Nickel carbonyl

What is Nickel carbonyl

It is an organonikel compound with the formula Ni(CO)4. This colorless liquid is the main carbonyl of nickel. It is an intermediate in the Mond process for the production of very high purity nickel carbonyl online and a reagent in organometallic chemistry, although the Mond Process has fallen into disuse due to the health risks of working with the compound. Nickel carbonyl is one of the most dangerous substances ever found in nickel chemistry due to its very high toxicity combined with high volatility and rapid absorption through the skin.

What are the signs of nickel poisoning?

Symptoms

• Rash or bumps on the skin.
• Itching, which may be severe.
• Redness or changes in skin color.
• Dry patches of skin that may resemble a burn.
• Blisters and draining fluid in severe cases.

Nickel carbonyl poisoning is characterized by a two-stage illness. The first consists of headaches and chest pain lasting a few hours, usually followed by a short remission. The second phase is a chemical pneumonitis which starts after typically 16 hours with symptoms of cough, breathlessness and extreme fatigue.

Acute nickel carbonyl poisoning

Nickel carbonyl [Ni(CO)4], is formed when metallic nickel combines with carbon monoxide. It is used in the refining process of nickel and as a catalyst in petroleum, plastic, and rubber production. Nickel carbonyl is considered to be one of the most toxic chemicals used industrially and the magnitude of its morbidity and mortality has been compared to that of hydrogen cyanide. A 46-year-old man presented to the emergency department 24 hours after accidental occupational exposure to nickel carbonyl. He admitted to dermal contamination and inhaling the vapor from his clothing after his respiratory protection was removed. On presentation the patient was alert and oriented, complained of shortness of breath, chest tightness, and paresthesias. Examination revealed decreased breath sounds bilaterally and arterial blood gas PO2 of 39% with calculated O2 saturation of 75%. After face mask O2 at 60% his PO2 increased to 85%. The patient required 60% O2 with continuous positive airway pressure of 5 for 4 days. Disulfiram (Antabuse) was administered for the first 2 days until sodium diethyldithiocarbamate (dithiocarb) was obtained. Disulfiram was used because it is metabolized to two molecules of dithiocarb and is hypothetically of value. Dithiocarb was obtained and continued over the next several days. The patient’s urine nickel level on the day of admission was 172 micrograms/dL (normal < 5 micrograms/dL) and a serum level of 14.6 micrograms/dL (normal .26-.46 micrograms/dL). The patient’s condition gradually improved over the next 10 days. Nickel carbonyl exposure produces mild transient initial symptoms which are followed within 24 hours by more severe life-threatening events.

Death occurs due to pulmonary and cerebral edema. Treatment with sodium diethyldithiocarbamate was not effective, perhaps due to the severity of exposure and the short interval between administration of the medication and death.

Nickel carbonyl, formed by the reaction of carbon monoxide with metallic nickel, is used in nickel refining, in the synthesis of acrylic and methacrylic esters, and for other organic synthesis. In air, nickel carbonyl rapidly decomposes to metallic nickel and carbon monoxide with a 50% decomposition at room temperature and total decomposition at 150-200 C. Its decomposition is inversely proportional to the concentration of carbon monoxide; in the absence of carbon monoxide, decomposition may occur in approximately 1 min. Thus, potential exposure to the parent nickel carbonyl is limited by its rapid conversion to airborne metallic nickel.

Human data are limited to case reports, primarily of nickel workers, that affirm the extreme toxicity of the compound. Definitive exposure terms are lacking in these reports. Available information suggests that there are very limited or no warning properties associated with exposure to nickel carbonyl. Significant signs and symptoms of toxicity are known to occur in the absence of recognizable odor. Human case studies have shown that a latency period often occurs between initial signs of toxicity and subsequent serious effects that may progress to death. The primary target of nickel carbonyl-induced acute toxicity appears to be the lungs, although extra pulmonary involvement also has been reported. The specific mechanism of toxicity is unclear but appears to involve damage to pulmonary tissue.