Nickel exposure

Human cells exposed to various nickel compounds have an increased frequency of chromosomal aberrations, although sister chromatid exchange frequency is unaffected. Cells from nickel refinery workers exposed to nickel monosulfide (0.2 mg Ni/m3) or nickel subsulfide (0.5 mg Ni/m3) showed a significant increase in the incidence of chromosomal aberrations (Boysen et al. 1980 WHO 1991 USPHS 1993). No correlation was evident between nickel exposure level and the frequency of aberrations (USPHS 1993). 

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... 

Overall, nickel is not an immediate threat to the health of plants, animals, and humans at environmentally encountered levels, except in the case of nickel carbonyl, and progress has been made toward minimizing or eliminating occupational nickel exposure. 

Bowser, D.H., K. Frenkel, and J.T. Zelikoff. 1994. Effects of in vitro nickel exposure on the macrophage-mediated immune functions of rainbow trout (Oncorhynchus mykiss). Bull. Environ. Contam. Toxicol. 52 367-373. 

Novelli, E.L.B., N.L. Rodrigues, and B.O. Ribas. 1995. Superoxide radical and toxicity of environmental nickel exposure. Human Exper. Toxicol. 14 248-251. 

In an evaluation of epidemiological studies to date, it was concluded that most of the respiratory cancer seen among the nickel refinery workers could be attributed to exposure to a mixture of oxidic and sulfidic nickel at very high concentrations. Exposure to large concentrations of oxidic nickel in the absence of sulfidic nickel was also associated with increased lung and nasal cancer risks. There was also evidence that soluble nickel exposure increased the risk of these cancers and that it may enhance risks associated with exposure to less soluble forms of nickel. There was no evi-... 

Food contains nickel and is the major source of nickel exposure for the general population. 

Other lung effects including chronic bronchitis and reduced lung function have been observed in workers breathing nickel. Current levels of nickel in workplace air are much lower than in the past, and few workers have symptoms from nickel exposure. 

See Chapter 2 for more information on the health effects of nickel exposure. 

Numerous studies in animals have investigated the respiratory effects of nickel exposure. Intermittent exposure (6 hours/day, 5 days/week) of rats and mice for 16 days or 13 weeks resulted in chronic active inflammation in the lungs, fibrosis, macrophage hyperplasia, interstitial infiltrates, and increased lung weight following exposure to 0.06 mg nickel/m as nickel sulfate, 0.11 mg nickelM as nickel subsulfide, and 0.4 mg nickel/m as nickel oxide (Benson et al. 1987, 1988, 1989 Durmick et al. 

Compared to rats, mice were more resistant to the development of lung lesions following nickel exposure. In this study, rats were exposed to 0, 0.5, 1, or 2 mg nickel/m as nickel oxide, 0, 0.11, or 0.73 mg nickel/m as nickel subsulfide, and 0, 0.03, 0.06, or 0.11 mg nickel/fti as nickel sulfate. Mice were exposed to 0, 1, 2, or 3.9 mg nickel/m as nickel oxide, 0, 0.44, or 0.88 mg nickel/rh as nickel subsulfide, and 0, 0.06, 0.11, or 0.22 mg nickel/m as nickel sulfate. Lung effects were observed in both rats and mice at all concentrations following exposure to nickel oxide and nickel subsulfide, and at concentrations >0.06 mg nickel/m for rats and mice exposed to nickel sulfate. Based on a NOAEL of 0.03 mg nickel/m for rats exposed to nickel sulfate for 2 years (NTP 1996c), a chronic-duration inhalation MRL of 2x10 " mg nickel/m for soluble nickel compounds was calculated as described in the footnote to Table 2-1. 

Dermal Effects. No studies were located regarding dermal effects in humans following inhalation exposure. However, contact dermatitis in persons exposed to nickel compounds is one of the most common effects of nickel exposure (see Section 2.2.3.2). In addition, immunological studies indicate that the dermatitis is an allergic response to nickel, and significant effects on the immune system have been noted in workers exposed to nickel (see Section 2.2.1.3). 

Exposure to nickel Exposure to nickel sulfate hexahvdrate tma nickel/m l subsulfide tma nickel/m l Exposure to nickel oxide tmu nickel/m l ... 

No gross or microscopic lesions were observed in the kidneys of rats treated dermally with 100 mg nickel/kg/day as nickel sulfate for 15 or 30 days (Mathur et al. 1977). In this study, there was no indication that the rats were prevented from licking the nickel from the skin therefore, the animals could have been orally exposed. Increased Mg ATPase was observed in the kidneys of guinea pigs treated with 100 mg nickel/kg/day as nickel sulfate placed on skin of the back for 30 days (Mathur and Gupta 1994). No effect was noted at 15 days, and dermal nickel exposure had no effect on kidney acid phosphatase or glucose-6-phosphatase activities. 

Sunderman (1993) reviewed all the biologieal monitoring data for niekel in humans and eoneluded that the most use l speeimens for biologieal monitoring are urine and semm. Levels of nickel in urine and serum ean provide the most information about levels of nickel exposure if the route, sources, and duration of exposure are known, if the ehemical identities and physical-chemieal properties of the nickel eompounds are known, and if physiologieal information, for example renal ftmetion, of the exposed population is known (Sunderman 1993). 

Information on nickel exposure from hazardous waste sites is lacking. The most probable route of exposure from hazardous waste sites would be dermal contact, inhalation of dust, and ingestion of nickel-contaminated soil. Groundwater contamination may occur where the soil has a coarse texture and where acid waste, such as waste from plating industries, is discarded. People using this water may be exposed to high levels of nickel. 

In discussing nickel exposure, it is important to consider what form of nickel a person is exposed to and its bioavailability. Such information is not often available. Although high concentrations of nickel may be found in contaminated soil and sediment, it may be embedded in a crystalline matrix or bound to hydrated iron, aluminum, and manganese oxides and, therefore, not bioavailable. 

Methods for Determining Biomarkers of Exposure and Effect. Nickel concentrations in hair, nails, blood, or urine are elevated in exposed individuals. A correlation has been established between nickel levels in urine, plasma, and feces in occupationally exposed workers and nickel levels in air (Angerer and Lehnert 1990 Bemacki et al. 1978 Hassler et al. 1983). If the identity of the nickel compounds to which workers are exposed is known, nickel levels in urine and plasma can be used as a biomarker for nickel exposure (Sunderman 1993). Available analytical methods can determine the nickel levels in these media in both unexposed and occupationally exposed persons. Methods to determine nickel speciation in biological media require further development. 

Angerer J, Lehnert G. 1990. Occupational chronic exposure to metals. II Nickel exposure of stainless steel welders—biological monitoring. Int Arch Occup Environ Health 62 7-10. 

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