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AMMONIUM PERCHLORATE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Ammonium perchlorate is an explosive agent. It is a direct irritant of eyes, skin, and mucous membranes. Irritating and toxic fumes of ammonia, chlorides, and oxides of nitrogen can be released in fires, and could cause severe respiratory tract irritation or pulmonary edema.
    B) It is produced by the interaction of sodium chlorate, ammonium hydroxide, and hydrochloric acid, and recovered by crystallization.

Specific Substances

    1) Ammonium perchlorate
    2) Perchloric acid, ammonium salt
    3) Molecular Formula: Cl-O4.H4-N
    4) NIOSH/RTECS SC 7520000
    5) Molecular Formula: NH4-Cl-O4
    6) CAS 7790-98-9
    1.2.1) MOLECULAR FORMULA
    1) Cl-O4.H4-N

Available Forms Sources

    A) FORMS
    1) Ammonium perchlorate is an odorless water soluble white crystalline solid (Bingham et al, 2001; Sax & Lewis, 1987; ITI, 1985; Fire Protection Guide, 1978). The perchlorate anion is a strong oxidant.
    B) SOURCES
    1) Ammonium perchlorate is produced by interaction of sodium chlorate, ammonium hydroxide, and hydrochloric acid, and recovered by crystallization (Sax & Lewis, 1987). A double-exchange reaction of sodium perchlorate and ammonium chloride is used in the manufacture of the commercial product. An extremely high purity ammonium perchlorate is made via the direct reaction of ammonia and pure perchloric acid solution (HSDB , 2001).
    C) USES
    1) Ammonium perchlorate is an explosive agent used as a component of fireworks, flash powders, explosives, smokeless jet and rocket propellants, as an oxidizing, engraving, or etching compound, as a reagent in analytical chemistry, and in pharmaceutical manufacturing (Bingham et al, 2001; Sax & Lewis, 1987; ITI, 1985).
    2) Drinking water supplies in parts of the United States have been found to be contaminated with perchlorate anion. It is suspected that the contamination is due to releases of ammonium perchlorate by defense contractors, military operations, and aerospace programs because it is used as a solid oxidant in missile and rocket propulsion systems. The perchlorate anion is persistent in the environment (Urbansky, 2002).

Overview

Laboratory Monitoring

    A) Monitoring kidney and thyroid function tests may be advisable in significant exposures.
    B) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) EMESIS: Ipecac-induced emesis is not recommended because there is so little information about the effects of overdose in humans.
    B) DILUTION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. Dilution may only be helpful if performed in the first seconds to minutes after ingestion. The ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting.
    C) 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.
    D) 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.
    E) ACUTE LUNG INJURY: Maintain ventilation and oxygenation and evaluate with frequent arterial blood gases and/or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed.
    F) Observe patients with ingestion carefully for the possible development of esophageal or gastrointestinal tract irritation or burns. If signs or symptoms of esophageal irritation or burns are present, consider endoscopy to determine the extent of injury.
    0.4.3) INHALATION EXPOSURE
    A) INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
    B) ACUTE LUNG INJURY: Maintain ventilation and oxygenation and evaluate with frequent arterial blood gases and/or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed.
    C) If bronchospasm and wheezing occur, consider treatment with inhaled sympathomimetic agents.
    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).
    2) Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines.

Range Of Toxicity

    A) Minimum lethal human exposure is unknown.

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Very little information is available on the toxicity of ammonium perchlorate. This agent is an irritant of eyes, skin, and mucous membranes. Hypothyroidism may occur following chronic exposures. Ammonium perchlorate has been found as a ground water contaminant, but has not been found to result in excess cancers or adverse effects on the thyroid or indirectly on other physiologic systems in epidemiologic studies.
    B) INHALATION - Irritating and toxic fumes of ammonia, chlorides, and oxides of nitrogen can be released in fires, and could cause severe respiratory tract irritation or pulmonary edema.
    C) INGESTION - Cases of ingestions have not been reported, but irritation of the esophagus or gastrointestinal tract may be predicted.
    0.2.4) HEENT
    A) Irritation of the eyes, nose, and throat may occur.
    0.2.6) RESPIRATORY
    A) Respiratory tract irritation or pulmonary edema may occur.
    0.2.8) GASTROINTESTINAL
    A) Esophageal or gastrointestinal tract irritation could occur following exposures.
    0.2.14) DERMATOLOGIC
    A) Dermal irritation may be noted.
    0.2.16) ENDOCRINE
    A) An antithyroid effect may occur following prolonged exposures.
    0.2.20) REPRODUCTIVE
    A) A study of maternal environmental exposure to perchlorate suggested that most cases of congenital hypothyroidism are caused by developmental defects and are not associated with exposure to perchlorate.
    B) Reproduction studies in experimental animals found the thyroid was the target organ. In rabbits, no fetal alterations, either malformations or variations, were attributed to ammonium perchlorate in the offspring.

Clinical Effects

Summary Of Exposure

    A) Very little information is available on the toxicity of ammonium perchlorate. This agent is an irritant of eyes, skin, and mucous membranes. Hypothyroidism may occur following chronic exposures. Ammonium perchlorate has been found as a ground water contaminant, but has not been found to result in excess cancers or adverse effects on the thyroid or indirectly on other physiologic systems in epidemiologic studies.
    B) INHALATION - Irritating and toxic fumes of ammonia, chlorides, and oxides of nitrogen can be released in fires, and could cause severe respiratory tract irritation or pulmonary edema.
    C) INGESTION - Cases of ingestions have not been reported, but irritation of the esophagus or gastrointestinal tract may be predicted.

Heent

    3.4.1) SUMMARY
    A) Irritation of the eyes, nose, and throat may occur.
    3.4.3) EYES
    A) Eye irritation may occur (HSDB , 2001; CHRIS , 1985).
    3.4.5) NOSE
    A) Irritation of the mucosa of the nose and throat may occur (HSDB , 2001) Prod Info Ammonium Perchlorate, 1996; (ITI, 1985).
    3.4.6) THROAT
    A) Irritation of the mucosa of the nose and throat may occur (HSDB , 2001) Prod Info Ammonium Perchlorate, 1996; (ITI, 1985).

Respiratory

    3.6.1) SUMMARY
    A) Respiratory tract irritation or pulmonary edema may occur.
    3.6.2) CLINICAL EFFECTS
    A) IRRITATION SYMPTOM
    1) Ammonium perchlorate is a mucous membrane irritant (Prod Info Ammonium Perchlorate, 1996) and may release irritating fumes of ammonia, chlorides, and oxides of nitrogen if involved in fires (Bingham et al, 2001). Severe respiratory tract irritation or pulmonary edema could develop (HSDB , 2001).
    a) Respiratory tract irritation, if severe, can progress to pulmonary edema which may be delayed in onset up to 24 to 72 hours after exposure in some cases.

Gastrointestinal

    3.8.1) SUMMARY
    A) Esophageal or gastrointestinal tract irritation could occur following exposures.
    3.8.2) CLINICAL EFFECTS
    A) GASTRITIS
    1) Esophageal and gastrointestinal tract irritation are expected following an ingestion exposure. Abdominal pain and nausea may occur (HSDB , 2001) Prod Info Ammonium Perchlorate, 1996).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) NEPHRITIS
    1) Because ammonium perchlorate is a strong oxidizer, significant overdoses or chronic intake may result in a delayed toxic effect on the kidneys (HSDB , 2001) Prod Info Ammonium Perchlorate, 1996).

Hematologic

    3.13.2) CLINICAL EFFECTS
    A) METHEMOGLOBINEMIA
    1) It is theoretically possible, although not yet reported, that absorption may result in methemoglobinemia since potassium perchlorates have been reported to cause this on rare occasions (HSDB , 2001).

Dermatologic

    3.14.1) SUMMARY
    A) Dermal irritation may be noted.
    3.14.2) CLINICAL EFFECTS
    A) ERUPTION
    1) Ammonium perchlorate exposure can cause dermal irritation (HSDB , 2001) Prod Info Ammonium Perchlorate, 1996; (Sax & Lewis, 1987; ITI, 1985; CHRIS , 1985).
    B) THERMAL BURN
    1) Ammonium perchlorate presents a significant explosion and fire hazard. Thermal burns and blast injuries could be seen in these circumstances (Bingham et al, 2001) Prod Info Ammonium Perchlorate, 1996).

Endocrine

    3.16.1) SUMMARY
    A) An antithyroid effect may occur following prolonged exposures.
    3.16.2) CLINICAL EFFECTS
    A) FINDING OF THYROID FUNCTION
    1) Symptoms of hypothyroidism (fatigue, weight gain, dry skin, coldness, constipation) may occur following prolonged exposures to high doses of ammonium perchlorate. Effects on the thyroid gland, which are due to competitive inhibition of thyroid iodine transport by the perchlorate anion, are reversible. The perchlorate ion, being similar in size to the iodide ion, can be taken up in place of iodide by the thyroid gland (Urbansky, 2002) Prod Info Ammonium Perchlorate, 1996; (Shigan, 1963). The effects of chronic low-level exposures are poorly defined.

Reproductive

    3.20.1) SUMMARY
    A) A study of maternal environmental exposure to perchlorate suggested that most cases of congenital hypothyroidism are caused by developmental defects and are not associated with exposure to perchlorate.
    B) Reproduction studies in experimental animals found the thyroid was the target organ. In rabbits, no fetal alterations, either malformations or variations, were attributed to ammonium perchlorate in the offspring.
    3.20.2) TERATOGENICITY
    A) PRIMARY CONGENITAL HYPOTHYROIDISM
    1) A 14-year study of maternal environmental exposure to perchlorate evaluated the concentrations of thyroid-stimulating hormone (TSH) and primary congenital hypothyroidism in newborns. Findings from this study suggested that most cases of elevated TSH or primary congenital hypothyroidism were caused by developmental defects independent of perchlorate environmental exposure (Kelsh et al, 2003).
    B) ANIMAL STUDIES
    1) RABBITS - A developmental (embryo-fetal toxicity) no-observable-adverse-effect (NOAEL) of 100 mg/kg/day was reported for ammonium perchlorate when given to pregnant rabbits in doses up to 102 mg/kg/day. No fetal alterations, either malformations or variations, were attributed to ammonium perchlorate in the offspring of these rabbits (York et al, 2001).
    2) RATS - At doses up to 30 mg/kg/day, ammonium perchlorate was not reported to be a reproductive toxicant. A two-generation reproduction study found the thyroid was the target organ, with increased thyroid weight and thyroid hyperplasia at doses equal to or greater than 3 mg/kg/day, which occurred at lower doses than those required to cause increased TSH or decreased T4. A NOAEL of 0.3 mg/kg/day was determined for ammonium perchlorate (York et al, 2001a).
    3) MICE - Breeding pairs of mice were dosed continuously with up to 1 mM ammonium perchlorate in drinking water, levels similar to those found in actual contaminated environments. Pups were sacrificed at postnatal day 21. Monitoring of body weight, organ weight, and litter survival were endpoints chosen based on the secondary thyroid toxicity effects of ammonium perchlorate. This study determined ammonium perchlorate to be a developmental toxicant. A biphasic effect on birth weight was shown, with lowering body weight up to a certain concentration, at which body weight begins to increase. Heart weights were decreased by in utero and lactational exposure, which is consistent with known effects of thyroid hormone alteration induced by ammonium perchlorate exposure. Accumulation of ammonium perchlorate was noted in the livers (Thuett et al, 2002).
    3.20.3) EFFECTS IN PREGNANCY
    A) ANIMAL STUDIES
    1) RABBITS - When ammonium perchlorate, doses up to 102 mg/kg/day, was administered to female rabbits on gestation days 6 through 28, the thyroid was reported as the target organ for perchlorate toxicity. Thyroid follicular hypertrophy was noted at an increased incidence in doses given >10 mg/kg/day, while significantly decreased T4 was noted in does given doses >30 mg/kg/day (York et al, 2001).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS7790-98-9 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
    1) Not Listed
    3.21.3) HUMAN STUDIES
    A) LACK OF EFFECT
    1) Long-time exposure to ammonium perchlorate in drinking water was assessed, for observed and expected numbers of new invasive cancer, between 1988 and 1998 by the Desert Sierra Cancer Surveillance Program (DSCSP). Levels of perchlorate in water had ranged between 5 and 98 ppb. For all cancers, including thyroid cancer, no significant difference was found between observed and expected numbers, with CI, 99% and SIR, 0.97 (Morgan & Cassady, 2002). The perchlorate anion is reported to block iodide uptake by the thyroid at high doses, but previously, it was unknown whether chronic low-level exposures would affect the thyroid (Renner, 1999).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitoring kidney and thyroid function tests may be advisable in significant exposures.
    B) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Evaluation of kidney and thyroid function tests may be advisable in cases of significant exposure.
    4.1.3) URINE
    A) URINALYSIS
    1) Monitoring urinalysis is suggested for patients with significant exposure.
    4.1.4) OTHER
    A) OTHER
    1) PULMONARY FUNCTION TESTS
    a) If respiratory tract irritation is present, it may be useful to monitor pulmonary function tests.
    b) If respiratory tract irritation is present, monitor arterial blood gases and chest x-ray.

Radiographic Studies

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

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

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

Monitoring

    A) Monitoring kidney and thyroid function tests may be advisable in significant exposures.
    B) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) EMESIS/NOT RECOMMENDED
    1) EMESIS: Ipecac-induced emesis is not recommended because there is so little information about the effects of overdose in humans.
    B) ACTIVATED CHARCOAL
    1) 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).
    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).
    6.5.2) PREVENTION OF ABSORPTION
    A) EMESIS/NOT RECOMMENDED
    1) Inducing emesis should be AVOIDED.
    B) DILUTION
    1) DILUTION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. Dilution may only be helpful if performed in the first seconds to minutes after ingestion. The ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting (Caravati, 2004).
    C) 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.
    D) 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) DILUTION
    1) DILUTION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. Dilution may only be helpful if performed in the first seconds to minutes after ingestion. The ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting (Caravati, 2004).
    B) IRRITATION SYMPTOM
    1) Observe patients with ingestion carefully for the possible development of esophageal or gastrointestinal tract irritation or burns. If signs or symptoms of esophageal irritation or burns are present, consider endoscopy to determine the extent of injury.
    C) ACUTE LUNG INJURY
    1) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
    2) NON-PHARMACOLOGIC TREATMENT: The treatment of acute lung injury is primarily supportive (Cataletto, 2012). Maintain adequate ventilation and oxygenation with frequent monitoring of arterial blood gases and/or pulse oximetry. If a high FIO2 is required to maintain adequate oxygenation, mechanical ventilation and positive-end-expiratory pressure (PEEP) may be required; ventilation with small tidal volumes (6 mL/kg) is preferred if ARDS develops (Haas, 2011; Stolbach & Hoffman, 2011).
    a) To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)
    3) FLUIDS: Crystalloid solutions must be administered judiciously. Pulmonary artery monitoring may help. In general the pulmonary artery wedge pressure should be kept relatively low while still maintaining adequate cardiac output, blood pressure and urine output (Stolbach & Hoffman, 2011).
    4) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
    5) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
    6) CALFACTANT: In a multicenter, randomized, blinded trial, endotracheal instillation of 2 doses of 80 mL/m(2) calfactant (35 mg/mL of phospholipid suspension in saline) in infants, children, and adolescents with acute lung injury resulted in acute improvement in oxygenation and lower mortality; however, no significant decrease in the course of respiratory failure measured by duration of ventilator therapy, intensive care unit, or hospital stay was noted. Adverse effects (transient hypoxia and hypotension) were more frequent in calfactant patients, but these effects were mild and did not require withdrawal from the study (Wilson et al, 2005).
    7) However, in a multicenter, randomized, controlled, and masked trial, endotracheal instillation of up to 3 doses of calfactant (30 mg) in adults only with acute lung injury/ARDS due to direct lung injury was not associated with improved oxygenation and longer term benefits compared to the placebo group. It was also associated with significant increases in hypoxia and hypotension (Willson et al, 2015).
    D) OBSERVATION REGIMES
    1) Carefully observe patients with ingestion exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    E) THYROID PANEL
    1) Monitoring thyroid function tests may be advisable in cases of significant exposure.

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) Move patient from the toxic environment to fresh air. Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for hypoxia, respiratory tract irritation, bronchitis, or pneumonitis.
    B) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    C) INITIAL TREATMENT: Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists, if bronchospasm develops. Consider systemic corticosteroids in patients with significant bronchospasm (National Heart,Lung,and Blood Institute, 2007). Exposed skin and eyes should be flushed with copious amounts of water.
    6.7.2) TREATMENT
    A) IRRITATION SYMPTOM
    1) Respiratory tract irritation, if severe, can progress to noncardiogenic pulmonary edema which may be delayed in onset up to 24 to 72 hours after exposure in some cases.
    2) There are no controlled studies indicating that early administration of corticosteroids can prevent the development of noncardiogenic pulmonary edema in patients with inhalation exposure to respiratory irritant substances, and long-term use may cause adverse effects (Boysen & Modell, 1989).
    a) However, based on anecdotal experience, some clinicians do recommend early administration of corticosteroids (such as methylprednisolone 1 gram intravenously as a single dose) in an attempt to prevent the later development of pulmonary edema.
    1) Anecdotal experience with dimethyl sulfate inhalation showed possible benefit of methylprednisolone in the TREATMENT of noncardiogenic pulmonary edema (Ip et al, 1989).
    3) Anecdotal experience also indicated that systemic corticosteroids may have possible efficacy in the TREATMENT of drug-induced noncardiogenic pulmonary edema (Zitnik & Cooper, 1990; Stentoft, 1990; Chudnofsky & Otten, 1989) or noncardiogenic pulmonary edema developing after cardiopulmonary bypass (Maggart & Stewart, 1987).
    4) It is not clear from the published literature that administration of systemic corticosteroids early following inhalation exposure to respiratory irritant substances can PREVENT the development of noncardiogenic pulmonary edema. The decision to administer or withhold corticosteroids in this setting must currently be made on clinical grounds.
    B) ACUTE LUNG INJURY
    1) Respiratory tract irritation, if severe, can progress to pulmonary edema which may be delayed in onset up to 24 to 72 hours after exposure in some cases.
    2) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
    3) 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)
    4) 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).
    5) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
    6) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
    7) 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).
    8) 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).
    C) BRONCHOSPASM
    1) If bronchospasm and wheezing occur, consider treatment with inhaled sympathomimetic agents.
    D) OBSERVATION REGIMES
    1) Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    E) 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) DERMAL DECONTAMINATION
    1) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).
    6.9.2) TREATMENT
    A) IRRITATION SYMPTOM
    1) Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines.
    B) SKIN ABSORPTION
    1) Some chemicals can produce systemic poisoning by absorption through intact skin. Carefully observe patients with dermal exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    C) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Enhanced Elimination

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

Range Of Toxicity

Summary

    A) Minimum lethal human exposure is unknown.

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) The minimum lethal human dose to this agent has not been delineated.

Maximum Tolerated Exposure

    A) GENERAL/SUMMARY
    1) The maximum tolerated human exposure to this agent has not been delineated.
    2) Due to the increased reports of ground water contamination with ammonium perchlorate, and its potential at high acute doses to block iodide uptake by the thyroid, the EPA is drafting toxicological assessments of potential health hazards. Concentrations as high as 3,700,000 micrograms/liter have been reported in groundwater. The California EPA has set a provisional action level of 18 micrograms/liter in drinking water (Renner, 1999). In 2002, the California Department of Health Services adopted a maximum accepted level of 4 parts per billion of perchlorate in drinking water, or 4 nanograms/milliliter (Morgan & Cassady, 2002; Urbansky, 2002).

Workplace Standards

    A) ACGIH TLV Values for CAS7790-98-9 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    B) NIOSH REL and IDLH Values for CAS7790-98-9 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    C) Carcinogenicity Ratings for CAS7790-98-9 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed
    2) EPA (U.S. Environmental Protection Agency, 2011): Not likely to be carcinogenic to humans. ; Listed as: Perchlorate and Perchlorate Salts
    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 CAS7790-98-9 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: RTECS, 2001
    1) LD50- (ORAL)MOUSE:
    a) 1900 mg/kg
    2) LD50- (ORAL)RAT:
    a) 4200 mg/kg
    3) LD50- (SUBCUTANEOUS)RAT:
    a) 1600 mg/kg

Pharmacology Toxicology

Toxicologic Mechanism

    A) Ammonium perchlorate is a direct irritant of eyes, skin, and mucous membranes (Prod Info Ammonium Perchlorate, 1996; (Sax & Lewis, 1987; ITI, 1985; CHRIS , 1985).
    B) A significant reversible pharmacological effect on thyroid tissue by the perchlorate ion may occur via competitive inhibition of thyroid iodine transport (York et al, 2001a; Renner, 1999) Prod Info Ammonium Perchlorate, 1996).
    C) In the presence of reducing materials, perchlorates can produce shock-sensitive explosive mixtures (Bingham et al, 2001).

Physicochemical

Physical Characteristics

    A) Ammonium perchlorate is an odorless water soluble white crystalline solid (HSDB , 2001; Sax & Lewis, 1987; ITI, 1985; Fire Protection Guide, 1978).
    1) Ammonium perchlorate crystals are orthorhombic (Budavari, 1996).

Molecular Weight

    A) 117.50 (RTECS , 2001)

Other

    A) ODOR THRESHOLD
    1) Not pertinent (CHRIS , 2002).

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