Ammonia Toxicity

http://emedicine.medscape.com/article/820298-overview#a0101

Ammonia Toxicity
Author: Steven Issley, MD, FRCPC; Chief Editor: Asim Tarabar, MD more... Updated: Jun 27, 2011

Background
At room temperature, ammonia (NH3) is a highly water-soluble, colorless, irritant gas with a unique pungent odor. Ammonia has a boiling point of -33C and an ignition temperature of 650C. 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 Freon largely has 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 by time-weighted average (TWA), short-term exposure limit (STEL), and concentration at which toxic gasses 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. Similarly, the STEL is the concentration to 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 ppm, an STEL of 35 ppm, and an IDLH of 500 ppm. Although injury from ammonia most commonly is caused by inhalation, it also may follow ingestion or direct contact with eyes or skin. The clinical presentations of these injuries and their investigation and treatment are discussed in this article; chloramine gas inhalation injury also is discussed.

Pathophysiology
The most common mechanism by which ammonia gas causes damage occurs when anhydrous ammonia (liquid or gas) reacts with tissue water to form the strongly alkaline solution, ammonium hydroxide. 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 Clinical). 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 mucosal 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 following exposure if the basal cell layer remains intact. However, damaged epithelium often is replaced by granular tissue, which may be one of the etiologies leading to chronic lung disease following ammonia inhalation injury.

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Ammonia Toxicity

http://emedicine.medscape.com/article/820298-overview#a0101

Liquid anhydrous ammonia (-33C) freezes tissue on contact. To put this in perspective, critical skin damage begins at -4C and becomes irreversible at -20C. 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. Ammonia is a product of protein catabolism and is metabolized by the liver. Normal blood ammonia levels range from 10-40 mol/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.

Epidemiology
Frequency
United States The 2009 Annual Report of the American Association of Poison Control Centers' National Poison Data System reported 2570 single exposures of ammonia. Of these, 97% were unintentional.[1] Similar to previous years, in 2002, US poison control centers reported nearly 6000 cases of toxic ammonia exposure.[2] Of exposures, 93% were unintentional, and 11% resulted in moderate to severe outcomes. Of note, in cases of household exposure, only 5% were moderate to severe.

Mortality/Morbidity
The 2009 Annual Report of the American Association of Poison Control Centers' National Poison Data System reported 3 deaths due to ammonia exposure.[1]

Age
According to the 2009 Annual Report of the American Association of Poison Control Centers' National Poison Data System, 976 exposures occurred in those younger than 6 years, 437 exposures occurred in those aged 6-19 years, and 1710 exposures occurred in those older than 19 years.[1] 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.

Contributor Information and Disclosures

Author Steven Issley, MD, FRCPC Attending Physician, Trauma Team Leader, Department of Emergency Medicine, Hotel Dieu Grace Hospital Disclosure: Nothing to disclose. Coauthor(s) 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, Canadian Association of Emergency Physicians, and Society for Academic Emergency Medicine Disclosure: Nothing to disclose. Specialty Editor Board

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Ammonia Toxicity

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Edmond A Hooker II, MD, DrPH, FAAEM 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. 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. John D Halamka, MD, MS Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine 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.

References
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