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Ammonia – When Something Smells Wrong

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Ammonia – When Something Smells Wrong Toxic Chemical Compounds Ammonia – When Something Smells Wrong Igor Makarovsky MSc1, Gal Markel PhD MD1,2, Tsvika Dushnitsky MD1 and Arik Eisenkraft MD1,3 1CBRN Medicine Branch, Medical Corps, Israel Defense Force, Israel 2Sheba Cancer Research Center and 3Safra Children's Hospital, Sheba Medical Center, Tel Hashomer, Israel Key words: ammonia, inhalational exposure, terror, frostbite, health effects IMAJ 2008;10:537–543 Ammonia (NH3, anhydrous ammonia) is one of the most abun- equipment against chemical weapons and were not affected. dant toxic chemicals. As such, it has the potential to be involved Although the toxic cloud could potentially have harmed civilians in a variety of toxicological mass events (e.g., industrial and in the center of the city, there is no record of injury. transportation accidents, water poisoning, terror attacks, bombing In this review we describe the clinical effects following ex- of industrial areas). Since a toxicological mass event is usually posure to ammonia and the appropriate treatment needed. In unpredictable, adequate preparedness is of utmost importance. addition, we review past events of massive ammonia releases Part of such preparedness is conveying information and knowl- from manufacturing facilities, highlighting the risk of chemical edge to clinicians, which is the objective of this review. terrorism [6]. Ammonia is the third most abundantly produced chemical in the world and is considered to be a Toxic Industrial Compound. Nowadays ammonia is used as a fertilizer, a precursor for other Ammonia is a gas with a urine-like odor fertilizers (i.e., urea, ammonium nitrate, etc.), explosives, as a chemical intermediate in the synthesis of other chemicals (such widely used for industrial purposes. Its as acrylonitrile), and in other industrial processes, including odor threshold is sufficiently low to acutely metallurgy, pulp and paper production, and refrigeration [1]. provide adequate warning of its presence. In previous centuries its carbonate salt [(NH4)2CO3.H2O] was used as a smelling salt and even today it is occasionally used in the boxing ring when boxers are knocked down unconscious. Smelling salts are a less common source of household ammonia Chemical and toxicological properties products. Often in capsule form, smelling salts, which contain Ammonia is a stable colorless gas at room temperature and approximately 20% ammonia, release a pungent odor upon break- is lighter than air. An ammonia cloud, on the other hand, has ing [2]. a white opaque appearance. It liquefies to a colorless fluid at The large-scale production of ammonia requires large storage -33ºC, or under at least 10 bar pressure. Ammonia gas is highly facilities, usually under pressure. The location of these tanks soluble in water, forming ammonium hydroxide (NH4OH). It is in an urban area is a potential strategic weak point as large a strong alkaline with high corrosive properties. The unique amounts of ammonia could be released as the result of a natural pungent odor of ammonia usually provides adequate warning of disaster, equipment failure, or accidental or intentional release. its presence [7]. Ammonia is usually considered a non-flammable This toxic chemical is transported throughout Israel or other gas, but in exceptional conditions it may become flammable, industrialized countries in big containers or trains that are prone exert noxious ammonia vapors and may even explode within a to accidents [3]. Thus, theoretically, it may be easily utilized by certain range of air concentrations (16–25%) [8]. terrorists to harm densely populated urban areas either through Ammonia is toxic to humans in all exposure scenarios. Its polluting the air, water reservoir poisoning or by other means odor threshold is sufficiently low to acutely provide adequate [4-6]. warning of its presence with an odor threshold of 5 ppm. Irritant gases have been used as chemical weapons. The However, ammonia causes olfactory fatigue or adaptation, making Russian military accused Chechen rebels of detonating bombs its presence difficult to detect when exposure is prolonged. Thus containing chlorine and ammonia in Grozny. The rebels had set the odor threshold may extend up to 53 ppm, according to the off several of these bombs during the night and early morning Agency for Toxic Substances and Disease Registry [9,10]. The near Russian positions, but the wind had blown the green cloud over the center of Grozny. The Russian troops had protective ppm = parts per million • Vol 10 • July 2008 Ammonia 537 Toxic Chemical Compounds Table 1. Summary of acute exposure guideline levels (AEGL) for by granular tissue, which may be one of the causes of chronic ammonia (in ppm)* lung disease following ammonia inhalation injury [2,14]. Classification 5 min 30 min 60 min 4 hrs 8 hrs Endpoint Liquid anhydrous ammonia (-33°C) freezes tissue on contact. AEGL 1 25 25 25 25 25 Odor It is known that critical skin damage begins at -4°C and becomes (ppm) irreversible at -20°C. Nevertheless, the degree of tissue injury is AEGL 2 380 160 110 110 110 Severe eye irritation, proportional to the duration and concentration of exposure [2]. (ppm) nasopharyngeal irritation Absorbed ammonia is well distributed throughout body AEGL 3 3,800 1,600 1,100 550 390 LC01 (in mice)* compartments and reacts with hydrogen ions, depending on (ppm) the pH of the compartment to produce the ammonium ions. * Ref. 35 These are endogenously produced in the gut from the bacterial LC01 = lethal concentration or lethality threshold breakdown of nitrogenous constituents of food. Almost all of this endogenous ammonium (approximately 99% of the 4 g produced daily) is absorbed by passive diffusion from the intestinal tract reported range of the ammonia odor threshold corresponds to before entering the hepatic portal vein [9,13]. In the liver, am- the range of occupational standards and guidelines for prolonged monium ions are extensively metabolized to urea and glutamine. exposure to ammonia. The American Conference of Governmental Consequently, levels of ammonia that reach the circulation are Industrial Hygienists has set an 8 hour exposure limit of 25 ppm low [9,13]. Moreover, hepatic insufficiency could affect ammonium and a short-term exposure limit (15 minutes) of 35 ppm for ion metabolism. ammonia in the workplace [11]. The U.S. National Institute for Ammonia reaching the circulation is excreted by humans as Occupational Safety and Health recommends that the level in urinary urea [9,13]. Small amounts of ammonia are excreted workroom air be limited to 50 ppm for 5 minutes of exposure via the urine; the average daily excretion for humans is ap- [9]. Table 1 summarizes the Acute Exposure Guideline Levels proximately 2–3 μg, about 0.01% of the total body burden. Small (AEGL) for inhaled ammonia at various concentrations set by the amounts of unabsorbed ammonia may also be excreted from the American Environmental Protection Agency. The drinking water gastrointestinal tract in the feces [9,13]. quality guideline is 0.5 mg/L as NH4+ [12]. Ammonia is not considered to be carcinogenic or teratogenic [13]. Mechanism of toxicity and pharmacology The major clinical effects include Ammonia is extremely soluble in water and dissolves in the mucus fluid covering the mucous lining of the respiratory system irritation symptoms of the eyes and to produce ammonium hydroxide, a strong base. The reaction is the respiratory tract, as well as exothermic in nature and may inflict significant thermal injury corrosive injuries to the skin and mucous [2]. membranes. Hypoxia and respiratory NH4OH causes severe alkaline chemical burns to the skin, eyes, and especially the respiratory system. Mild exposure primar- failure are common and require ily affects the upper respiratory tract, while more severe exposure prompt intervention tends to affect the entire respiratory system. The gastrointestinal tract may also be affected if ammonia is ingested [2]. Tissue damage from such bases is caused by liquefaction necrosis and penetrates far deeper than that caused by an equipotent acid. In the case of ammonium hydroxide, the tissue Health effects breakdown liberates water, thus bringing about the conversion of Ammonia is readily absorbed through mucous membranes, ammonia to ammonium hydroxide. In the respiratory tract, this especially of the gastrointestinal tract [13]. Although ammonia results in the destruction of cilia and the mucosal barrier, leading rapidly enters the eye, systemic absorption is considered not to to infection. Moreover, secretions, sloughed epithelium, cellular be quantitatively significant [13]. Nevertheless, its main route to debris, edema, and reactive smooth muscle contractions cause damage is through the respiratory system. There are hardly any significant airway obstruction. Airway epithelium can regain bar- systemic toxicity findings following acute skin exposure [9]. rier integrity within 6 hours after exposure if the basal cell layer Damage to the respiratory system, the skin or other organs remains intact. However, damaged epithelium is often replaced that come in contact with ammonia is proportional to depth of inhalation or direct contact, duration of exposure, concentration AEGL 1 = a level at or above which the general population (including and pH of the gas or liquid. Following a short-term inhalation susceptible individuals) may have some discomfort. exposure, ammonia is almost entirely retained in the upper AEGL 2 = a level at or above which the above-mentioned population may experience long-lasting
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