Nickel acute effect

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. 

Acute effects of water-soluble nickel compounds... 

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

Some nonmalignant respiratory effects have been observed in experimental animals during acute or subchronic exposures. Soluble and moderately soluble compounds were more toxic than were insoluble compounds and produced different effects. Sulfate and subsulftde produced fibrosis whereas nickel oxide did not. 

Systemic effects of nickel exposure include hyperglycemia, increased levels of plasma glucagon, damage to the pancreatic islet cells, decreased body weight, reduced food and water intake, and hypothermia (NAS 1975 USEPA 1980 USPHS 1993). Acute administration of nickel salts caused prompt hyperglucagonemia and subsequent hyperinsulinemia in rats, rabbits, and guinea pigs (WHO... 

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. ... 

Several chronic inhalation and oral studies and acute dermal studies in animals are reported in the literature. These studies exposed several species of animals to both soluble and less-soluble nickel compounds. The target organs were found to be the respiratory system for inhalation exposure and the respiratory system, gastrointestinal tract, hematological system, and kidneys for oral exposure at high levels. Reproductive and developmental effects were observed in animals after inhalation exposure and after oral exposure to nickel. Nickel sensitivity and dermatitis were also observed. 

Acute oral studies in animals are limited to LDjg studies (Haro et al. 1968 Mastromatteo 1986). Accidental oral exposure of humans to nickel (Sunderman et al. 1988) and a longer term study in which dogs vomited during the first few days of the study (Ambrose et al. 1976) indicate that an acute dose of nickel is a gastrointestinal irritant. Therefore, animals that are capable of vomiting may be the most appropriate for further studies of the effects of nickel following acute oral exposure. 

Wade, A.E., Evans, J.S., Stemson, L.A. Gammans, R.E. (1977) Interaction of nitromethane with reduced hepatic microsomal cytochrome P 450. Biochem. Pharmacol., 26, 963-967 Zitting, A., Nickels, J. Savolainen, H. (1982) Comparison of acute toxic effects of intia-peritoneally injected nitromethane and nitroethane in rats. Toxicol. Lett., 13, 189-194... 

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... 

Lung cancer is probably the most lethal manifestation of toxic effect from chronic exposure to certain chemicals. Asbestos fibers, coke oven emissions, arsenic, chromates, nickel and the radioactive gas, radon, are some of the substances known to cause lung cancer. For a detailed discussion of carcinogenesis, see Part A, Section VI, while specific compounds are discussed in Part B of this text. Acute and chronic effects of some common pulmonary toxicants are presented in Table V.3. 

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). 

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. 

Animal experimental models of nickel-induced skin sensitivity are few and have been conducted only under very specialized conditions. Studies examining the mechanism of nickel contact sensitization and its extent in wildlife are needed. The importance of the surface properties and crystalline strac-ture of nickel compounds in relation to their reactivity and protein-binding activities is well documented. It is therefore necessary to identify clearly the nickel compounds to which exposure occurs. Acute and chronic dermal and inhalation studies using all nickel compounds would determine if certain compounds are more effective in eliciting allergic dermatitis. 

Cadmium and nickel can produce delayed effects in human cells in vitro, which are characteristic if gnomic instabihty (Cone et al. 2001). The effects even occur at levels where no acute toxic effects can be demonstrated. The consequences of this gnomic instabihty are not yet known but it is possible that many of the systemic symptoms associated with exposure to low concentrations of these metals could... 

The toxicity of cobalt and cobalt-nickel alloys in experimental hard metal pneumoconiosis is well documented. Metallic cobalt powder instilled in-tratracheally in the lungs of rats had an acute irritant action and lead to severe alterations in capillaries (Harding 1950, Schiller 1958,1961). The solubility of cobalt in plasma is some 500 times greater than in saline, but a fairly large (10 ml) intraperito-neal dose of plasma saturated with cobalt was without evident effects on the rat (Harding 1950). 

Kozlova, T., C.M. Wood, and J.C. McGeer. 2009. The effect of water chemistry on the acute toxicity of nickel to the cladoceran Daphnia pulex and the development of a biotic ligand model. Aquat. Toxicol. 91 221-228. 

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