ACGIH: TWA 10 mg/m3; STEL 20 mg/m3NIOSH: TWA 10 mg/m3; STEL 20 mg/m3
物理描述:
Ammonium chloride is a white crystalline solid. It is soluble in water(37%). The primary hazard is the threat posed to the environment. Immediate steps should be taken to limit its spread to the environment. It is used to make other ammonium compounds, as a soldering flux, as a fertilizer, and for many other uses.
颜色/状态:
Colorless crystals or crystalline masses, or white, granular powder
气味:
Odorless
味道:
Cooling, saline
蒸汽压力:
1 Pa at 91 °C (solid); 10 Pa at 121 °C (solid); 100 Pa at 159 °C (solid); 1kPa at 204.7 °C (solid); 10 kPa at 263.1 °C (solid); 100 kPa at 339.5 °C (solid)
When ammonium ion is converted to urea, liberated hydrogen ion reacts with bicarbonate and other body buffers ... chloride ion displaces bicarbonate ion; latter is converted to carbon dioxide ... chloride load to kidneys is increased and appreciable amount escapes reabsorption along with equivalent amount of cation ... and isoosmotic quantity of water.
The toxicity of ammonium chloride depends on the ammonia which enters the living organism and hence the cell. This substance is readily absorbed by the gastrointestinal tract, and utilized in the liver to form amino acids and proteins. When ammonium ions are converted to urea, liberated hydrogen ion reacts with bicarbonate ion to form water and carbon dioxide. The chloride ion displaces the bicarbonate ion. Chloride is loaded into the kidneys. The increased chloride concentration in the extracellular fluid produces an increased load to the renal tubules. Increase excretion of electrolytes and water causes loss of extracellular fluid and promotes the mobilization of edema fluid.
Male Sprague-Dawley rats gavaged with 1000 umol (15)N ammonium chloride each day for 5 days were found to excrete low, but significant amounts of excess (15)N nitrate in their urines on the five days of treatment and on the five subsequent days. A total of 0.28 + or - 0.03 umol excess (15)N nitrate (mean + or - SE) per rat was recovered which indicates that ammonia is converted to nitrate in a yield of approximately 0.0080%.
IDENTIFICATION AND USE: Ammonium chloride is a white, fine or coarse, crystalline powder. it is a good fertilizer for important crops in rainy climates, particularly for rice. It is not registered for current use in the U.S., but approved pesticide uses may change periodically and so federal, state and local authorities must be consulted for currently approved uses. Ammonium chloride is used also as a flux in zinc and tin plating; electroplating, electrolytic refining of zinc; etching solutions in manufacture of printed circuit boards; in dry and Leclanche batteries; manufacturing of explosives; flame suppressant; hardener for formaldehyde-based adhesives; mordant for dyes and printing. It is used as medication particularly in diuretics, expectorants. HUMAN EXPOSURE AND TOXICITY: Potential symptoms of overexposure to fumes are irritation of eyes, skin, and respiratory system; cough, dyspnea, pulmonary sensitization. Large doses of ammonium chloride may cause metabolic acidosis secondary to hyperchloremia, especially in patients with impaired renal function. Other adverse effects of excessive ammonium chloride dosage include rash, headache, hyperventilation, bradycardia, progressive drowsiness, mental confusion, and phases of excitement alternating with coma. Calcium-deficient tetany, hyperglycemia, glycosuria, twitching, hyperreflexia, and EEG abnormalities have also been reported. Most of these adverse effects are secondary to ammonia toxicity resulting from inability of the liver to convert the ammonium ion to urea. Because rapid IV injection may increase the likelihood of ammonia toxicity, IV infusions of ammonium chloride should be administered slowly to permit metabolism of ammonium ions by the liver. Patients receiving ammonium chloride should be closely monitored for signs and symptoms of ammonia toxicity such as pallor, sweating, irregular breathing, vomiting, bradycardia, cardiac arrhythmias, local or generalized twitching, asterixis, tonic seizures, and coma. ANIMAL STUDIES: Acute exposure in mice by intravenous administration resulted in hyperventilation and clonic movements which were followed sometimes by tonic extensor convulsions, but usually by profound coma; death was preceded by convulsions, but survivors made complete and rapid recovery. This syndrome was potentiated by short periods of hypoxia. In rabbits, replacement of aq. humor with 1% solution of ammonium chloride has caused considerable hyperemia of iris, but by next day eyes were almost normal, and in another day were completely recovered. The ingestion of ammonium chloride in doses of around 500-1000 mg/kg bw/day, for periods ranging from 1 to 8 days, has induced metabolic acidosis in mice, guinea-pigs, rats, rabbits, and dog. Pulmonary edema, central nervous system dysfunction, and renal changes are reported to have occurred after ingestion of ammonium chloride. Ammonium chloride is reported to cause alterations in calcium and bone metabolism in various species. Specific toxic effects on the kidneys as renal hypertrophy were found in rats receiving ammonium chloride in the diet. Other salts (ammonium citrate or sodium chloride) did not induce such effects. Rabbits showed cellular swelling and karyolysis of kidney tubulus cells after two daily oral administrations of 16.2 g/animal ammonium chloride. One-sixth molar ammonium chloride was given to mice orally in the drinking water after day 7 during pregnancy and although the offspring were small sized no congenital defects were found. In other study mice were given 600 mg/kg orally at 8 and 10 am and 12 and 1 pm on day 10 of gestation and produced 7% ectrodactyly in the offspring. Negative in the Ames test using Salmonella typhimurium TA 98, TA 100, TA 1535, TA 1537, TA 1538 at doses with and without metabolic activation. Negative in the Ames test using Escherichia coli WP2uvrA with and without metabolic activation. ECOTOXICITY STUDIES: Four simultaneous early life-stage ammonia tests with small mouth bass were carried out at 4 different pH levels ranging from 6.6 to 8.7. Exposure to ammonium chloride solutions began on 2 to 3-day old embryos and lasted for 32 days. Concentrations found to retard growth ranged from 0.056 mg/L at pH 6.60 to 0.865 mg/L at pH 8.68. Groups of 180 Coho salmon were exposed to ammonium chloride at concentrations of 0.019-0.33 mg/L for 91 days. In high dose animals the hemoglobin content and hematocrit was significantly reduced and the percentage of immature erythrocytes in blood was increased. The key species, the earthworm Eisenia fetida, was subjected to a series of tests in solid phase mesocosms and full-scale units. The solid phase tests showed a relatively low toxicity to ammonium with ammonium chloride having an LC50 for ammonium of 1.49 g/kg.
参考文献:M Chen, V Vijay, Q Shi, Z Liu, H Fang, W Tong. 用于研究药物诱导肝损伤的FDA批准药物标签,药物发现今日,16(15-16):697-703, 2011. PMID:21624500 DOI:10.1016/j.drudis.2011.05.007
M Chen, A Suzuki, S Thakkar, K Yu, C Hu, W Tong. DILIrank:按在人类中发展药物诱导肝损伤风险排名的最大参考药物清单。药物发现今日2016, 21(4): 648-653. PMID:26948801 DOI:10.1016/j.drudis.2016.02.015
References:M Chen, V Vijay, Q Shi, Z Liu, H Fang, W Tong. FDA-Approved Drug Labeling for the Study of Drug-Induced Liver Injury, Drug Discovery Today, 16(15-16):697-703, 2011. PMID:21624500 DOI:10.1016/j.drudis.2011.05.007
M Chen, A Suzuki, S Thakkar, K Yu, C Hu, W Tong. DILIrank: the largest reference drug list ranked by the risk for developing drug-induced liver injury in humans. Drug Discov Today 2016, 21(4): 648-653. PMID:26948801 DOI:10.1016/j.drudis.2016.02.015
Completely absorbed within 3–6 h. In healthy persons, absorption of ammonium chloride given by mouth was practically complete. Only 1 to 3% of the dose was recovered in the feces.
From human incidentally exposures it was learnt that following oral administration, ammonium chloride is rapidly absorbed from the GI tract, complete absorption occurring within 3 -6 hours. Only 1 -3% of the dose was recovered in the feces. Substantial first pass metabolism occurs in the liver. For animals, after repeated oral administration, ammonium chloride enters readily the body and main targets for its toxicity are kidneys.