Registration Dossier
Registration Dossier
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EC number: 258-054-8 | CAS number: 52628-25-8
Endpoint summary
Administrative data
Link to relevant study record(s)
Description of key information
Key value for chemical safety assessment
Additional information
Ammonium:
In aqueous environments, such as the body the ammonium chloride is completely dissociated into the ammonium (NH4 +) and the chloride (Cl-) ions. The ammonium cation is not an essential ion, but a toxic waste product from animal metabolism that is re-used in protein synthesis via glutamate. Depending on the animal species, ammonium will be directly excreted to the environment or it will first be converted to urea, which is less toxic and can be stored more efficiently. Ammonium does not exist in the blood in relevant amounts unless in case of liver failure. The chloride ion is needed for metabolisms in the human body and it also helps to keep the acid-base balance of the body. It also has several physiological roles in the central nervous system and biological transport protein. The amount of chloride is controlled by the kidneys. The EPA Secondary Drinking Water Regulations recommend a maximum concentration of 250 mg/1 for chloride ions.
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.
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 teh mobilisation of edema fluid.
Based on the above data, the oral absorption is set at 100%. However, based on low MW (53.46), high water solubility, and assumed low logPow a low dermal absorption is expected. In addition, the ion formation of the substance inmediately when in contact with a fluid decreases the absorption too.Therefore, 10% dermal absorption is taken, and 100% (default) inhalation absorption.
Zinc:
In aqueous environments, such as the body the ammonium chloride is completely dissociated into the ammonium (NH4 +) and the chloride (Cl-) ions. The ammonium cation is not an essential ion, but a toxic waste product from animal metabolism that is re-used in protein synthesis via glutamate. Depending on the animal species, ammonium will be directly excreted to the environment or it will first be converted to urea, which is less toxic and can be stored more efficiently. Ammonium does not exist in the blood in relevant amounts unless in case of liver failure. The chloride ion is needed for metabolisms in the human body and it also helps to keep the acid-base balance of the body. It also has several physiological roles in the central nervous system and biological transport protein. The amount of chloride is controlled by the kidneys. The EPA Secondary Drinking Water Regulations recommend a maximum concentration of 250 mg/1 for chloride ions.
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.
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 teh mobilisation of edema fluid.
Based on the above data, the oral absorption is set at 100%. However, based on low MW (53.46), high water solubility, and assumed low logPow a low dermal absorption is expected. In addition, the ion formation of the substance inmediately when in contact with a fluid decreases the absorption too.Therefore, 10% dermal absorption is taken, and 100% (default) inhalation absorption.
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