Distribution

The kinetic processes that govern transport and distribution of nickel in the body are dependent on the site of absorption, rate and concentration of nickel exposure, solubility of the nickel compound, and physiological status of the body. Nickel is mainly transported in the blood through binding with serum albumin and, to a lesser degree, histidine. The nickel ion may also bind with body proteins to form a nickel-rich metalloprotein (Sunderman et al., 1986).

Postmortem analysis of tissues from ten individuals who, with one exception, had no known occupational exposure to nickel, showed highest nickel concentrations in the lungs, thyroid gland, and adrenal gland, followed by lesser concentrations in the kidneys, heart, liver, brain, spleen and pancreas (Rezuke et al., 1987). These values are in general agreement with other autopsy studies that have shown highest concentrations of nickel in lung, followed by lower concentrations in kidneys, liver, heart, and spleen (Nomoto, 1974; Zober et al., 1984a; Seemann et al., 1985).

The distribution of various nickel compounds to tissues has been studied in animals. Such studies reveal that the route of exposure can alter the relative amounts of nickel deposited in various tissues. Animal studies indicate that inhaled nickel is deposited primarily in the lung and that lung levels of nickel are greatest following inhalation of relatively insoluble NiO, followed by moderately soluble Ni3S2 and soluble NiSO4 (as NiSO4•6H2O) (Dunnick et al., 1989). Following intratracheal administration of Ni3S2 and NiSO4, concentrations of nickel were found to be highest in the lung, followed by the trachea, larynx, kidney, and urinary bladder (Valentine and Fisher, 1984; Medinsky et al., 1987). Kidney nickel concentrations have been shown to increase in proportion to exposure to NiSO4 via inhalation, indicating that a significant portion of soluble nickel leaving the respiratory tract is distributed to the kidneys (Benson et al., 1988). There is also some evidence that the saturation of nickel binding sites in the lung or saturation or disruption of kidney reabsorption mechanisms in rats administered NiSO4 results in more rapid clearance (Medinsky et al., 1987).

Not surprisingly, predictions of body burden have varied depending upon the analytical methods used and the assumptions made by investigators to calculate burden. Bennett (1984) estimates the average human nickel body burden to be about 0.5 mg (0.0074 mg/kg x 70 kg). In contrast, values of 5.7 mg have been estimated by Sumino et al. (1975) on the basis of tissue analyses from autopsy cases.