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Ammonia Toxicity

  • Author: Steven Issley, MD, FRCPC; Chief Editor: Asim Tarabar, MD  more...
Updated: Dec 29, 2015

Practice Essentials

Injury from ammonia most commonly is caused by inhalation, but it also may follow ingestion or direct contact with eyes or skin.

Signs and symptoms

Symptoms of exposure to gaseous ammonia include the following:

  • Rhinorrhea
  • Scratchy throat
  • Chest tightness
  • Cough
  • Dyspnea
  • Eye irritation

Symptoms usually subside within 24-48 hours. Absence of symptoms following inhalational exposure to ammonia essentially rules out significant injury.

Ingestion of ammonia can produce the following symptoms:

  • Oropharyngeal, epigastric, and retrosternal pain
  • Abdominal pain and other GI symptoms, with viscus perforation (perforation may occur up to 24-72 hours post ingestion)
  • Respiratory symptoms, if aspiration pneumonia or pneumonitis complicates ingestion

On physical examination, inhalation injury from ammonia is marked by the following findings:

  • Head, ears, eyes, nose, throat (HEENT) - Facial and oral burns and ulcerations
  • Respiration - Tachypnea, oxygen desaturation, stridor, drooling, cough, wheezing, rhonchi, and decreased air entry
  • Central nervous system (CNS) - Loss of consciousness (if exposure is massive)

Alkali burns to the skin from ammonia are yellow, soapy, and soft in texture; with severe burns, skin turns black and leathery.

Manifestations of ocular toxicity from ammonia include the following:

  • Iritis
  • Corneal edema
  • Semi-dilated fixed pupil
  • Eventual cataract formation
  • Hepatic encephalopathy [1]

See Clinical Presentation for more detail.


Serum ammonia levels are of little value in patients with ammonia toxicity because they do not correlate with clinical condition. Laboratory studies in patients with ammonia exposure include the following:

  • Serum acetaminophen level in intentional exposures
  • CBC
  • Electrolytes, BUN, and creatinine
  • Serum lactic acid
  • Serial arterial blood gases (ABGs) in cases of significant respiratory distress - Metabolic acidosis, respiratory alkalosis, increased alveolar-arterial gradient

Patients with eye injury should have a slit-lamp examination with fluorescein staining. Perform tonometry to determine if intraocular pressure is elevated. Measure conjunctival pH.

Depending on the clinical presentation, other tests and procedures may include the following:

  • Chest radiography
  • Abdominal series – To rule out perforation following ingestion
  • Cardiac monitoring
  • Pulse oximetry
  • Pulmonary capillary wedge pressure (PCWP) monitoring – In cases of severe acute lung injury (ALI) or ARDS
  • Pulmonary function tests
  • Ventilation/perfusion (V/Q) scan
  • Bronchoscopy – In severe acute inhalation injury
  • Endoscopy – In significant ingestion exposures

See Workup for more detail.


Management of toxic exposure to ammonia is largely supportive, as follows:

  • Decontaminate the patient (if that was not done at the site of exposure)
  • Support the ABCs as necessary
  • Provide warmed humidified oxygen

Indications for tracheal intubation include the following:

  • Severe respiratory distress (hypoxemia, hypercapnia)
  • Stridor
  • Hoarseness
  • Deep facial burns
  • Burns identified by bronchoscopy or endoscopy
  • Depressed mental status

Treat ingestions using the following steps:

  • Rinse mouth and dilute ingestion with approximately 250 mL of water or milk
  • Do not induce emesis, so as not to worsen injury with a second pass of toxin
  • Promptly arrange a gastroenterology consultation for subsequent endoscopic evaluation (not often performed before 12 hours post ingestion)

Corticosteroids are controversial therapies for ammonia toxicity, and should be used only after appropriate expert consultation. Accepted indications include the following:

  • Acute bronchospasm in patients with underlying reactive airways disease
  • Chronic respiratory complications from acute inhalation injury
  • Symptomatic airway edema after caustic exposure

See Treatment and Medication for more detail.



At room temperature, ammonia (NH3) is a highly water-soluble, colorless, irritant gas with a unique pungent odor. Ammonia has a boiling point of -33°C and an ignition temperature of 650°C. Injury from ammonia most commonly is caused by inhalation, but it also may follow ingestion or direct contact with eyes or skin.

Anhydrous ammonia is one of the most widely produced chemicals in the United States, one third of which is used by the farming industry as a component of fertilizer and animal feed. Before the 1970s, liquid ammonia stored under high pressure was widely used for refrigeration. Although chlorofluorocarbons (eg, Freon) have largely replaced ammonia as a refrigerant, ammonia refrigeration is still used and numerous case reports exist of severe toxicity following unintentional exposure.

Ammonia also is used in the production of explosives, pharmaceuticals, pesticides, textiles, leather, flame-retardants, plastics, pulp and paper, rubber, petroleum products, and cyanide. Furthermore, ammonia is a major component of many common household cleaning and bleaching products (eg, glass cleaners, toilet bowel cleaners, metal polishes, floor strippers, wax removers, smelling salts).

Permissible levels of exposure to toxic gases are defined as follows:

  • Time-weighted average (TWA)
  • Short-term exposure limit (STEL)
  • Concentration at which toxic gases are immediately dangerous to life or health (IDLH)

The TWA is defined as the concentration for an 8-hour workday of a 40-hour workweek that nearly all workers can be exposed to without adverse effects. The STEL is the concentration at which an exposure of longer than 15 minutes is potentially dangerous and may produce immediate or chronic compromise to health. Anhydrous ammonia has a TWA of 25 parts per million (ppm), a STEL of 35 ppm, and an IDLH of 500 ppm.

The clinical presentations of these injuries and their evaluation and treatment are discussed in this article. Chloramine gas inhalation injury also is discussed. For patient education resources, see the First Aid and Injuries Center, as well as Thermal (Heat or Fire) Burns.



Ammonia most commonly causes damage when anhydrous ammonia (liquid or gas) reacts with tissue water to form the strongly alkaline solution, ammonium hydroxide. The formula for this is as follows:

NH3 + H2 O ⇒ NH4 OH

This reaction is exothermic and capable of causing significant thermal injury.

Ammonium hydroxide can cause severe alkaline chemical burns to skin, eyes, and especially the respiratory system. Mild exposures primarily affect the upper respiratory tract, while more severe exposures tend to affect the entire respiratory system (see Presentation). The gastrointestinal tract also may be affected if ammonia is ingested.

Tissue damage from alkali is caused by liquefaction necrosis and theoretically can penetrate deeper than that caused by an equipotent acid. In the case of ammonium hydroxide, the tissue breakdown liberates water, thus perpetuating the conversion of ammonia to ammonium hydroxide. In the respiratory tract, this results in the destruction of cilia and the mucosa, eliminating the barrier to infection. Furthermore, secretions, sloughed epithelium, cellular debris, edema, and reactive smooth muscle contraction cause significant airway obstruction.

Airway epithelium can regain barrier integrity within 6 hours after exposure if the basal cell layer remains intact. However, damaged epithelium often is replaced by granular tissue, which may be one of the causes of chronic lung disease following ammonia inhalation injury.

Liquid anhydrous ammonia (-33°C) freezes tissue on contact. To put this in perspective, critical skin damage begins at -4°C and becomes irreversible at -20°C. The degree of tissue injury, however, is proportional to the duration and concentration of exposure. Similarly, damage to the respiratory system is proportional to depth of inhalation, duration of exposure, concentration, and pH of the gas or liquid.

Chloramines (NH2 Cl, NHCl2) are highly water-soluble irritant gases formed when household bleach (5.25% sodium hypochlorite [NaOCl]) is mixed with 5-10% ammonia solutions (usually cleaning products). When inhaled, the gases react with the water in airway mucous membranes to produce free ammonia gas, hypochloric acid, and hypochlorous acid. In turn, hypochlorous acid reacts with water to form hydrochloric acid and nascent oxygen, a strong oxidizing agent with corrosive effects.

Ammonia is a product of protein catabolism and is metabolized by the liver. Normal blood ammonia levels range from 10-40 µmol/L. This increases 10% with exposure to 25 ppm but is not considered harmful. Theoretically, patients with liver dysfunction are at increased risk for ammonia toxicity; however, currently no sufficient clinical evidence can confirm this.

Chloramine gas

Chloramines (NH2 Cl, NHCl2) are highly water-soluble irritant gases formed when household bleach (5.25% sodium hypochlorite [NaOCl]) is mixed with 5-10% ammonia solutions (usually cleaning products). When inhaled, the gases react with the water in airway mucous membranes to produce free ammonia gas, hypochloric acid, and hypochlorous acid. In turn, hypochlorous acid reacts with water to form hydrochloric acid and nascent oxygen, a strong oxidizing agent with corrosive effects.



Agriculture-related ammonia injury most often results from either ammonia leaks in fertilizer tanks and hoses or toxic ammonia levels in animal confinement buildings, where ammonia is adsorbed by dust particles that transport it more directly to small airways. Because of this synergistic effect, symptoms have reportedly developed within minutes of entering animal confinement buildings.

Firefighters are at risk for exposure this irritant gas. Anhydrous ammonia may be released in industrial fires (eg, at fertilizer plants). In addition, ammonia is liberated during combustion of nylon, silk, wood, and melamine.

Household exposure may occur because ammonia is a major component of many common household cleaning and bleaching products, including the following:

  • Glass cleaners
  • Toilet bowel cleaners
  • Metal polishes
  • Floor strippers
  • Wax removers

Smelling salts are a less common source of household ammonia ingestion. Often in capsule form, smelling salts, which contain approximately 20% ammonia, release a pungent odor when broken. Smelling salts are found in many first-aid kits as a treatment for syncope; unfortunately, children sometimes bite into them, resulting in minor esophageal burns and mild respiratory symptoms.



The 2014 Annual Report of the American Association of Poison Control Centers' National Poison Data System reported 2,083 single exposures of ammonia, with no deaths. In addition, 89 single exposures to ammonia-containing glass cleaners and 555 single exposures to all-purpose ammonia cleaners were reported, with no deaths.[2]

Of note, ingestion of household solutions usually is unintentional and occurs in young children; adult ingestions, however, most often are suicide attempts. In contrast, inhalation injury is almost always unintentional and generally occurs in an industrial setting; therefore, it is far more common in adults than children.

Ammonia exposure may be one factor in an elevated risk for chronic bronchitis and chronic obstructive pulmonary disease (COPD) seen in livestock farmers. Susceptibility to farming-related COPD appears to be heightened in farmers with underlying atopy.[3]



Most individuals with ammonia inhalation who survive the first 24 hours will recover. Patients begin showing improvement within 48-72 hours and may recover fully during this time if exposure was mild. For patients with more significant respiratory symptoms, recovery can be expected within several weeks to months.

Interestingly, Arwood et al found that initial chest radiography findings and oxygenation level correlate poorly with outcome and that physical examination on arrival provides more sensitive prognostic information.[4] Montague and MacNeil, however, note that patients who do not develop chest radiograph abnormalities are less likely to have chronic respiratory sequelae.[5]

In a study of 12 patients exposed to anhydrous ammonia as a result of the same accident, Close and colleagues found that patients exposed to high concentrations of ammonia over a short period of time manifested upper airway obstruction and required early intubation or tracheostomy but recovered with few pulmonary sequelae. In contrast, patients exposed to lower concentrations of gas over a prolonged period did not manifest upper airway obstruction, but suffered significant long-term pulmonary sequelae.[6]

Patients in this case series who developed long-term pulmonary sequelae experienced gradual deterioration of pulmonary function during the first 2-6 months after exposure.[6] A period of slight improvement was then observed, followed by stabilization of symptoms.[6]

Long-term effects of ammonia inhalation injury include the following:

  • Cough
  • Hoarseness
  • Obstructive and/or restrictive lung disease
  • Hyper-reactive airway disease and reactive airway dysfunction syndrome (RADS)
  • Impaired gas exchange
  • Residual parenchymal damage
  • Bronchiectasis and bronchiolitis obliterans (following massive exposure)
  • Pulmonary fibrosis

Chronic obstructive disease from ammonia toxicity is often only minimally improved by bronchodilators. The reason is thought to be that this sequela results from airway lesions more than from hyperreactivity.

Contributor Information and Disclosures

Steven Issley, MD, FRCPC Attending Physician, Department of Emergency Medicine, University Health Center, Toronto, ON

Disclosure: Nothing to disclose.


Eddy S Lang, MDCM, CCFP(EM), CSPQ Associate Professor, Senior Researcher, Division of Emergency Medicine, Department of Family Medicine, University of Calgary Faculty of Medicine; Assistant Professor, Department of Family Medicine, McGill University Faculty of Medicine, Canada

Eddy S Lang, MDCM, CCFP(EM), CSPQ is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine, Canadian Association of Emergency Physicians

Disclosure: Nothing to disclose.

Joel Lockwood, MD Resident Physician, Department of Emergency Medicine, University of Toronto Faculty of Medicine, Canada

Joel Lockwood, MD is a member of the following medical societies: American College of Emergency Physicians, Emergency Medicine Residents' Association, Canadian Association of Emergency Physicians

Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD Assistant Professor, Director, Medical Toxicology, Department of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital

Disclosure: Nothing to disclose.


Michael J Burns, MD Instructor, Department of Emergency Medicine, Harvard University Medical School, Beth Israel Deaconess Medical Center

Michael J Burns, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Emergency Physicians, American College of Medical Toxicology, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Edmond A Hooker II, MD, DrPH, FAAEM Associate Professor, Department of Health Services Administration, Xavier University, Cincinnati, Ohio; Assistant Professor, Department of Emergency Medicine, University of Cincinnati College of Medicine

Edmond A Hooker II, MD, DrPH, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American Public Health Association, Society for Academic Emergency Medicine, and Southern Medical Association

Disclosure: Nothing to disclose.

John T VanDeVoort, PharmD Regional Director of Pharmacy, Sacred Heart and St Joseph's Hospitals

John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists

Disclosure: Nothing to disclose.

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