (Smith & Oehme, 1991).

Range Of Toxicity

    11.3.2) MINIMAL TOXIC DOSE
    A) DOG
    1) Dogs given 0.5 gram/kg of sodium chlorate orally survived. One of two dogs given 1 g/kg died (Sheahan et al, 1971).

Continuing Care

    11.4.1) SUMMARY
    11.4.1.2) DECONTAMINATION/TREATMENT
    A) GENERAL TREATMENT
    1) Treatment consists of removing the animal from the toxic environment, administering sodium thiosulfate to inactivate the chlorate ion, demulcents to relieve gastric irritation, and methylene blue to combat formation of methemoglobin (Smith & Oehme, 1991).
    11.4.2) DECONTAMINATION
    11.4.2.2) GASTRIC DECONTAMINATION
    A) GASTRIC DECONTAMINATION
    1) GENERAL TREATMENT
    a) GASTRIC LAVAGE -
    1) Mineral oil with 1% sodium thiosulfate is recommended via gastric lavage for monogastric animals. Mineral oil may prevent further GI absorption of chlorates and help speed unabsorbed chlorate through the intestinal tract (Smith & Oehme, 1991).

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