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OCR for page 345
Nickel
Nickel (Ni) is a hard silver-white ferromagnetic metal that can be
polished to a lustrous finish. It occurs in several ores (chalcopyrite,
py~rhotite, pentlandite, garnierite, niccolite, and millerite) and the
element constitutes 0.008 percent of the earth's crust. Nickel is used in
alloys, storage batteries, for electroplating, and in Raney nickel, a
catalyst used for hydrogenation of organic compounds. In 1971 the
United States produced over 15,000 tons of nickel; however, the total
consumption in this country during 1972 was estimated to be 159,286
tons (National Research Council, 1975~.
With diets very low in nickel, animals maintained in specially clean
environments have failed to grow, develop, and reproduce normally;
however, nickel deficiencies have not been observed under typical
laboratory or practical conditions. Nickel in various forms is relatively
nontoxic when consumed orally; however, workers exposed to air-
borne nickel have an increased incidence of respiratory disease, includ-
ing cancer. Some individuals develop very marked dermal sensitivity to
nickel. The sources, distribution, industrial uses, and biological ejects
of nickel were reviewed in detail by the National Research Council
(1975), and Nielsen (1977) reviewed nickel toxicity.
ESSENTIALITY
Nielsen and co-workers obtained the first evidence of nickel defi-
ciencies in chicks; the early studies of these and other workers were
345
OCR for page 346
346 MINERAL TOLERANCE OF DOMESTIC ANIMALS
reviewed (Nielsen, 1974; Nielsen and Ollerich, 1974; Underwood,
1977).
The diets used to produce deficiency have been very low, ranging
from 2 to 40 ppb nickel. It was generally necessary to maintain the
animals in filtered air environments with nickel sources rigorously
excluded ancl/or to feed the diet throughout a lifetime or through more
than one generation. The requirement has been estimated to be 50 80
ppb for the rat and chick (Nielsen and Sandstead, 19741.
Deficiencies of nickel have been produced in chicks, pigs, goats, and
rats, as reviewed by Nielsen and Sandstead (1974), and sheep (Spears
et al., 197Sa,b). Abno~alities observed in deficient animals have
varied markedly between species, between laboratories, and within
laboratories in successive experiments. The differences appear to be
related to degree of deficiency, adequacy of the diet in nutrients other
than nickel, other aspects of dietary composition, and inadequacies in
the filtered environment. The problems of dietary adequacy and envi-
ronment have been significantly improved for chicks (Nielsen et al.,
1975a) and rats (Nielsen et al., 1975b).
Abnormalities observed in deficient chicks inclucied depressed
hematocrits, less yellow lipochrome pigment in the shank skin, and
abnormalities in the rough endoplasmic reticulum of the liver (Nielsen
et al., 1975a). Similar liver pathology had been described in nickel-
deficient chicks by Sunderman et al. (19721. Nickel deficiency has
caused reproductive problems in goats and swine (Anke et al., 19741.
Delayed sexual maturity occurred in the sows; there was high mortality
of the young pigs. Nickel-deprived lambs showed depressed growth,
total serum proteins, erythrocyte counts, total liver lipids and choles-
terol, serum alanine transaminase levels, dietary nitrogen utilization,
and liver copper concentration (Spears et al., 1978a,b).
Deficient rats had increased per~natal mortality, a rough ha* coat,
and ultrastructural changes in the liver (Nielsen et al., 1975b). In
deficient rats, Schnegg and Kirchgessner (1978) observed depressed
growth, hematocrits, hemoglobin levels, and erythrocyte counts;
serum levels of urea, ATP, and glucose; liver levels of triglycerides,
glucose, and glycogen; liver, kidney, and spleen levels of zinc, iron,
and copper; and activities of several liver and kidney enzymes. They
also found marked impairment of iron absorption.
OCR for page 347
Nic/ce'
347
METABOLISM
Underwood (1977) has reviewed information on nickel absorption and
tissue distribution. Absorption of normal dietary nickel levels are 10
percent or less. Daily urinary excretion appears to equal amounts of
nickel absorbed when nickel intake is normal. There was little accumu-
lation of nickel in tissues of rats receiving 5 ppm nickel in their drinking
water throughout their lifetime (Schroeder et al., 1974~.
Nickel was shown to be a component of urease. Lambs fed a low
nickel diet had lower levels of ruminal urease than lambs fed 5 ppm
nickel (Spears et al., 19771.
The metabolic mechanisms for any essential functions of nickel have
not been established.
SOURCES
Relatively few data are available on the nickel content of animal feeds.
Whole oats and rye seeds contained 2-3 ppm nickel, whereas concen-
trations in wheat ranged from 0 to 0.5 ppm (Schroeder et al., 1962; Zook
et al., 1970~. Commercial dog and rat diet contained 2.1 and 3.3 ppm
nickel, respectively (Schroeder et al., 1962~. Nickel in a purified rat diet
containing 20 percent casein was 0.21 ppm (Whanger, 1973), and in an
unrefined diet for cattle it was 0.9 ppm (O'Dell et al., 1970b). Nickel
concentrations in components used in diets for cattle were corn, 0.4
ppm; oats, 1 ppm; soybean meal, 3.6 ppm; alfalfa meal, 1.4 ppm; and
cottonseed hulls, 0.6 ppm (O'Dell et al., 1971~.Plant foods are generally
higher in nickel than foods of animal origin. Nickel in common pasture
plants ranged from 0.5 to 3.5 ppm (Underwood, 1977~.
The nickel content of water is typically very low. The concentrations
in the major river basins and water supplies of the United States were
usually less than 10 ppb (National Research Council, 1975~. Higher
concentrations may occur in water of industrial areas.
There is no need to add nickel to practical animal diets. Nickel from
food machinery can contribute significant amounts of nickel to pro-
cessed foods. Nickel chloride has been used in studies of nickel essen-
tiality. Little is known about the form of nickel in foods and its
bioavailability.
Nickel from industrial operations can contribute locally to the nickel
level in air, water, and soil. There appear to be no widespread problems
for either man or animals from exposure to these sources.
OCR for page 348
348 MINERAL TOLERANCE OF DOMESTIC ANIMALS
TOXICOSIS
LOW LEVELS
Nickel is relatively nontoxic in terms of the quantities required above
typical dietary intakes to produce adverse effects in a few weeks.
Lactating dairy cows were unaffected by 145, 365, or 1,835 mg nickel
per day (Archibald, 1949; O'Dell et at., 1970a). The latter two levels
represented 50 and 250 ppm nickel in the diet, respectively. Young
calves were not affected by 250 ppm dietary nickel as the carbonate or
50 ppm as the chloride; however, they consumed less food when the
diet contained 500 or 1~000 ppm nickel as the carbonate or 100 and 200
ppm as the chloride (O'Dell et al., 1970c). In these experiments, the
calves were offered a choice of basal diet or nickel-supplemented diet.
A linear depression of palatability, as judged by consumption of nickel-
containing diet, was observed as nickel in the diet increased. Total food
consumption was unaffected. Levels of 62.5 and 250 ppm nickel as the
carbonate caused no adverse health effects or increases in tissue nickel
levels of calves after X weeks of feeding (O'Dell et al., 1970b, 1971)e
The young growing chick responded similarly to the young calf.
Dietary levels of 100 and 300 ppm nickel as either the carbonate or the
acetate had no adverse effects when fed from hatching to 4 weeks of age
(Weber and Reid, 1968~. Levels of 500 ppm or more reduced growth.
Dogs fed either 100 ppm or 1,000 ppm nickel as the sulfate showed
no adverse effects after 2 years (Ambrose et al., 19761.
Schroeder et al. (1974) gave weanling rats 5 ppm nickel in their
drinking water for their remaining lifetime. No adverse effects were
observed. When weanling rats received 5 ppm nickel in their drinking
water and were carried through three generations, more young rats died
in each generation (Schroeder and Mitchener, 1971~. Significant num-
bers of runts occurred in the Fl and F3 generations.
Phatak and Patwardhan (1950) fed 250, 500, or 1,000 ppm nickel to
rats for 3 to 4 months. They tested nickel carbonate, nickel soap, and
nickel catalyst. The soap was prepared from nickel carbonate and
mixed fatty acids obtained from refined groundnut oil. The nickel
catalyst was finely divided nickel suspended in vegetable oil and sup-
ported on kieselguhr. These represent forms that could be present in
small amounts in hydrogenated fats. They observed no adverse effects
with these levels of nickel. The experimental period encompassed one
reproductive cycle. Nickel concentrations in nine tissues were not
detectable in the controls; however, all nine tissues of supplemented
rats contained nickel concentrations that were generally dose-related.
OCR for page 349
Nickel
349
Nickel in the bodies of newborn rats was measurable only with the
highest level of catalyst or the two upper levels of nickel carbonate.
Body weights of the pups were not affected by nickel.
Phatak and Patwardhan (1952) fed nickel catalyst at 250 ppm to
young rats for 16 months. No adverse effects on growth, gross ap-
pearance, or vigor were observed. Soft tissues and bone accumulated
nickel, with maximal concentrations attained by 8 months.
No adverse effects occurred in weanling rats fed 100 ppm nickel as
the acetate for 6 weeks (Whanger, 19731. Ambrose et al. (1976)
observed no adverse effects in rats fed 100 ppm nickel as the sulfate for
2 years.
A low level of nickel, 5 ppm, was administered to mice in their
drinking water throughout their lifetime (Schroeder et al., 1963, 19641.
No adverse effects were observed. Weber and Reid (1969) fed 1,100
ppm nickel to young mice and observed decreased growth of females by
4 weeks. Adult weights were unaffected by this level of nickel and no
adverse effects occurred by the end of one reproductive cycle.
The adult monkey, like the cow, was resistant to high dietary levels
of nickel. Phatak and Patwardhan (1950) observed no adverse effects of
250, 500, or 1,000 ppm nickel in the diet. They tested the same nickel
carbonate, nickel soap, and nickel catalyst that they fed to rats.
HIGH LEVELS
Due to numerous factors that influence nickel toxicity, as discussed
below, there is no sharp demarcation between levels of dietary nickel
that produce minimal or no adverse effects and those that produce
marked adverse effects. The delineation between this and the previous
section is therefore based on severity of response and involves a large
overlap of nickel intakes.
O'Dell e! al. (1970b, 1971) found decreases in feed intake, organ
size, and nitrogen retention in calves fed 1,000 ppm nickel as the car-
bonate for 8 weeks. Even though the calves lost weight, they were not
emaciated but simply looked younger than the control group. The con-
centrations of nickel in 9 of 10 tissues and body fluids was significantly
increased above those of control calves. The total nickel intake was not
different from that of calves fed 250 ppm nickel, which had no effect on
tissue nickel; however, the nickel intake per unit body weight was
much higher for calves fed 1,000 ppm nickel. The homeostatic mech-
anism regulating nickel thus ceased to function at intake levels some-
where between 250 and 1,000 ppm.
Weber and Reid (1968) fed chicks nickel as the sulfate or acetate at
OCR for page 350
350 MINERAL TOLERANCE OF DOMESTIC ANIMALS
seven graded levels from 100 to 1,300 ppm for 4 weeks. Growth rate
was decreased in all birds fed 500 ppm or more nickel. Nitrogen reten-
tion was decreased by 500 ppm or more nickel as the sulfate and by 900
ppm or more nickel as the acetate. When controls were pair-fed to birds
consuming 1,100 ppm nickel, there was no effect of nickel on growth,
but there was a significant reduction of nitrogen retention.
When Ambrose e! al. (1976) fed dogs 2,500 pun nickel as the sulfate,
the dogs vomited and salivated excessively. After return to the control
diet followed by a gradual increase to 2,500 ppm nickel, there were no
acute problems. The dogs continued for 2 years, exhibiting a moder-
ately reduced growth rate. They developed a mild anemia, granulocytic
hyperplastic bone marrow, increased urine volume, and severe lung
lesions.
Young rats of both sexes rapidly decreased their food intake and lost
weight by 13 days after receiving diets with 1,000 ppm nickel as the
chloride (Schnegg and Kirchgessner, 1976~. There were increases in
many measurements of physiological responses; these included red
blood cell counts, hematocrit, hemoglobin, serum protein, nitrogen in
tissues, and nickel, copper, zinc, and iron concentrations in some tis-
sues. Somewhat different changes were produced in weanling rats fed
SOD and 1,000 ppm nickel as the acetate for 6 weeks (Whanger, 1973~.
Growth rate was markedly decreased by 500 ppm nickel, but there was
a mean 23-g weight loss by rats fed 1,000 ppm nickel. Decreased hemo-
globin and heart cytochrome oxidase were found in rats fed 1,000 ppm
nickel. They also had consistently increased tissue nickel and iron
levels and increased zinc in the liver. In all subcellular fractions of liver
and kidney, the concentrations of iron and nickel were increased by 500
and 1,000 ppm dietary nickel. The zinc concentration increased in the
nuclei and debris of the kidneys from rats fed excess nickel; however,
zinc in the intact kidney was not significantly increased by high nickel.
Ambrose et al. (1976) observed mild changes in rats fed 1,000 ppm
nickel as the sulfate for 2 years. Females had reduced body weight and
liver weight and increased heart weight. Males receiving the same diet
exhibited no adverse effect. Increased numbers of stillborn pups
occurred in the Fla generations of rats fed 250, 500, or 1,000 ppm nickel
as sulfate through three generations. Decreased numbers of pups were
weaned with each of the higher levels of nickel. With 1,000 ppm nickel,
weaning weight was decreased; however, the eject was less severe in
F2 and F3 generations.
The oral Also of nickel acetate for rats was 350 mg/kg of body weight
(Fairchild et al., 1977~.
Young mice fed 1,600 ppm nickel as the acetate had depressed
OCR for page 351
Nickel
351
growth by 4 weeks (Weber and Reid, 1969~. Activities of cytochrome
oxidase, malic dehydrogenase, isocitric dehydrogenase, and succinic
dehydrogenase were determined in liver, kidney, and heart and NADH
cytochrome c reductase in liver. Values for succinic dehydrogenase
were not affected by nickel; however, 1,600 ppm nickel caused de-
creased levels of the other enzymes in one or all tissues. Almost no
enzyme changes were produced by 1,100 ppm nickel. There was no
effect of 1,600 ppm nickel on the number of pups born, but there was
a marked decrease in the number of pups weaned. The oral LD50 of
nickel acetate for mice was 136 mg/kg of body weight (Fairchild et al.,
1977).
FACTORS INFLUENCING TOXICITY
The above data show a wide range in response to given levels of dietary
nickel. This appears to reflect differences in form of nickel fed, duration
of feeding, species, age, reproductive status, and diet composition.
In the studies summarized in Table 26, six forms of nickel were used.
All were simple salts except for two. O Dell et al. (1970c) found nickel
as the chloride to be approximately 5 times more toxic than nickel as
the carbonate. Nickel as the carbonate appeared to have a somewhat
greater effect in decreasing nitrogen retention by chicks than did nickel
as the acetate (Weber and Reid, 1968~. Phatak and Patwardhan (1950)
found the following decreasing order of nickel toxicity in rats: car-
bonate, soap, and catalyst. Overall conclusions regarding the order of
toxicity are not possible.
Most studies of nickel toxicity were relatively short, and high levels
of nickel were required to produce toxicosis. Nickel at 5 ppm in the
drinking water was given to mice and rats throughout their lifetime
without ill effects (Schroeder et al., 1963, 1964, 19741. Schroeder and
Mitchener (1971) found deaths of the young and/or runts in each of
three successive generations of rats given 5 ppm nickel in the drinking
water from weaning. Weber and Reid (1969) and Phatak and Patward-
han (1950) gave higher amounts of nickel salts to young rats through one
reproductive cycle without difficulties based on gross indices of re-
sponse (body weight, number of young, etc.~.
It is likely that diet composition may have a significant effect on
nickel toxicity. When Phatak and Patwardhan (1952) fed diets with
protein at 14 or 11 percent, the lower protein was associated with lower
concentrations of nickel in some of the rats tissues. This effect ap-
peared to be greater after 4 months as compared with 8 months of
feeding 250 ppm nickel as a catalyst. The effect of dietary protein
OCR for page 352
352 MINERAL TOLERANCE OF DOMESTIC ANIMALS
should be investigated further, particularly since nickel markedly
reduces nitrogen retention (Weber and Reid, 1968, 1969; O'Dell et al.,
1970b). Changes in tissue concentrations of zinc, iron, manganese,
copper, and chromium may mean that alterations in dietary levels of
these elements would modify nickel toxicity.
When long-term nickel poisoning is discovered, an immediate switch
to diets with low or normal nickel levels should be made. O'Dell et al.
(1970b) removed excess nickel from the diet of male calves after 8
weeks of feeding. Those previously fed 1,000 ppm nickel as the car-
bonate had suffered a small weight loss; however, they gained the same
amount of weight as the controls during a Week recovery
period. Phatak and Patwardhan (1952) fed young rats 250 ppm nickel as
the catalyst for 8, 12, or 16 months, and then the nickel was removed.
Nickel was excreted in urine and feces until nondetectable levels were
found for feces by 20 days and urine by 40 days. The kidney still
retained significant nickel at this point.
TISSUE LEVELS
Animals fed basal diets with no added nickel had tissue concentrations
of nickel that were generally below 1 ppm fresh weight (Phatak and
Patwardhan, 1950, 1952; Schroeder et al., 1963, 1964, 1974; O'Dell et
al., 1971; Whanger, 19731. For general purposes of comparison, a 70
percent moisture content was assumed for values reported on a dry
weight basis. Tissues or body fluids with the lowest concentrations
were bile, serum, vitreous humor, brain, pancreas, red blood cells,
skin, and tongue. Tissues in the moderate to high range included heart,
kidney, liver, and lung. The spleen and testes varied between studies
from low to high and moderate nickel concentrations, respectively.
Schroeder et al. (1974) observed no significant increases oftissue nickel
in rats given 5 ppm nickel in drinking water throughout their lifetime
after weaning. There appeared to be higher levels of nickel in some
tissues of mice receiving nickel in drinking water for a lifetime
(Schroeder et al., 1963, 19641.
With supplemental nickel, the gastrointestinal tract of calves ac-
cumulated nickel in relation to dose (O'Dell et al., 1971~. Significant
increases occurred in the rumen-reticulum, omasum, and abomasum.
There was a progressive decline in nickel concentration from the
duodenum to the upper half of the remaining small intestine and the
lower small intestine. In most studies, high levels of dietary nickel, such
OCR for page 353
Nickel
353
as 1,000 ppm, caused significant increases (typically 10-fold) of nickel
in the tissues that were assayed. Severe growth depression was also
found in these animals, which complicates interpretation of the data.
Whanger (1973) found increased nickel in liver and kidneys of rats fed
500 ppm nickel; the limited data of Phatak and Patwardhan (1950)
support this observation. When Phatak and Patwardhan (19S2) ana-
lyzed rats after 4, 8, 12, and 16 months of feeding 250 ppm nickel as the
catalyst, maximal concentrations of nickel in the liver, kidney, and
spleen were attained by 8 months. Phatak and Patwardhan (1950) found
significant nickel in newborn pups of mothers fed 500 or 1,000 ppm
nickel as the carbonate.
Nickel was not increased in the milk of dairy cows fed 145 mg nickel
per day for 2 months (Archibald, 1949) or 365 or 1,835 mg per day for
6 weeks (O'Dell et al., 1970a).
MAXIMUM TOLERABLE LEVELS
In only one study, S ppm nickel in the drinking water of rats from
weaning caused death of young in three generations and runting in the
first and third generations. Mice tolerated this level. Although 100 ppm
nickel as the chloride decreased food intake of calves, 500 ppm nickel
as the carbonate were required for this effect. Five hundred parts per
million nickel reduced growth and nitrogen retention of chicks. In most
experiments 1,000 ppm had marked adverse effects. These included
decreased growth rate or even weight loss, changes in red blood
cell numbers and hemoglobin (both increases and decreases were re-
ported), accumulation of nickel, and alterations in tissue concentra-
tions of several essential elements. Emesis was produced in dogs by
2,500 ppm nickel. Adaptive tolerance to high levels of nickel was
observed in dogs and rats. The single oral dose mso of nickel as the
acetate was 1 16 mg per kilogram of body weight for rats and 136 mg per
kilogram of body weight for mice. For cattle, the maximum tolerable
level was set at 50 ppm, based on the lack of adverse eject with nickel
chloride at this level. Additional data are needed for other species.
SUMMARY
Nickel is an essential element required for growth and iron absorption.
There is no evidence that nickel is ever deficient under practical condi-
OCR for page 354
354 MINERAL TOLERANCE OF DOMESTIC ANIMALS
lions and that nickel supplements would be beneficili. Data on the
toxicity of nickel have shown very wide variation in the amounts of
nickel to produce harTnfill effects. The toxicity can be affected by the
form of nickel, species, age, reproductive status, duration of adminis-
tration, and nutrient content of the diet.
OCR for page 355
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OCR for page 362
362 MINERAL TOLERANCE OF DOMESTIC ANIMALS
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Representative terms from entire chapter:
rats fed
