| Regulatorische Informationen | Chemical: Zinc cyanide (Zn(CN)2)Zinc cyanide: HSNO Approval: HSR006723 Approved with controls |
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| Weitere Sicherheitsinformationen | IMAP assessments - Zinc cyanide (Zn(CN)2): Human health tier I assessment |
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| CSL Reaction Information | CSL00046N,N-DIMETHYLFORMAMIDE + 2-CHLORO-5-FLUOROPYRIMIDINE + ZINC CYANIDEViolent thermal exotherm at >100oCHarmful,ToxicHeteroaryl chlorideCyanation |
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| Minimum Risk Level | Intermediate Oral: 0.3 mg/kg/day (L134)
Chronic Oral: 0.3 mg/kg/day (L134) |
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| Treatment | Zinc poisoning is treated symptomatically, often by administering fluids such as water or milk, or with gastric lavage. Antidotes to cyanide poisoning include hydroxocobalamin and sodium nitrite, which release the cyanide from the cytochrome system, and rhodanase, which is an enzyme occurring naturally in mammals that combines serum cyanide with thiosulfate, producing comparatively harmless thiocyanate. Oxygen therapy can also be administered. (L49, L97) |
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| Gesundheitliche Auswirkungen | Chronic exposure to zinc causes anemia, atazia, lethargy, and decreases the level of good cholesterol in the body. It is also believed to cause pancreatic and reproductive damage. Exposure to high levels of cyanide for a short time harms the brain and heart and can even cause coma, seizures, apnea, cardiac arrest and death. Chronic inhalation of cyanide causes breathing difficulties, chest pain, vomiting, blood changes, headaches, and enlargement of the thyroid gland. Skin contact with cyanide salts can irritate and produce sores. (L49, L96, L97) |
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| Expositionspfade | Inhalation (L96)oral (L96)dermal (L96) |
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| Toxizitätsübersicht | Anaemia results from the excessive absorption of zinc suppressing copper and iron absorption, most likely through competitive binding of intestinal mucosal cells. Unbalanced levels of copper and zinc binding to Cu,Zn-superoxide dismutase has been linked to amyotrophic lateral sclerosis (ALS). Stomach acid dissolves metallic zinc to give corrosive zinc chloride, which can cause damage to the stomach lining. Metal fume fever is thought to be an immune response to inhaled zinc. Organic nitriles decompose into cyanide ions both in vivo and in vitro. Consequently the primary mechanism of toxicity for organic nitriles is their production of toxic cyanide ions or hydrogen cyanide. Cyanide is an inhibitor of cytochrome c oxidase in the fourth complex of the electron transport chain (found in the membrane of the mitochondria of eukaryotic cells). It complexes with the ferric iron atom in this enzyme. The binding of cyanide to this cytochrome prevents transport of electrons from cytochrome c oxidase to oxygen. As a result, the electron transport chain is disrupted and the cell can no longer aerobically produce ATP for energy. Tissues that mainly depend on aerobic respiration, such as the central nervous system and the heart, are particularly affected. Cyanide is also known produce some of its toxic effects by binding to catalase, glutathione peroxidase, methemoglobin, hydroxocobalamin, phosphatase, tyrosinase, ascorbic acid oxidase, xanthine oxidase, succinic dehydrogenase, and Cu/Zn superoxide dismutase. Cyanide binds to the ferric ion of methemoglobin to form inactive cyanmethemoglobin. (L48, L49, A49, L97) |
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| Signs and Symptoms | Ingestion of large doses of zinc causes stomach cramps, nausea, and vomiting. Acute inhalation of large amounts of zinc causes metal fume fever, which is characterized by chills, fever, headache, weakness, dryness of the nose and throat, chest pain, and coughing. Dermal contact with zinc results in skin irritation. Cyanide poisoning is identified by rapid, deep breathing and shortness of breath, general weakness, giddiness, headaches, vertigo, confusion, convulsions/seizures and eventually loss of consciousness. (L49, L96, L97) |
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| Carcinogen Classification | No indication of carcinogenicity to humans (not listed by IARC). |
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