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ACUTE EXPOSURE INFORMATION
- USES: Nickel carbonyl is a nickel compound used as a chemical reagent that is toxic by inhalation. It is an intermediate in nickel refining. Exposure often occurs to vapor or gas. It is used as a catalyst or reagent in organic synthesis and chemical manufacture, used in glass plating, a chemical intermediate for the manufacture and refining of high purity nickel (Mond process), and used for vapor plating in other metallurgical and electronic industries. It is also used in continuous nickel coatings on steel and other metals.
- TOXICOLOGY: Nickel carbonyl is an extremely toxic gas which can produce significant but delayed effects. Most poisonings involve inhalation with or without dermal exposure. Animal studies have found that the pulmonary parenchyma is the target tissue for nickel carbonyl toxicity regardless of route of exposure. Type I alveolar cells are principally affected, but type II alveolar cells are also damaged as a direct effect of nickel carbonyl. The cause of most deaths has been attributed chiefly to impaired gas exchange in the lungs secondary to the parenchymal tissue damage. Nickel carbonyl inhibits numerous enzyme activities and disrupts other pathways involved in RNA synthesis.
- EPIDEMIOLOGY: Exposure are rare, but fatalities have been reported following inadvertent exposures.
- WITH POISONING/EXPOSURE
- MILD EXPOSURE: INHALATION: Chronic low dose inhalational exposure can result in asthma. Diffuse pulmonary infiltrates or fibrosis can be seen on chest radiograph. DERMAL: Contact of the liquid with the skin may produce adverse effects. There is little information concerning dermal exposure in the absence of inhalational exposure; it is unknown if systemic effects might develop. OCULAR: Severe irritation or damage to the eyes can occur from vapor exposure. INGESTION: Although ingestion reportedly may result in toxicity, no cases of ingestion have been found and ingestion is highly unlikely.
- SEVERE EXPOSURE: INHALATION: Nickel carbonyl is a severe pulmonary irritant which is rapidly absorbed following inhalation. Immediate effects include nausea, vomiting, abdominal pain, headache, dizziness, blurred vision, weakness, paresthesias, chest tightness, cough and chest pain. These effects usually subside once the victim is in fresh air, although more severe effects may develop over the next few days. Delayed effects generally occur 12 to 36 hours postexposure in patients with severe poisoning, but may be delayed longer to as long as 5 or more days after exposure and can include weakness, myalgias, fatigue, cough, dyspnea, sore throat, fever, tachypnea, hoarseness, cyanosis, hypoxemia, gastrointestinal disturbances and pneumonitis. In severe cases, delirium, CNS depression, seizures, transaminitis, acute lung injury and seizures may develop. Toxic myocarditis and dysrhythmias occasionally occur. EEG abnormalities have been reported in nickel carbonyl workers. Late changes involve pulmonary edema and interstitial fibrosis. Severe irritation or damage to the eyes can occur from exposure. In fatal exposures, death has occurred within 3 to 13 days of exposure. Recovery from acute exposure may require several months.
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