CAS RN: 7664-41-7

Toxicity Summary

IDENTIFICATION AND USE: Ammonia is a colorless gas or liquid. Ammonia is used in the production of ammonium sulfate and ammonium nitrate for fertilizers; and in the manufacture of nitric acid, soda, synthetic urea, synthetic fibers, dyes, and plastics. Ammonia, or dissociated ammonia, is used in such metal treating operations as nitriding, carbo-nitriding, bright annealing, furnace brazing, sintering, sodium hydride descaling, atomic hydrogen welding, and other applications where protective atmospheres are required. The petroleum industry utilizes anhydrous ammonia in neutralizing the acid constituents of crude oil and in protecting equipment such as bubble plate towers, heat exchangers, condensers, and storage tanks from corrosion. It is also used as medication. Ammonia in an aqueous environment exists in equilibrium between ionized ammonium cation and the non-ionized ammonia. This equilibrium can be affected by buffers, pH, temperature, and salinity. Thus, in many cases it is not possible to assign the associated toxicity to the ionized or non-ionized form of the ammonia-nitrogen. HUMAN EXPOSURE AND TOXICITY: Studies using low levels of ammonia show that inhaled ammonia is temporarily dissolved in the mucus of the upper respiratory tract, and then a high percentage of it is released back into the expired air. Following exposure to 500 ppm ammonia for 10-27 min, healthy male subjects eliminated 70-80% of the inspired ammonia by this route. Short term exposure: eye or skin contact with ammonia can cause irritation, burns, frostbite (anhydrous), and permanent damage. Irritates the respiratory tract causing coughing, wheezing, and shortness of breath. Higher exposure can cause pulmonary edema, a medical emergency, that can be delayed for several hours and is life-threatening. Exposure can cause headache, loss of sense of smell, nausea, and vomiting. Inhalation: nose and throat irritation have been reported at 72 ppm after 5 min exposure. Exposures of 500 ppm for 30 min have caused upper respiratory irritation, tearing, increased pulse rate, and blood pressure. Death has been reported after an exposure to 10,000 ppm for an unknown duration. Skin: Solutions of 2% ammonia can cause burns and blisters after 15 min of exposure. These burns may be slow to heal. Anhydrous ammonia may cause skin to freeze. Eyes: Levels of 70 ppm (gas) have caused eye irritation. If not flushed with water immediately, contact with eye may cause partial or complete blindness. Ingestion: ammonia will cause pain if swallowed and burning of the throat and stomach. May cause vomiting. One teaspoon of 28% aqua ammonia may cause death. Long term exposure: repeated exposure can cause chronic eye, nose, and throat irritation. Repeated lung irritation can result in bronchitis with coughing, shortness of breath, and phlegm. Analysis of blood samples from 22 workers exposed to ammonia in a fertilizer factory and 42 control workers not exposed to ammonia showed increased frequency of chromosomal aberrations (CAs) and sister chromatid exchanges (SCEs), increased mitotic index (MI), and increased frequency of CAs and SCEs with increasing length of exposure. ANIMAL STUDIES: Analysis of endogenous ammonia levels in the expired air of rats showed concentrations ranging from 10-353 ppb (mean = 78 ppb) in nose-breathing animals. The quantitative difference between inspired and expired ammonia suggests that small amounts are absorbed across the nasopharyngeal membranes into the systemic circulation. Absorbed ammonia is excreted by the kidneys as urea and urinary ammonium compounds, as urea in feces, and as components of sweat. Toxic levels do not develop as a result of chronic inhalation exposure because the body has multiple effective mechanisms for detoxifying and excreting it. Cardiovascular changes that may be analogous to those observed in humans have been observed in rabbits exposed to high concentrations of ammonia. Bradycardia was seen at 2,500 ppm, and hypertension and cardiac arrhythmias leading to cardiovascular collapse followed acute exposures to concentrations exceeding 5,000 ppm. Pathological correlates for these effects have not been demonstrated. Atrophy of pericardial fat has been observed in mice exposed to 4,000 ppm ammonia. Hepatic effects are usually not seen in animals exposed to ammonia gas. Liver necrosis has been observed following acute lethal exposure of mice to 3,440 ppm ammonia for 1 hour. Levels of 170 ppm of ammonia vapor caused mild changes in the spleens, kidneys, and livers of guinea pigs. Static exposures of cats and rabbits for 1 hr at 7000 mg/cu m resulted in the death of approx 50%. Postmortem exam showed severe effects on the upper respiratory tract. Less severe effects in the lower respiratory tract included damage to bronchioles and alveolar congestion, edema, atelectasis, hemorrhage, emphysema, and fluid. The search for the peripheral toxins responsible for the CNS impairment present in hepatic encephalopathy has shown that the administration of ammonia in normal rats reproduced behavioral and electrophysiological changes similar to those seen in galactosamine induced encephalopathy. No statistically significant differences were noted in ovarian or uterine weights of pigs exposed to about 7 or 35 ppm ammonia for 6 weeks. Female pigs that were continuously exposed to about 35 ppm ammonia from 6 weeks before breeding until day 30 of gestation had no statistically significant differences in age at puberty, number of live fetuses, or fetus-to-corpus luteum ratio compared to pigs exposed to only about 7 ppm. No unexposed controls were included in that study. No statistically significant difference in fetal length was evident at 30 days of gestation in offspring of pig dams that were continuously exposed to about 7 or 35 ppm ammonia from 6 weeks before breeding until day 30 of gestation. The mutagenicity of anhydrous ammonia was investigated in a Ames test in S. typhimurium TA98, TA100, TA1535, TA1537 and TA1538, and in E. coli WP2uvrA. The test method was modified appropriately to investigate a volatile test substance. Studies were performed in duplicate in the presence and absence of an exogenous metabolic activation system. No evidence of mutagenicity was seen under the conditions of this assay. ECOTOXICITY STUDIES: Ammonia is an environmental pollutant that is toxic to all aquatic animals. The major sources for atmospheric NH3 are agricultural activities and animal feedlot operations, followed by biomass burning (including forest fires) and to a lesser extent fossil fuel combustion. Close to its sources, acute exposures to NH3 can result in visible foliar injury on vegetation.
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