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Brief Communication |
Correspondence: 1Corresponding Author: Scott D Fitzgerald, Diagnostic Center for Population and Animal Health, 4125 Beaumont Road, Lansing, MI 48910-8104
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Abstract |
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 TOPSources and manufacturers Abstract References |
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Key Words: Anhydrous ammonia • cattle • intoxication • pathology • pneumonia
Anhydrous ammonia (AA) is a common, inexpensive chemical widely used as a nitrogen fertilizer and a refrigerant. The petroleum industry uses AA in neutralizing acid constituents of crude oil. It has also become widely used in the illegal manufacture of methamphetamine, and this use has resulted in an increase in illegal activities to obtain AA including theft from on-farm storage facilities. Anhydrous ammonia is a gas, which is stored in large tanks under conditions of high pressure and low temperature (–33°C) to keep it in its liquid phase.9 Whereas farmers and fertilizer applicators undergo specialized training in the safe handling of AA and the use of proper personal protective equipment, most illegal drug manufacturers do not. When storage tank valves are damaged or left open after illicit access the AA is released in its gaseous phase, forming colorless to white vapor clouds with a sharp penetrating odor.6,9 If AA comes into contact with animal mucous membranes the AA combines rapidly with water to form highly caustic ammonium hydroxide, resulting in liquefactive necrosis of contacted tissues.8 There are only a handful of published reports detailing the effects of AA on animals6; in this report a recent incident occurring on a cattle feedlot is described.
Multiple 2-ton AA transport tanks were parked adjacent to a barn containing approximately 260 feeder cattle. The barn was enclosed on 3 sides, with a feeding alley along the open fourth side. One night in May 2005, thieves broke into one of the tanks to obtain AA for the illegal manufacture of methamphetamine. The valve was left open through the night, and the next morning 12 Holstein-cross feeder cattle were found dead, with dozens more exhibiting blindness, recumbency, or labored respiration. During the next few days 64 cattle died or had to be euthanatized because of AA exposure, and several dozen more were left blind, inappetent, or with respiratory symptoms including deep labored breathing, coughing, and ocular-nasal discharge.7
Two 16-month-old Holstein-cross feeder cattle were submitted to the Diagnostic Center for Population and Animal Health at Michigan State University 3 days after initial exposure to the AA gas. Both cattle were clinically blind, had lost significant weight, and were exhibiting labored breathing. Both cattle had bilateral corneal ulcerations, 2–3 cm in diameter (Fig. 1). On necropsy, both cattle had fibrinonecrotic membranes affecting the proximal half of the nasal septum/nasal turbinates (Fig. 2). One animal had multiple hemorrhagic bullae up to 6 cm in diameter within its nasal sinuses. Both cattle had petechial hemorrhages throughout the pharyngeal and tracheal mucosa, and one animal had bilateral 2 x 3 cm erosions of the mucosa over the arytenoid cartilage in its larynx. Both cattle had bilateral congestion and consolidation affecting 20–30% of their cranioventral lung lobes (Fig. 3).
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Postmortem samples of plasma, cerebrospinal fluid, and vitreous humor were collected from each animal, stored at 4°C, and analyzed 24 hours later for ammonium concentrations using an automated chemistry analyzera and a standard commercial enzymatic assayb based on the conversion of NH+4 and 2-oxoglutamate to glutamate by glutamate dehydrogenase. Samples of all 3 fluids from affected and reference cattle are presented in Table 1. Because samples were not kept on ice and tested within 2–4 hours as is generally recommended, samples from 9 reference cattle were collected and processed similarly for comparison. All values from the affected cattle were within the intervals spanned by the reference individuals. These reference intervals are quite broad, likely because of the variable effects of sample age on ammonium concentration. With increasing sample age, some ammonia gas may escape the sample, but ammonium concentrations typically rise because of the generation of ammonium from cell metabolism and from the degradation of labile proteins and amino acids.1,10 The magnitude of increase is expected to vary with the state of the individual, sample cellularity, temperature, and time.
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When AA gas comes into contact with the mucous membranes of humans or animals it rapidly combines with water to form the corrosive and alkaline chemical ammonium hydroxide.8 Humans exposure to AA has been reported to result in a variety of signs depending on the tissue contacted.4,11 Dermal exposure produces erythema to full thickness dermal burns. Eye exposure may result in conjunctivitis, lacrimation, corneal irritation and ulceration, and temporary or permanent blindness. Respiratory exposure can lead to bronchospasm, laryngitis, tracheitis, dyspnea, chest pain, and burns to the respiratory mucosa. Treatment of exposed people requires rapid and aggressive irrigation to remove the caustic chemical and reduce the severity of resultant burns.3,11 These cattle did not develop grossly visible skin burns, but the corneal ulcers and upper respiratory lesions are similar to those reported in humans with ammonia burns. Because the exposure occurred during the night, these cattle were exposed to the vapor cloud for several hours and primary irrigation therapy was not instituted. Instead, the valve was repaired and closed to prevent further AA leakage, and all barn doors were opened to maximize ventilation of the barn to decrease further animal exposure until the vapor cloud dissipated.
Secondary bacterial pneumonia likely contributed to the pulmonary lesions and mortality in these cases. Because the upper respiratory system suffered deciliation and erosions, the protective effects of the mucociliary apparatus were likely compromised. Furthermore, the suppurative nature of the pulmonary exudates supports the presence of a bacterial infection, although bacterial culture from the lung tissue was not attempted. Although specific morphologic lesions were not found in either animal's brains, recent experimental studies have shown neurotoxicity caused by excessive activation of N-methyl-D-aspartate receptors occurs in laboratory animals dying of acute ammonia toxicity.2,5 Some of the acute mortality in these cattle may likely have been associated with neurotoxicity and other metabolic derangements.
Anhydrous ammonia induces skin burns and respiratory disease as severe sequelae in both human and animal cases.3,4,8 Although relatively few animal cases have been reported in the veterinary literature, it is likely that more cases of this type will be encountered because of the highly profitable market for illegal methamphetamine drugs. Anhydrous ammonia theft is reaching epidemic levels in some farming communities.7 Although farmers are instructed to store AA storage tanks near their homes to deter thieves, many farmers locate these storage tanks near outbuildings in case of leaks resulting in toxic AA gas release. Often these outbuildings also serve as animal housing units. Whereas some facilities using AA storage tanks have invested in high-tech security camera systems, others have simply stopped using AA as a nitrogen fertilizer. A recently developed deterrent is the addition of a commercial substancec that can be added to AA for a relatively small fee. This additive results in everything that comes in contact with the AA being stained a bright pink color. In addition, when the AA is used for methamphetamine production, the resulting product is a gummy pink substance, rather than the fine white powder its manufacturers and users prefer.7 This pink residue is less concentrated, harder to smoke, and much more difficult to sell than the desired white powder.
This case illustrates the clinical, gross, and histologic effects of AA gas exposure on cattle. This particular producer lost nearly 25% of his feedlot cattle to a relatively minor AA gas leak that only lasted a few hours; many additional animals had long-term visual and respiratory effects that resulted in poor growth and production losses. Furthermore, the potential for farm animal exposure is becoming more likely because of the widespread illegal use of this common fertilizer for the production of methamphetamine. It is hoped that this case report will aid diagnosticians in their recognition of this condition, but also might point out the dangers involved in using AA on animal production facilities and also offer a suggestion for an additive that would decrease the likelihood of their farm being targeted for AA thievery.
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Sources and manufacturers |
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a. Olympus AU640; Olympus Corporation, Irvine, TX.
b. Raichem Ammonia Kit; Raichem, Division of Hemagen Diagnostics, San Diego, CA.
c. GloTell; Royster-Clark, Norfolk, VA.
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