Acute nickel carbonyl

A close correlation exists between the clinical severity of acute nickel carbonyl intoxication and the urinary concentration of nickel during the first 3 days after exposure hospitalization should be considered in all cases where the urinary nickel content exceeds 0.5 mg/liter of urine. ... 

Acute effects of nickel carbonyl The lung is the primary target organ for acute nickel carbonyl toxicity in rats, following administration either by intravenous... 

Animal studies have demonstrated that sodium diethyldithiocarbamate is an effective antidote to acute nickel carbonyl poisoning when the chelating drug is administered parenterally soon after the exposure (Baselt and Hanson 1982, Baselt et al. 1977, West and Sunderman 1958). Based on this evidence, sodium diethyldithiocarbamate has been used for many years to treat patients with acute nickel carbonyl poisoning (Sunderman 1971, 1979, 1992, Sunderman and Sunderman 1958). In a critique of the published experimental and clinical data. Brad-berry and Vale (1999) concluded that adequately controlled clinical trials of the drug have never been performed they suggested... 

Beadbeeey SM and Vale JA (1999) Therapeutic review do diethyldithiocarbamate and disulflram have a role in acute nickel carbonyl poisoning Clin Toxicol 37 259-264. 

Sunderman FW (1971) The treatment of acute nickel carbonyl poisoning with sodium diethyldithiocarba-mate. Ann Clin Res 3 182-185. 

Sunderman FW (1979) Efficacy of sodium diethyl-dithiocarbamate (Dithiocarb) in acute nickel carbonyl poisoning. Ann Clin Lab Sd 9 1 — 10. 

The toxic symptoms from inhalation of nickel carbonyl are beUeved to be caused by both nickel metal and carbon monoxide. In many acute cases the symptoms ate headache, di22iQess, nausea, vomiting, fever, and difficulty in breathing. If exposure is continued, unconsciousness follows with subsequent damage to vital organs and death. Iron pentacarbonyl produces symptoms similar to nickel carbonyl but is considered less toxic than nickel carbonyl. 

Nickel carbonyl Carbonylation of acetylene and alcohols to produce acrylic and methacrylic acids Acute respiratory failure carcinogenic... 

The Reppe process for manufacture of acrylic esters uses acetylene and carbon monoxide, with a nickel carbonyl catalyst having high acute and longterm toxicity, to react with an alcohol to make the corresponding acrylic ester ... 

By analogy to nickel carbonyl, acute effects from animal exposures are expected to be pulmonary edema, congestion, and hemorrhage. In humans, nickel carbonyl causes an acute flulike syndrome that subsides and is followed after 12-36 hours by an acute respiratory syndrome. Exposure to cobalt hydrocarbonyl may be expected to produce similar effects. 

In rodent studies iron pentacarbonyl was found to have approximately one-third the acute toxicity of nickel carbonyl. At 33 ppm for 5.5 hours three of eight rats died at 18 ppm four of eight died after two 5.5-hour exposures. Multiple 5.5-hour exposures at 7ppm caused no apparent effects. 

The severe acute systemic effects found with nickel carbonyl exposure are not associated with inorganic nickel. ... 

Some toxic substances such as sulfur dioxide, nitrogen dioxide, and ozone cause acute, direct damage to lung tissue, whereas others, such as nickel carbonyl, may lead to the formation of tumors. 

There are over 40 different cell types in the respiratory system, and those particularly susceptible are the lining cells of trachea and bronchi, endothelial cells and the interstitial cells (fibroblasts and fibrocytes). Some toxic substances such as sulphur dioxide, nitrogen dioxide and ozone cause acute, direct damage to lung tissue, whereas others, such as nickel carbonyl may lead to the formation of tumours. 

Baselt RC, Sunderman FW Jr, Mitchell J and Horak E (1977) Comparisons of antidotal efficacy of sodium diethyldithiocarbamate, D-penidUamine and triethylenetetramine upon acute toxicity of nickel carbonyl in rats. Res Commun Chem Pathol Pharmacol 18 677-688. 

Hagkett RL and Sunderman FW Jr (1967) Acute pathological reactions to administration of nickel carbonyl. Arch Environ Health 14 604-613. 

Iron penlacarbonyl (Iron caibonyl [CAS 13463-40-6]) Acute toxicity resembles that of nickel carbonyl. Inhalation of vapors can cause lung and systemic injury without warning signs. Symptoms of overexposure include headache, nausea and vomiting, and dizziness. Symptoms of severe poisoning are fever, extreme weakness, and pulmonary edema effects may be delayed for up to 36 hours. 0.1 ppm Colorless to yellow viscous liquid. Vapor pressure is 40 mm Hg at 30.3°C (86.5°F). Highly flammable. 

The chemical and physical forms of nickel and its salts strongly influence bioavailability and toxicity. In general, nickel compounds have low hazard when administered orally. In humans and other mammals, however, nickel-inhalable dust, nickel subsulflde, nickel oxide, and especially nickel carbonyl induce acute pneumonitis, central nervous system disorders, skin disorders such as dermatitis, and cancer of the lungs and nasal cavity (Table 22.1). Nickel carbonyl is acutely lethal to humans and animals within 3-13 days of exposure recovery is prolonged in survivors. An excess... 

The toxic effects are similar to those of nickel tetracarbonyl or iron pentacarbonyl. The acute toxicity, however, is lower than that of these two carbonyls. Inhalation of the gas can cause dizziness, giddiness, and headache. It readily decomposes at room temperature producing toxic carbon monoxide. A 30-minute LC50 in rats is 165 mg/m (Palmes et al. 1959). 

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