Guidelines for Metals and Metalloids in Ambient ... - ARCHIVE: Defra

Nickel
The normal body burden of nickel approximates 0.1 µg/g in
non-occupationally exposed individuals, with much of this in the lung.
Svenes and Andersen (1998) reported that the nickel content of
lung tissue taken from a group of ex- nickel refinery workers was 50 ±
150 µg/g (dry weight), compared with 0.74 ± 0.44 µg/g in a similar
group unconnected with the industry.
126. There have been no specific studies to determine whether children are
more susceptible than adults to the effects of nickel. Limited evidence
of an increased susceptibility from dermal exposures is considered
more likely to reflect potential for exposure (via body piercing) than
increased sensitivity (ATSDR, 2003).
3.2 Absorption and excretion
3.2.1 Pulmonary absorption
127. The measured particle size for atmospheric nickel indicates that most
of the inhaled particulate matter will deposit in the lung (WHO, 2000)
with up to 40% being retained in the deep lung where clearance is more
prolonged. There are marked differences in the solubility of nickel
compounds. In general, nickel chloride and nickel sulphate are soluble
while nickel oxide and nickel subsulphide are insoluble. Soluble nickel
compounds are rapidly removed from the lung (Carvalho and Ziemer,
1982). Menzel et al. (1987) demonstrated a saturable clearance
mechanism for soluble nickel compounds from rat lungs, calculating a
maximum clearance velocity of 34.6 ng/g of lung tissue per hour for
nickel chloride. In contrast approximately 50% of a dose of nickel
oxide, which is much less soluble, was still present in the lungs of
golden hamsters after 45 days. Moreover, only 10% nickel sulphide,
which is of intermediate solubility, is retained after 35 days (Valentine
and Fisher, 1984).
3.2.2 Metabolism
128. The biological half-life of nickel depends on the compound tested and
thus its solubility as discussed above. Once in blood, nickel binds to the
blood proteins, albumin and α-2-macroglobulin. The bound nickel can
exchange with free histidine, leading to a pool of low molecular weight
nickel-L-histidine complexes, which can cross biological membranes.
Tissue based metabolism of nickel has been extensively studied in
animals and has been shown to involve oxidation/reduction (redox)
reactions generating the trivalent form, nickel (Ni 3+ ). The extent of
redox cycling within different tissues is likely to be influenced by the
availability of other oxidising and reducing species.
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