Ammonia is widely used as a refrigerant, a fertilizer, and a household or commercial cleaning agent. Anhydrous ammonia (NH3) is a highly irritating and pungent gas that is water soluble. It is also a key ingredient in the illicit production of methamphetamine. Aqueous solutions of ammonia may be strongly alkaline, depending on the concentration. Solutions for household use are usually 5-10% ammonia, but commercial solutions may be 25-30% or more. The addition of ammonia to chlorine or hypochlorite solutions will produce chloramine gas, an irritant with properties similar to those of chlorine gas.

Ammonia gas is highly water soluble and rapidly produces an alkaline corrosive effect on contact with water in tissues. Mucosal tissue such as the eyes and upper respiratory tract are highly sensitive. Exposure to aqueous solutions can cause corrosive alkaline injury to the eyes, skin, or GI tract (see “Caustic and Corrosive Agents”).

1. Ammonia gas. The odor of ammonia is detectable at 5 ppm, and without protective gear a person will experience respiratory irritation at 50 ppm and usually self-evacuate the area. Eye irritation is common at 100 ppm. The ACGIH Threshold Limit Value (TLV-TWA) for anhydrous ammonia gas is 25 ppm as an 8-hour time-weighted average, and the short-term exposure limit (STEL) is 35 ppm. OSHA sets the permissible exposure limit (PEL) at 50 ppm. The level considered immediately dangerous to life or health (IDLH) is 300 ppm. The Emergency Response Planning Guidelines (ERPG) suggest that 25 ppm will cause no more than mild, transient health effects for exposures of up to 1 hour.
2. Aqueous solutions. Diluted aqueous solutions of ammonia (eg, <5%) rarely cause serious burns but are moderately irritating. More concentrated solutions (eg, 25-30% ammonia) are much more likely to cause serious corrosive injury.

Clinical manifestations depend on the physical state and route of exposure.

1. Inhalation of ammonia gas. Symptoms are rapid in onset owing to the high water solubility of ammonia and include immediate burning of the eyes, nose, and throat, accompanied by coughing. With serious exposure, swelling of the upper airway can occur and cause airway obstruction, laryngospasm, and stridor. Bronchospasm with wheezing can occur. Massive inhalational exposure may cause noncardiogenic pulmonary edema and desquamation of airway.
2. Ingestion of aqueous solutions. Immediate burning in the mouth and throat is common. With more concentrated solutions, serious esophageal and gastric burns are possible, and victims may have dysphagia, drooling, and severe throat, chest, and abdominal pain. Hematemesis and perforation of the esophagus or stomach may occur. The absence of oral burns does not rule out significant esophageal or gastric injury.
3. Skin or eye contact with gas or solution. Serious alkaline corrosive burns may occur. Contact with liquefied ammonia can cause frostbite injury.

Is based on a history of exposure and description of the typical ammonia smell, accompanied by typical irritative or corrosive effects on the eyes, skin, and upper respiratory or GI tract.

1. Specific levels. Blood ammonia levels may be elevated (normal, 8-33 mcmol/L) but are not predictive of toxicity. Samples should be placed on ice and testing performed on a stat basis because ammonia levels increase after blood collection owing to the breakdown of proteins.
2. Other useful laboratory studies may include electrolytes, arterial blood gases or pulse oximetry, and chest radiographs.

1. Emergency and supportive measures. Treatment depends on the physical state (aqueous vs. gas) of the ammonia and the route of exposure.
   1. Inhalation of ammonia gas
      1. Observe carefully for signs of progressive upper airway obstruction and intubate early if necessary.
      2. Administer humidified supplemental oxygen and bronchodilators for wheezing. Treat noncardiogenic pulmonary edema if it occurs.
      3. Asymptomatic or mildly symptomatic patients may be discharged after a brief observation period.
   2. Ingestion of aqueous solution. If a solution of 10% or greater has been ingested or if there are any symptoms of corrosive injury (dysphagia, drooling, or pain), perform flexible endoscopy to evaluate for serious esophageal or gastric injury. Obtain chest and abdominal radiographs to look for mediastinal or abdominal free air, which suggests esophageal or GI perforation.
   3. Eye exposure. Irrigate until eye pH normalizes (pH 7.0-7.4). Perform fluorescein examination and refer the patient to an ophthalmologist if there is evidence of corneal injury.
2. Specific drugs and antidotes. There is no specific antidote for these or other common caustic burns. The use of corticosteroids in alkaline corrosive ingestions is controversial. While prolonged courses of steroids are associated with esophageal perforation and serious infection, recent studies indicate that a short course of steroids may benefit select patient populations (Grade 2B alkaline injuries).
3. Decontamination
   1. Inhalation. Remove immediately from exposure and give supplemental oxygen if available.
   2. Ingestion
      1. Immediately give water by mouth to dilute the ammonia. Do not induce vomiting because this may aggravate corrosive effects. Do not attempt to neutralize the ammonia (eg, with an acidic solution).
      2. Nasogastric suction may be useful to remove excess ammonia in the stomach (in cases of deliberate ingestion of large quantities) and to prepare for endoscopy; use a small, flexible tube and pass it gently to avoid injury to damaged mucosa.
      3. Do not use activated charcoal; it does not adsorb ammonia, and it may obscure the endoscopist's view.
   3. Skin and eyes. Remove contaminated clothing and irrigate exposed skin with water. Irrigate exposed eyes with copious amounts of tepid water or saline.
4. Enhanced elimination. There is no role for dialysis or other enhanced elimination procedures.