Nickel (Ni) is an essential nutrient for higher animals. Although a
number of cellular effects of nickel have been documented, a deficiency
disease has not been described in man. Nickel is found in highest
concentrations in lung, kidney and some hormone-producing tissues.
Although nickel-specific enzymes have yet to be identified in higher
animals, nickel can activate or inhibit a number of enzymes that usually
contain other elements. The production or action of some hormones (prolactin,
adrenaline, noradrenaline, aldosterone) responds to changes in nickel
concentration. Within cells, nickel alters membrane properties and
influences oxidation/reduction systems. Nickel has great affinity for
cellular structures such as chromosomes and ion channels, but its
influence on them at normal tissue concentrations is not known.
Deficiencies: It is difficult to induce a deficiency
because the requirement is low and nickel comes from a variety of sources.
Feeding a low nickel diet has reduced the growth of several species of
animals. At the cellular level structures become disorganized and membrane
properties change. Nickel deficiency has been linked to low blood glucose
levels, abnormal bone growth, poor absorption of ferric iron, and altered
metabolism of calcium, vitamin B-12 and energy nutrients.
Diet recommendations: Based on animal experiments, the
human requirement for nickel probably does not exceed 100 µg/day. Nickel
content of Western self-selected and institutional diets ranges from 60 to
260 µg/day. Adequacy of the lower intakes may depend on the
bioavailability of nickel (the nickel compounds ingested and foods
consumed with them).
Food sources: Rich food sources of nickel include
oatmeal, dried beans and peas, nuts, and chocolate. The apparent
absorption from test meals is about 1%. Up to 27% is absorbed from water
but the daily intake of water provides only 1-2 µg Ni. Absorption is
influenced by the amount fed, the acidity of the gut, and the presence of
various binding agents (as phytate) or competing substances. In
particular, the levels of other minerals such as iron, magnesium, zinc and
calcium may alter nickel absorption from the gut.
Toxicity: Toxicity has occurred in workers exposed to
nickel dust or nickel carbonyl formed in refining. Increased risk of nasal
and lung cancers was linked to occupational nickel exposure before current
workplace safety standards were set. Environmental sources of lower levels
of nickel include tobacco, dental or orthopedic implants, stainless-steel
kitchen utensils and inexpensive jewelry. Repeated exposures may lead to
asthma and contact dermatitis, symptoms of which may worsen if the diet is
high in nickel. The oral toxic dose is about 1000 times the amount
consumed in food. Different chemical forms vary widely in toxicity.
Excessive nickel in tissues is pro-oxidant (damaging chromosomes and other
cell components) and alters hormone and enzyme activities, movement of
ions through membranes, and immune function. These effects can change
glucose tolerance, blood pressure, response to stress, growth rate, bone
development and resistance to infection. Under some conditions, large
amounts of nickel may precipitate magnesium deficiency or cause
accumulation of iron or zinc.
Recent research: Additional information is needed to
establish more precisely an intake/exposure range that is both adequate
and safe, and to account for other factors that affect the need and
tolerance for nickel.