Lung nickel

Nickel Nose, lung Nickel smelters, mboers, roasters, electrolysis workers... 

Poirier LA, Theiss JC, Arnold LJ, et al. 1984. Inhibition by magnesium and calcium acetates of lead subacetate and nickel acetate-induced lung tumors in strain A mice. Cancer Res 44 1520-1522. 

Increased frequency of lung and nasal cancers reported among English nickel refinery 1, 5, 6... 

Nickel carbonyl (Ni(CO)4) is a volatile, colorless liquid readily formed when nickel reacts with carbon monoxide it boils at 43°C and decomposes at more than 50°C. This compound is unstable in air and is usually not measurable after 30 min (NRCC 1981 Norseth 1986 USPHS 1993). The intact molecule is absorbed by the lung (USEPA 1980) and is insoluble in water but soluble in most organic solvents (WHO 1991). 

During occupational exposure, respiratory absorption of soluble and insoluble nickel compounds is the major route of entry, with gastrointestinal absorption secondary (WHO 1991). Inhalation exposure studies of nickel in humans and test animals show that nickel localizes in the lungs, with much lower levels in liver and kidneys (USPHS 1993). About half the inhaled nickel is deposited on bronchial mucosa and swept upward in mucous to be swallowed about 25% of the inhaled nickel is deposited in the pulmonary parenchyma (NAS 1975). The relative amount of inhaled nickel absorbed from the pulmonary tract is dependent on the chemical and physical properties of the nickel compound (USEPA 1986). Pulmonary absorption into the blood is greatest for nickel carbonyl vapor about half the inhaled amount is absorbed (USEPA 1980). Nickel in particulate matter is absorbed from the pulmonary tract to a lesser degree than nickel carbonyl however, smaller particles are absorbed more readily than larger ones (USEPA 1980). Large nickel particles (>2 pm in diameter) are deposited in the upper respiratory tract smaller particles tend to enter the lower respiratory tract. In humans, 35% of the inhaled nickel is absorbed into the blood from the respiratory tract the remainder is either swallowed or expectorated. Soluble nickel compounds... 

Nickel retention in the body of mammals is low. The half-time residence of soluble forms of nickel is several days, with little evidence for tissue accumulation except in the lung (USEPA 1980, 1986). Radionickel-63 (63Ni) injected into rats and rabbits cleared rapidly most (75%) of the injected dose was excreted within 24 to 72 h (USEPA 1980). Nickel clears at different rates from various tissues. In mammals, clearance was fastest from serum, followed by kidney, muscle, stomach, and uterus relatively slow clearance was evident in skin, brain, and especially lung (Kasprzak 1987). The half-time persistence in human lung for insoluble forms of nickel is 330 days (Sevin 1980). 

About 727,000 workers were potentially exposed to nickel metal, nickel alloys, or nickel compounds during the period 1980 to 1983 (USPHS 1993). Worker exposure differs from that of the general population in that the major route of exposure for nickel workers is inhalation and for the general population it is dermal contact (Sevin 1980). Nickel workers with lung cancer had elevated concentrations of 1.97 mg/kg DW in their lungs when compared to the general population (0.03 to 0.15 mg/kg DW USPHS 1977). Plasma concentrations of nickel quickly reflect current exposure history to nickel (USEPA 1980). Mean nickel concentrations in plasma of humans occupationally exposed to nickel have declined by about 50% since 1976, suggesting decreased exposure due to improved safety (Boysen et al. 1980). 

Inhaled nickel is at least 100 times more toxic than ingested nickel because it is more readily absorbed from the lungs than from the gastrointestinal tract, and death is more often the result of respiratory failure than of nervous system effects. For example, oral ingestion of 0.05 mg Ni/kg BW and inhalation at 0.005 Ni/m3 are equally effective threshold doses in rats (USPHS 1977). 

Threshold effects on lung function or morphology in several species of laboratory mammals occur at airbome nickel concentrations of 0.1 to 0.2 mg/m3, depending on nickel compound and duration of exposure. 

Local effects noted in guinea pigs, rats, mice, and hamsters caused by inhalation of metallic nickel powder (15 mg/m3), nickel subsulfide (0.97 mg/m3), or nickel oxide (53 mg/m3) include nasal sinus inflammations, ulcers, lung irritation, nickel accumulations in lungs, emphysema, and... 

After 24 h, no increase in nickel content of lungs, liver, kidney or carcass... 

Nickel aerosols, occupational exposure Lung cancer, nasal sinusitis, chronic rhinitis 10... 

Single injection of ultrafine particles of nickel metal (20 nm diameter) at 5 mg Severe lung inflammation, cytotoxicity, and increased epithelial permeability 42... 

Nickel chloride 1.0 mg/kg BW examined 6 and 72 h after injection At 6 h, tissue nickel concentrations were elevated in kidneys, lungs, adrenals, liver, pancreas, spleen, heart, and testes, in that order by 72 h, 90% of the nickel was excreted, mostly (75%) in the urine 7... 

Johansson, A., T. Curstedt, and P. Camner. 1991. Lung lesions after combined inhalation of cobalt and nickel. Environ. Res. 54 24-38. 

McDowell, S. A. et al., The role of the receptor tyrosine kinase Ron in nickel-induced acute lung injury, Am. J. Respir. Cell. Mol. Biol., 26, 99, 2002. 

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