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AMMONIUM CHLORIDE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Ammonium chloride is a systemic acidifier.

Specific Substances

    1) Ammonii chloridum
    2) Ammonium chloratum
    3) Ammonium muriate
    4) Sal ammoniac
    5) Salmiac
    6) CAS 12125-02-9
    7) AMMON CHLOR
    8) CHLORAMMONIAC (FRENCH)
    9) CLARURO DE AMONIO (MEXICAN)
    1.2.1) MOLECULAR FORMULA
    1) H4-N.Cl
    2) NH4Cl

Available Forms Sources

    A) FORMS
    1) Ammonium chloride injection is available as 267.5 mg ammonium chloride per mL supplied in 20 mL single dose containers for intravenous administration (Prod Info ammonium chloride intravenous injection solution concentrate, 2009).
    B) USES
    1) Ammonium chloride is used as a fertilizer, a dye mordant, in electroplating, washing powders, ammonia compounds, soldering as flux, melt-retarding show treatment to slow melting on ski slopes, urea-formaldehyde adhesives, and in the manufacture of dry batteries (ACGIH, 1983; ITI, 1988) Budavari, 1996).
    2) Ammonium chloride is used as a flux for coating sheet iron with zinc; in tinning; in dry and Leclanche batteries; in dyeing, freezing mixtures, electroplating, cleaning soldering irons, safety explosives, lustering cotton, tanning; in washing powders; in the manufacture of dyes; in cement for iron pipes; for snow treatment (slows melting on ski slopes); and, therapeutically, as a systemic acidifier, expectorant, diaphoretic, and acidifying diuretic (Budavari, 1996).
    3) The fume is frequently evolved in galvanizing operations (ACGIH, 1986).
    4) Ammonium chloride has been used to acidify blood and urine in severe cases of phencyclidine toxicity to shift the gradient causing movement of phencyclidine out of the brain and to enhance its renal excretion (Done et al, 1979; Giannini et al, 1987).
    5) After dilution with isotonic sodium chloride solution, ammonium chloride injection is indicated for treatment of patients with hypochloremia or metabolic alkalosis (Prod Info ammonium chloride intravenous injection solution concentrate, 2009).

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) RISK - Ammonium chloride is usually not a serious industrial hazard. It can produce mild irritation of the skin and respiratory tract. Systemic toxicity may occur by ingestion but is usually not severe.
    2) ROUTE - Toxicity may occur by eye, inhalation, ingestion, or skin exposure.
    3) SIGNS/SYMPTOMS - Hyperchloremic hypokalemic metabolic acidosis is the most common manifestation of systemic toxicity. Initial symptoms are nausea, vomiting, headache, progressive drowsiness, and hyperventilation. A transient diuresis may occur.
    4) PREDISPOSITION - In patients with renal or liver failure, ammonia may accumulate with symptoms of pallor, sweating, irregular respirations and/or apnea, bradycardia, and hyperreflexia.
    0.2.5) CARDIOVASCULAR
    A) WITH THERAPEUTIC USE
    1) In patients with renal or liver disease ammonia may accumulate, producing bradycardia.
    0.2.6) RESPIRATORY
    A) WITH POISONING EXPOSURE
    1) Hyperventilation reflects respiratory compensation for metabolic acidosis and may not be present for several hours after acidosis is evident. It is often one of the presenting symptoms observed.
    2) Ammonium ions may accumulate in patients with liver or kidney disease producing jerky respirations and periods of apnea.
    3) Inhalation of soldering fume containing ammonium chloride may cause asthma.
    0.2.7) NEUROLOGIC
    A) WITH POISONING EXPOSURE
    1) Drowsiness, headache and mental confusion are often presenting symptoms. These may progress to coma. Tremor and hyperreflexia have been seen in patients with kidney or liver disease.
    0.2.8) GASTROINTESTINAL
    A) WITH THERAPEUTIC USE
    1) Nausea and vomiting can occur with therapeutic use. Anorexia and thirst may be present.
    B) WITH POISONING/EXPOSURE
    1) Nausea, vomiting, and abdominal pain occur commonly following large doses.
    0.2.11) ACID-BASE
    A) WITH POISONING/EXPOSURE
    1) Hyperchloremic hypokalemic metabolic acidosis is the most common finding.
    0.2.12) FLUID-ELECTROLYTE
    A) WITH THERAPEUTIC USE
    1) Hypokalemia and hyperchloremia are the most common findings; hyperkalemia may occur in the presence of acidosis. Transient hypocalcemic tetany have been observed. Diuresis may occur.
    0.2.13) HEMATOLOGIC
    A) WITH THERAPEUTIC USE
    1) Leukocytosis may occur.
    0.2.16) ENDOCRINE
    A) WITH THERAPEUTIC USE
    1) Transient hyperglycemia may occur.
    0.2.20) REPRODUCTIVE
    A) Ammonium chloride is classified as FDA pregnancy category C. Acidosis has been reported as an adverse fetal effect in humans following maternal administration. Congenital anomalies were observed in animal offspring with maternal exposure.
    0.2.21) CARCINOGENICITY
    A) At the time of this review, no studies were found on the possible carcinogenic activity of ammonium chloride in humans or experimental animals.

Laboratory Monitoring

    A) Monitor serum electrolytes. Monitor arterial blood gases in patients with metabolic acidosis. Monitor serum ammonia levels in patients with evidence of encephalopathy.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) 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.
    B) Given that NH4CL is a readily ionized inorganic salt, activated charcoal would theoretically not absorb it well.
    C) Potassium salts should be given to correct hypokalemia.
    D) ACIDOSIS - Severe metabolic acidosis may be cautiously corrected with IV sodium bicarbonate in D5W. Begin aggressive repletion of serum potassium before administering bicarbonate to hypokalemic patients, as bicarbonate will worsen hypokalemia. Initial bicarbonate doses are 1 to 2 mEq per kilogram in adults and 1 mEq/kg in children. Repeat every 1 to 2 hours as required with close monitoring of serum electrolytes, arterial blood gases, pH, bicarbonate, and base deficits.
    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.

Range Of Toxicity

    A) Ingestion of 40 to 50 g over a short period would be expected to exhaust available body buffers of the average adult and produce potentially fatal acidosis. Mild acidosis occurs at a dose of 2 g.

Clinical Effects

Summary Of Exposure

    A) WITH POISONING/EXPOSURE
    1) RISK - Ammonium chloride is usually not a serious industrial hazard. It can produce mild irritation of the skin and respiratory tract. Systemic toxicity may occur by ingestion but is usually not severe.
    2) ROUTE - Toxicity may occur by eye, inhalation, ingestion, or skin exposure.
    3) SIGNS/SYMPTOMS - Hyperchloremic hypokalemic metabolic acidosis is the most common manifestation of systemic toxicity. Initial symptoms are nausea, vomiting, headache, progressive drowsiness, and hyperventilation. A transient diuresis may occur.
    4) PREDISPOSITION - In patients with renal or liver failure, ammonia may accumulate with symptoms of pallor, sweating, irregular respirations and/or apnea, bradycardia, and hyperreflexia.

Heent

    3.4.3) EYES
    A) WITH THERAPEUTIC USE
    1) NO EFFECTS - Solutions of 5 to 10% ammonium chloride have been used therapeutically to irrigate the eyes with no adverse effect (Grant & Schuman, 1993).
    B) WITH POISONING/EXPOSURE
    1) IRRITATION - Ammonium chloride is listed as a severe eye irritant (concentration not specified) (Lewis, 2000).
    2) ANIMAL STUDY
    a) CORNEAL EDEMA - Continuous ocular exposure by dripping into rabbit eyes for several hours produced corneal epithelium edema (Grant & Schuman, 1993).

Cardiovascular

    3.5.1) SUMMARY
    A) WITH THERAPEUTIC USE
    1) In patients with renal or liver disease ammonia may accumulate, producing bradycardia.
    3.5.2) CLINICAL EFFECTS
    A) BRADYCARDIA
    1) WITH THERAPEUTIC USE
    a) In patients with renal or liver disease, ammonia may accumulate, producing bradycardia (Sollmann, 1957).

Respiratory

    3.6.1) SUMMARY
    A) WITH POISONING EXPOSURE
    1) Hyperventilation reflects respiratory compensation for metabolic acidosis and may not be present for several hours after acidosis is evident. It is often one of the presenting symptoms observed.
    2) Ammonium ions may accumulate in patients with liver or kidney disease producing jerky respirations and periods of apnea.
    3) Inhalation of soldering fume containing ammonium chloride may cause asthma.
    3.6.2) CLINICAL EFFECTS
    A) HYPERVENTILATION
    1) WITH POISONING/EXPOSURE
    a) Hyperventilation reflects respiratory compensation for metabolic acidosis and may not be present for several hours after acidosis is evident (Relman et al, 1961). Along with mental confusion, this is often the presenting symptom observed.
    B) APNEA
    1) WITH POISONING/EXPOSURE
    a) In patients with renal or liver disease ammonia may accumulate, producing irregular respirations and periods of apnea (Solmann, 1957).
    C) BRONCHOSPASM
    1) WITH POISONING/EXPOSURE
    a) Chronic inhalation of soft corrosive soldering flux fumes containing ammonium chloride may cause asthma (Weir et al, 1989). These fluxes also had zinc chloride; the contribution of each agent is unknown.
    1) Symptoms developed after exposure of 12 to 18 months and would appear several hours after occupational exposure. Decrease in FEV1 caused by the flux was partially accounted for upon challenge testing with ammonium chloride alone in one patient (Weir et al, 1989).
    D) ACUTE LUNG INJURY
    1) WITH POISONING/EXPOSURE
    a) Pulmonary edema may occur and it does not seem to be related to the acidosis (Solmann, 1957).
    E) IRRITATION SYMPTOM
    1) WITH POISONING/EXPOSURE
    a) Inhalation of ammonium chloride fumes, such as in amounts evolved in galvanizing operations, may result in mild respiratory irritation (ACGIH, 1986).

Neurologic

    3.7.1) SUMMARY
    A) WITH POISONING EXPOSURE
    1) Drowsiness, headache and mental confusion are often presenting symptoms. These may progress to coma. Tremor and hyperreflexia have been seen in patients with kidney or liver disease.
    3.7.2) CLINICAL EFFECTS
    A) DROWSY
    1) WITH POISONING/EXPOSURE
    a) Progressive drowsiness, headache, and mental confusion are often presenting signs and symptoms (Relman et al, 1961). If untreated, progressive obtundation and coma may ensue.
    B) COMA
    1) WITH THERAPEUTIC USE
    a) CASE REPORT - Coma was reported in a patient with normal hepatic and renal function following intravenous administration of 15 grams (Warren et al, 1979).
    b) CASE REPORT - A 67-year-old woman developed impaired language and level of consciousness, oliguria and dyspnea and presented with coma (GCS 7) from chronic ammonium chloride poisoning (Megarbane et al, 2000).
    C) TREMOR
    1) WITH THERAPEUTIC USE
    a) In patients with renal or liver disease, this agent is contraindicated because ammonia may accumulate, producing local and generalized tremor and hyperreflexia.
    2) Signs/symptoms of ammonia toxicity include focal or generalized twitching, asterixis, tonic seizures, and coma.

Gastrointestinal

    3.8.1) SUMMARY
    A) WITH THERAPEUTIC USE
    1) Nausea and vomiting can occur with therapeutic use. Anorexia and thirst may be present.
    B) WITH POISONING/EXPOSURE
    1) Nausea, vomiting, and abdominal pain occur commonly following large doses.
    3.8.2) CLINICAL EFFECTS
    A) NAUSEA AND VOMITING
    1) WITH THERAPEUTIC USE
    a) Gastric irritation including nausea and vomiting will be more severe following ingestion of non-enteric-coated formulations.
    2) WITH POISONING/EXPOSURE
    a) Nausea, vomiting and abdominal pain are commonly seen (Relman et al, 1961).
    B) LOSS OF APPETITE
    1) WITH THERAPEUTIC USE
    a) Anorexia and thirst may be present.

Acid-Base

    3.11.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Hyperchloremic hypokalemic metabolic acidosis is the most common finding.
    3.11.2) CLINICAL EFFECTS
    A) ACIDOSIS
    1) WITH THERAPEUTIC USE
    a) SYSTEMIC ACIDOSIS - Administration of spironolactone and ammonium chloride concomitantly may produce a systemic acidosis (Ellenhorn & Barceloux, 1988).
    2) WITH POISONING/EXPOSURE
    a) HYPERCHLOREMIC HYPOKALEMIC metabolic acidosis is the most common finding (Megarbane et al, 2000; Wong et al, 2001). Acute ingestion of 40 to 50 grams in an adult is sufficient to totally deplete body buffers and produce serious acidosis (Relman et al, 1961).
    b) Mixed metabolic and respiratory acidosis may develop in patients who have severe hypokalemia, with weakness of respiratory muscles preventing the normal degree of hyperventilation in response to metabolic acidosis (Wong et al, 2001).
    c) CASE REPORT - A 56-year-old woman with dialysis dependent renal failure developed recurrent episodes of hyperchloremia metabolic acidosis after ingesting throat lozenges that contained 20 mg NH4Cl per lozenge. She was ingesting 10 g (about 500 lozenges) between dialysis sessions (Luth & Luft, 2006).
    B) ABNORMAL URINE
    1) WITH THERAPEUTIC USE
    a) URINE PH - The urine pH is decreased following oral administration of 2 grams.

Hematologic

    3.13.1) SUMMARY
    A) WITH THERAPEUTIC USE
    1) Leukocytosis may occur.
    3.13.2) CLINICAL EFFECTS
    A) LEUKOCYTOSIS
    1) WITH THERAPEUTIC USE
    a) Leukocytosis may occur.

Endocrine

    3.16.1) SUMMARY
    A) WITH THERAPEUTIC USE
    1) Transient hyperglycemia may occur.
    3.16.2) CLINICAL EFFECTS
    A) HYPERGLYCEMIA
    1) WITH THERAPEUTIC USE
    a) Transient hyperglycemia and glycosuria may occur.

Reproductive

    3.20.1) SUMMARY
    A) Ammonium chloride is classified as FDA pregnancy category C. Acidosis has been reported as an adverse fetal effect in humans following maternal administration. Congenital anomalies were observed in animal offspring with maternal exposure.
    3.20.2) TERATOGENICITY
    A) ANIMAL STUDIES
    1) LACK OF EFFECT
    a) No teratogenicity was observed in rats (Goldman & Yakovac, 1964).
    2) CONGENITAL ANOMALY
    a) Pregnant mice administered ammonium chloride in drinking water produced small offspring (Goldman & Yakovac, 1964). It caused missing digits in mice when given at a very high dose which may have been close to the LD50 (Weaver & Scott, 1984). When injected into pregnant rats, it produced fewer living pups with lower weight and CNS damage (Maros, 1978).
    3.20.3) EFFECTS IN PREGNANCY
    A) ACIDOSIS
    1) Acidosis has been reported as an adverse effect on the human fetus (Schardein, 1985).
    2) PREGNANCY CATEGORY
    a) Ammonium chloride is classified as FDA pregnancy category C. It is recommended that ammonium chloride be given to a pregnant woman only if clearly necessary (Prod Info ammonium chloride intravenous injection solution concentrate, 2009).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS12125-02-9 (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
    3.21.2) SUMMARY/HUMAN
    A) At the time of this review, no studies were found on the possible carcinogenic activity of ammonium chloride in humans or experimental animals.

Genotoxicity

    A) At the time of this review, no genetic studies were found for ammonium chloride.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor serum electrolytes. Monitor arterial blood gases in patients with metabolic acidosis. Monitor serum ammonia levels in patients with evidence of encephalopathy.

Radiographic Studies

    A) ABDOMINAL RADIOGRAPH
    1) Enteric coated ammonium chloride tablets may be visible on abdominal x-rays.

Methods

    A) OTHER
    1) AIR - A sample is collected on a filter and analyzed by colorimetric techniques (ITI, 1988).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) Monitor serum electrolytes. Monitor arterial blood gases in patients with metabolic acidosis. Monitor serum ammonia levels in patients with evidence of encephalopathy.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) 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) 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) HYPOKALEMIA
    1) POTASSIUM salts should be given to correct hypokalemia 40 milliequivalents/liter may be added to the initial infusion. Oral potassium may also be given.
    B) ACIDOSIS
    1) Severe metabolic acidosis may be cautiously corrected with IV sodium bicarbonate in D5W. Begin aggressive repletion of serum potassium before administering bicarbonate to hypokalemic patients, as bicarbonate will worsen hypokalemia. Initial doses are 1 to 2 milliequivalents/kilogram in adults and 1 milliequivalent/kilogram in children. Repeat every 1 to 2 hours as required with close monitoring of blood gases and blood pH.
    a) Another recommendation for the initial bicarbonate dose would be half the base deficit or one quarter times body weight (in Kilograms) times (24-serum bicarbonate).
    2) Sodium bicarbonate infusion to correct acute metabolic acidosis induced by ammonium chloride in a rat model, increased plasma bicarbonate concentration and repaired the natriuresis, kaluresis, chloruresis, and diuresis (Cogan & Mueller, 1983).
    C) DISORDER OF BRAIN
    1) SOURCE - Accumulation of ammonia in patients with poor renal or hepatic function may lead to ammonia encephalopathy. Ammonia toxicity may also result from rapid intravenous administration.
    2) MONITOR - Mental status and ammonia concentrations in the blood as an indicator of severity of accumulation.
    3) Encephalopathy should be readily reversible with sodium bicarbonate therapy in patients with normal hepatic and renal function (other measures would be of minor importance).
    a) Dialysis should be considered in patients with renal failure who are not able to excrete ammonium ions.
    4) MEDICAL MANAGEMENT - Of hepatic encephalopathy includes reduction of dietary intake of protein, reduction of ammonia-producing microorganisms in the intestine (i.e., neomycin), or addition of a source of organic acid production (lactulose is metabolized to organic acids by intestinal bacteria) in intestinal tract to retard the nonionic diffusion of ammonia and amines from the colon to the blood (Gilman et al, 1990).
    a) ARGININE - May be of benefit because it acts as a precursor of ornithine in the urea cycle in the liver (Gilman et al, 1990).
    b) GLUTAMATE - May react with ammonia in the enzymatic synthesis of glutamine (Gilman et al, 1990).

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) BRONCHOSPASM
    1) If bronchospasm and wheezing occur, consider treatment with inhaled sympathomimetic agents.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Eye Exposure

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

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) 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).

Abstracts

Case Reports

    A) ADULT
    1) An 18-year-old woman who chronically intermittently ingested up to 15 g/d and acutely ingested 82 g over 48 hours developed nausea, vomiting, headache, drowsiness, and confusion.
    a) Laboratory values included a urine pH of 4.82, potassium 5.2, chloride 137, blood sugar 237, and blood pH 6.78. She became comatose. Following sodium bicarbonate infusion the serum potassium fell to 2.1 with EKG changes consistent with hypokalemia (Relman et al, 1961).
    2) A 69-year-old consuming 250 mL Benylin(R) syrup (14 mg diphenhyramine, 135 mg ammonium chloride, and 57 mg sodium citrate per 5 mL) daily and 60 to 80 mg temazepam nightly for several months presented with confusion, metabolic acidosis, and non-ketotic hyperglycemia (MacRury et al, 1987).

Range Of Toxicity

Summary

    A) Ingestion of 40 to 50 g over a short period would be expected to exhaust available body buffers of the average adult and produce potentially fatal acidosis. Mild acidosis occurs at a dose of 2 g.

Therapeutic Dose

    7.2.1) ADULT
    A) For treatment of hyperchloremia or metabolic alkalosis, 1 to 2 vials (100 to 200 mEq) ammonium chloride should be added to 500 to 1000 mL of 0.9% sodium chloride, and intravenously infused at a rate not to exceed 5 mL/minute (approximately 3 hours for infusion of 1000 mL). Monitor dosage with repeated serum sodium bicarbonate determinations (Prod Info ammonium chloride intravenous injection solution concentrate, 2009).

Minimum Lethal Exposure

    A) ADULT
    1) Ingestion of 40 to 50 grams over a short period would be expected to exhaust available body buffers of the average adult and produce potentially fatal acidosis (Relman et al, 1961).
    2) Administration of more than 15 to 20 grams to an adult has produced obtundation.

Maximum Tolerated Exposure

    A) GENERAL/SUMMARY
    1) Mild acidosis occurs at a dose of 2 grams.
    B) CASE REPORTS
    1) Severe metabolic acidosis (pH 7.07 three hours postingestion) was reported in a 10-month-old boy given 150 milliequivalents/square meter by nasogastric tube (Dibona & Kelsch, 1977).
    C) ROUTE OF EXPOSURE
    1) INDUSTRIAL - Ammonium chloride is usually not a serious industrial hazard. It can produce mild irritation of the skin and respiratory tract (ACGIH, 1986).
    2) OTHER - Ammonium chloride is poisonous by subcutaneous, intravenous, and intramuscular routes. It is moderately toxic by other routes (Sax & Lewis, 1989). Toxicity may occur by eye, inhalation, ingestion, or skin exposure (ITI, 1988). Systemic toxicity can occur by ingestion, but is usually not severe (ACGIH, 1986).

Workplace Standards

    A) ACGIH TLV Values for CAS12125-02-9 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.
    a) Adopted Value
    1) Ammonium chloride fume
    a) TLV:
    1) TLV-TWA: 10 mg/m(3)
    2) TLV-STEL: 20 mg/m(3)
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: Not Listed
    2) Codes: Not Listed
    3) Definitions: Not Listed
    c) TLV Basis - Critical Effect(s): Eye and URT irr
    d) Molecular Weight: 53.5
    1) For gases and vapors, to convert the TLV from ppm to mg/m(3):
    a) [(TLV in ppm)(gram molecular weight of substance)]/24.45
    2) For gases and vapors, to convert the TLV from mg/m(3) to ppm:
    a) [(TLV in mg/m(3))(24.45)]/gram molecular weight of substance
    e) Additional information:

    B) NIOSH REL and IDLH Values for CAS12125-02-9 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Ammonium chloride fume
    2) REL:
    a) TWA: 10 mg/m(3)
    b) STEL: 20 mg/m(3)
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s):
    3) IDLH: Not Listed

    C) Carcinogenicity Ratings for CAS12125-02-9 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Ammonium chloride fume
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
    3) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Ammonium chloride fume
    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 CAS12125-02-9 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: RTECS, 2002
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 485 mg/kg
    2) LD50- (ORAL)MOUSE:
    a) 1300 mg/kg
    3) LD50- (INTRAMUSCULAR)RAT:
    a) 30 mg/kg
    4) LD50- (ORAL)RAT:
    a) 1650 mg/kg

Pharmacology Toxicology

Pharmacologic Mechanism

    A) Ammonium chloride serves as a proton donor in the maintenance of acid-base balance. Ammonium chloride has a dissociation constant of 9.3 (pKa). Ninety-nine percent of ammonium chloride will exist in the blood as NH4+ (Gilman et al, 1990).

Toxicologic Mechanism

    A) Elevated concentrations of ammonia in the blood have been associated with an encephalopathy (disturbance of consciousness, asterixis, and EEG abnormalities), which may represent ammonia toxicity to the brain (Gilman et al, 1990).
    B) Ammonium chloride increases the acid of the body by 1. the conversion of part of the ammonium into urea, leaving an excess of chloride anions, which neutralize a corresponding amount of the alkali reserve and 2. directly as a salt of a strong acid and weak base (Sollmann et al, 1957).
    C) The chloride load, which is excreted along with cations and water, accounts for the diuretic effect. Sodium is the primary cation excreted but potassium excretion may also increase.
    D) The kidney compensates for loss of sodium by the deamination of amino acids and excretion of hydrogen ions (in the form of ammonium chloride) in exchange for sodium.
    E) With chronic ammonium chloride therapy, the renal excretion of ammonium chloride eventually (within 3 days) matches its intake.

Physicochemical

Physical Characteristics

    A) White granular powder or colorless, odorless crystals with a cooling, saline taste (CHRIS, 2005; Budavari, 1989).
    B) Ammonium chloride is somewhat hygroscopic with a tendency to cake (Budavari, 1989).

Ph

    A) 5.5 (at 25 degrees C) (1% solution) (Budavari, 1989)
    B) 5.1 (at 25 degrees C) (3% solution) (Budavari, 1989)
    C) 4.6-6 (5% solution) (JEF Reynolds , 1990)
    D) 5.0 (at 25 degrees C) (10% solution) (Budavari, 1989)

Molecular Weight

    A) 53.50

Other

    A) ODOR THRESHOLD
    1) Odorless (CHRIS, 2005)

Animal Toxicology

Clinical Effects

    11.1.13) OTHER
    A) OTHER
    1) MONOGASTRIC ANIMALS - Ammonium chloride may produce nausea and vomiting (Rossoff, 1974).

Range Of Toxicity

    11.3.1) THERAPEUTIC DOSE
    A) CATTLE
    1) No harm was noted in cattle with repeated doses of 75 g of ammonium chloride or with daily doses of 31 to 47 g to calves (Clarke et al, 1981).
    B) SHEEP
    1) No harm was noted in sheep given daily doses of 8 g of ammonium chloride (Clarke et al, 1981).
    11.3.2) MINIMAL TOXIC DOSE
    A) LACK OF INFORMATION
    1) No specific information on a minimal toxic dose was available at the time of this review.

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