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OCR for page 553
Z.
1nc
Zinc (Zn) has been used by man for utilitarian or ornamental purposes
for almost 2,000 years. Semitic bronzes dating from 1400 to 1000 B.C.
have been found to contain as much as 23 percent zinc. The metal is
bluish-white, lustrous, relatively soft, and forms distorted hexagonal
closely packed structures. Zinc constitutes 0.002 percent of the earth's
crust. The principal zinc-bearing ores are sphalerite and wurzite and
their weathering products, particularly smithsonite and hemimorphite.
Minor ores include zincite and willemite.
The principal commercial uses of zinc are for galvanizing iron, as a
component of alloys (bronze, brass, Babbitt metal, Ghan silver, and
special alloys for die casting), and in dry cell batteries, castings, and
printing plates. Zinc oxide is used in rubber because of its high heat
capacity, conductivity, and capacity for scavenging free sulfur. In-
organic salts of zinc are used in ceramic glazes and in dyeing. Two
fungicides, zineb and ziram, are organozinc compounds. The zinc on
galvanized iron is a sacrificial coating that is stable in dry atmospheres,
but forms a film of gray hydrated basic carbonate in moist atmospheres.
The American Society of Testing Materials has established maximal
levels of lead, iron, and cadmium for five grades of slab zinc. The
permissible levels for the highest and lowest grades are 0.003 and 1.60
percent lead, 0.003 and 0.05 percent iron, and 0.003 and O.SO percent
cadmium, respectively. Contact of foods with galvanized metal can
lead to contamination, not only with zinc, but also with the toxic
elements lead and cadmium. Zinc usage in the United States in 1975
553
OCR for page 554
554 MINERAL TOLERANCE OF DOMESTIC ANIMALS
(metric tons) was as follows: for galvanizing, 341,906; in zinc-base
alloys, 3 12,516; in brass, 236,172; as the oxide, 120,048; as rolled zinc,
24,773; and other uses, 82,069.
Zinc is known to be an important essential mineral for numerous
species. Many animal diets require supplementation with a concen-
trated form of the element due either to low total amounts of zinc or to
its low bioavailability from the diet. The level of available dietary zinc
can influence the net absorption, metabolism, and function of other
elements. Signs of zinc toxicity include decreased growth rate, anemia,
decreased bone mineralization, bone deformities, and decreased
feather pigmentation. The choice of appropriate forms and levels of
zinc supplements poses numerous practical problems ranging from
adequacy to safety.
The most extensive reviews of zinc are those by the National Re-
search Council (1978), two symposia edited by A. S. Prasad (1966,
1976), and a chapter by Underwood (19771.
ESSENTIALITY
Zinc is required for normal growth, development, and function in all
animal species that have been studied. Severe deficiency can lead to
death. Lesser degrees of deficiency are most pronounced during
periods of rapid growth and in those cells or tissues that either turn over
or grow most rapidly. Characteristics of deficiency include growth
retardation, delayed sexual maturation, alopecia, abnormal feathering,
skin lesions, hyperkeratinization of the esophagus, reduced numbers of
circulating lymphocytes, skeletal abnormalities, impaired reproduction
in both males and females, and fetal- abnormalities.
The importance of zinc supplementation for a food-producing animal
was demonstrated in 1955, when it was shown that parakeratosis in
swine was due to inadequate dietary zinc (Tucker and Salmon, 19551.
This disease, which caused great economic losses, was precipitated by
high levels of dietary calcium in the presence of vegetable proteins
containing phytate. The bioavailability of zinc was markedly reduced
so that a severe deficiency resulted.
Zinc requirements for young domestic animals and fowl range from
approximately 40 to 100 ppm in the diet.
OCR for page 555
Z.
Inc
METABOLISM
555
Zinc is absorbed from the intestinal tract in relation to need and the
primary route of excretion is in the feces. In addition to unabsorbed
zinc, small amounts of fecal zinc derive from bile, pancreatic secre-
tions, desquamated epithelial cells, and zinc secreted directly into the
gut along its length. Small amounts of zinc are lost in urine, sweat and
shed integumental tissues. The highest concentrations of zinc are found
in the tapetum ~uci~um~.S and 13.8 percent dry weight for the dog
and fox' respectively. The iris and choroid also contain high concentra-
tions. The prostate and its secretions are high in zinc. Otherwise, soft
tissue concentrations range from approximately 12 to 55 ppm wet
weight, varying somewhat between studies and species (Underwood,
1977).
The movement of zinc into and within the body is precisely regulated
at levels of intake within the requirement range. Zinc binds to sulf-
hydry1, amino, imidazole, and phosphate groups; thus, amino acids,
proteins, nucleic acids, and other organic molecules bind zinc under
physiological conditions. In general, readily available stores of zinc are
quite small, as dramatically reflected by drops In the plasma zinc values
to the deficiency range within 24 hours after changing to diets very low
In zmc.
Zinc activates some enzymes and is a component of a large number
of important metaDoenzymes (Riordan and Vallee, 19761. The latter
include carbonic anhydrase, carboxypeptidases A and B. alcohol de-
hydrogenase, glulamic dehydrogenase, mglyceraldehyde-3-phosphate
dehydrogenase, lactic dehydrogenase, malic dehydrogenase, alkaline
phosphatase, aldolase, superoxide dismutase, ribonuclease, DNA poly-
merase, and others. The metal is located at the active site of the zinc
metaDoenzymes and is involved In the catalytic process. Zinc
may function in maintaining the secondary, tertiary, or quaternary
structure, depending on the enzyme. Zinc also plays a role In the
configuration of DNA and RNA. The biochemical functions of zinc have
recently been reviewed (Cheaters, 19781.
SOURCES
Underwood (1977) summarized information on the zinc content of ani-
mal feeds. Values for pasture herbage ranged between 17 and 60 ppm
dry weight, with most values faking between 20 and 30 ppm. Industrial
pollution increased the zinc content of grass from 5- to 50-fold (Milis
OCR for page 556
556 MINERAL TOLERANCE OF DOMESTIC ANIMALS
and Dalgan~o, 1972). Cereal grains typically contain 20 and 30 ppm
zinc, whereas soybean, peanut, and linseed meal contain 5~70 ppm.
Fish meal, whale meal, and meat meal may contain 9~100 ppm zinc.
The present drinking water standard is 5 ppm zinc (National Re-
search Council, 19781. This concentration of zinc is almost never found
In surface water, municipal drinking water supplies, or in drinking
water collected at the home tap. Industnal polBution, such as that
derived from dumping plating baths or mining operations, can produce
very high concentrations of zinc. Streams tend to become purified by
precipitation of zinc with clay sediments or hydrous iron and manga-
nese oxides. A concentration of 25 ppm zinc was recommended as a
safe upper limit in drinking water for livestock and poultry (National
Research Council, 19741.
Inorganic salts of zinc, such as the oxide, carbonate, acetate, chIo-
r~de, or sulfate, and even metallic zinc serve as readily available
sources for the animal. Even those salts that are insoluble in water are
solubilized by gastric juice. Only the zinc in a few ores was found to be
unavailable to the chick (Edwards, 19591. Crucle sources of zinc should
be checked for cadmium and lead. Dietary phytate, which can be sum
plied by whole seeds and certain seed fractions, decreases the avail-
ability of zinc for animals without a functional rumen.
Contamination of food and water with large amounts of zinc can
occur upon storage in galvanized containers, particularly under acidic
conditions. This type of exposure can be fatal but most frequently
produces gastrointestinal distress, emesis, and/or refusal of the animal
to eat the food. Other potential sources of excess zinc include pesti-
cides, fungicides, and industrial pollution.
TOXICOSIS
LOW LEVELS
In most of the studies summarized in Table 41, no adverse physiological
effects were observed at dietary concentrations lower than 600 ppm
zinc. In several studies animals appeared grossly normal with far larger
dietary zinc concentrations. In studies where graded levels of zinc were
given, the most sensitive response was an increase in tissue zinc con-
centrations. In studies with low zinc levels that did not affect body
weight, decreases in rate of gain or losses of body weight were first
observed with dietary zinc levels of 900 ppm in cattle (Ott et al., 1966a);
OCR for page 557
Z.
Inc
557
19500 ppm in sheep (Ott et al.9 1966b); 2,000 ppm in swine (Brink et al.9
1959); 800, 1,500, and 2,000 ppm in chicks (Berg and Martinson, 1972;
Roberson and Schaible, 1960; and Johnson et al.9 1962, respectively);
4,000 ppm in turkeys (Vohra and Kratzer, 1968); and 270 ppm in young
Japanese quail (Hamilton et al., 1979). Davies et al. (1977) found that
week-old lambs were very sensitive to high zinc levels.
Miller et al. (1965) observed no adverse health effects or changes in
milk quantity or composition in cows fed 372 to 1,279 ppm zinc as the
oxide for 6 weeks. Small increases of zinc in milk with higher doses
were less than corresponding increases in plasma.
Dogs fed excess zinc in meals were unaffected by 400 mg zinc per
day, and the only effect of 800 mg zinc was to increase tissue concen-
trations of zinc (Drinker e' al., 1927~. Daily intakes of 59-196, 180, or
200 mg zinc did not affect cats (Drinker et al., 1927; Scott and Fisher,
1938; Mannell, 1967~.
Mice receiving 500 ppm zinc as the sulfate in their drinking water
appeared grossly normal after 1-14 months (Aughey et al., 19771.
Histological examination revealed hypertrophy of the adrenal cortex
and pancreatic islets. There was also evidence of pituitary hyper-
activity. This level of zinc would be similar to about 1,000 ppm in the
diet based on total consumption.
HIGH LEVELS
In most studies, supplemental zinc at 1,000 ppm in the diet or more
caused some adverse physiological effect. Reduced weight gains;
anemia; reduced bone ash; decreased tissue concentrations of iron,
copper, and manganese; and diminished utilization of calcium and
phosphorus were observed. Increased consumption of a mineral mix-
ture available ad libitum was observed in cattle and sheep fed excess
zinc (Ott et al., 1966a,b). The cattle also chewed wood. Sheep fed 750
ppm zinc, beginning with the sixth week of pregnancy, produced almost
no viable lambs (Campbell and Mills, 1979~. Sheep dosed intraruminally
with zinc sulfate developed diarrhea, lost weight? and died (Smith,
1977~. These changes were slow to develop with 20 mg zinc per kilo-
gram of body weight, but rapid with 180 mg per kilogram.
Grimmett et al. (1937) and Sampson et al. (1942) observed arthritis
and severe bone and cartilage abnormalities in the joints of the long
bones in pigs fed milk containing 268 ppm zinc plus small amounts of
grains. Brink et al. (1959) also observed an artl~itis-like syndrome,
internal hemorrhaging, and some mortality in swine receiving 2,000 or
OCR for page 558
558 MINERAL TOLERANCE OF DOMESTIC ANIMALS
4,000 ppm zinc. Cox and Hale (1962) and Hsu et al. (1975) did not
observe these changes in swine fed the same high levels of zinc.
Willoughby et al. (1972) produced severe swelling in the epiphyseal
region of long bones in horses receiving high levels of zinc that were
increased gradually from 25 to 186 mg per kilogram of body weight. The
horses became lame, anemic, had increased tissue levels of zinc, and
grew more slowly. Lameness was also observed in mallard ducks fed
3,000 to 12,000 ppm zinc (Gasaway and Buss, 19721. The ducks were
anemic, lost weight, and most of them eventually died.
Human beings exposed to excess zinc by the oral route have de-
scribed an unpleasant taste, gastrointestinal discomfort, and dizziness,
responses that animals cannot communicate. Cats were found to vomit
or refuse to eat a meal containing 320 or 400 mg zinc as the oxide (Scott
and Fisher, 1938~. Cows in two dairy herds accidentally received feed
in which magnesium oxide was replaced by zinc oxide (Allen, 1968~.
These high levels of zinc, 72 and 145 g per day, immediately produced
scours and declines in food consumption and milk production. With
the higher level, pulmonary emphysema, hemolytic anemia, and death
were observed.
Table 42 summarizes data on acute toxicosis of single oral doses of
zinc salts in small animals.
FACTORS INFLUENCING TOXICITY
Variability in response to excess levels of zinc is not unexpected when
one examines the extensive literature dealing with factors that can
affect zinc toxicity. Most of these studies have been carried out in rats
rather than food-producing or companion animals, which are the sub-
ject of this report.
The first defense against orally administered excess zinc is the
homeostatic mechanisms that limits absorption. By the use of 65 Zn, it
was shown that the initial whole-body retention of zinc by rats after
dosing was reduced by a factor of 3 when the dietary intake was 6 to 10
times normal (Furchner and Richmond, 19621. By more extensive
studies in Holstein bull calves, Miller et al. (1970, 1971) showed that
homeostatic mechanisms regulating zinc metabolism became markedly
less elective with 600 ppm dietary zinc as compared with 200 ppm.
Neither excess level caused any physiological abnormalities. With
tracer doses of 65ZnCI2 given at various time periods after feeding 600
ppm zinc to calves, Stake et al. (1975) showed that deterioration in
homeostasis affected specific tissues and organs at different rates.
OCR for page 559
Z.
Inc
559
Numerous studies in rats have shown decreases in tissue levels of
iron, copper, and copper-containing enzymes when excess zinc was
fed. Supplements of iron and copper were usually beneficial. The
antagonism of copper by zinc is very sensitive. This was shown
dramatically by Hill and Matrone (1962) in the chick. With a low-copper
diet that permitted normal growth but with slightly lowered hemoglo-
bin, the dietary addition of 100 ppm zinc caused growth depression and
mortality. With 200 ppm supplemental zinc, there was still further
reduction of growth and hemoglobin and an increase in mortality.
Young Japanese quail (Coturnix coturnix japonica ~ fed 1 ppm cop-
per, a marginally deficient level, were more sensitive to the effects of
excess zinc than birds fed 1.5 ppm, the requirement, or 3.6 ppm copper
(Hamilton et al., 1979~. The greater sensitivity with low-copper intake
was manifested by decreased body weight, lack of feather pigmenta-
tion, and in some cases by perosis. As little as 31.2, 62.5, and 125 ppm
zinc (in excess of the 20 ppm in the basal diet) produced significant
adverse effects with 1 ppm dietary copper. Concentrations of zinc and
manganese in the duodenum and liver were not affected by dietary
copper level; however, iron concentration in the liver was consistently
lower with the higher level of copper. Supplements of ascorbic acid
augmented the adverse effect of excess zinc on growth, feather pig-
mentation, and bone deformities in young quad! fed a diet marginally
deficient in copper (Fox et al., 1978~. The sensitive bone-joint abnor-
malities described in swine (Grimmest e! al., 1937; Sampson et al.,
1942) probably were related to a low-copper intake. Rats fed 1,200 ppm
zinc had decreased concentrations of elastin in aorta, skin, and
cartilage, changes suggestive of copper antagonism (Philip and Kurup,
1978).
All possible interactions between normal and high levels of zinc,
lead, and cadmium, and deficient and normal levels of calcium and
vitamin D, were studied in rats (Thawley et al., 19771. High zinc plus
high cadmium produced more severe anemia than either alone. A low-
serum iron level due to feeding high zinc was further reduced by low
calcium or high vitamin D. In rats deficient in calcium, high zinc aug-
mented the porotic process (Ferguson and Leaver, 1972~. With a defi-
ciency of calcium and vitamin D, zinc caused both porosis and osteo-
malacia, whereas in vitamin D deficiency zinc had a porotic effect on
bone and a mineralizing effect on dentine.
The level of dietary selenium was shown to be important in zinc
toxicity (Jensen, 19751. Chicks fed a natural-ingredient diet containing
0.2 ppm selenium and 8.8 flu added vitamin E showed exudative
OCR for page 560
560 MINERAL TOLERANCE OF DOMESTIC ANIMALS
diathesis, muscular dystrophy, decreased weight gains, and mortality
beginning with 2,000 ppm excess zinc. The mortality, exudative dia-
thesis, and muscular dystrophy did not occur when 0.5 ppm selenium
was added to the diet with zinc levels up to 4,000 ppm. The supple-
mental selenium did not affect body weight.
With the exception of the paper by Hamilton et al. (1979), diets fed
in the studies summarized in Table 41 were composed of nonpurif~ed
ingredients supplemented with minerals. The basal diet of Hamilton et
al. (1979) was a casein gelatin diet that contained required levels only
of zinc, iron, manganese, and magnesium. Copper was fed at various
levels, as discussed above, and other nutrients were near the required
amounts insofar as known. It is thought that sensitivity to excess zinc
with this diet reflects the level of essential nutrients, although the rapid
growth rate of the young quail may have been a contributory factor.
McCall et al. (1961) reported that rats fed diets containing 20 and 30
percent protein from soybean of} meal responded more favorably to
high dietary zinc than when casein supplied the same levels of protein.
Berg and Martinson (1972) reported greater sensitivity of chicks to
excess zinc with a sucrose-fish meal diet than with corn-fish meal,
sucrose-soybean, or corn-soybean diets. Growth of control birds was
somewhat less with the sucrose-fish meal diet. Replacement of sucrose
with corn (15 to 67 percent of the diet) effected incremental improve-
ments in growth of birds fed the basal diet alone or with 2,000 ppm zinc.
Very young sheep were affected more adversely by zinc in the form of
yeast than as zinc sulfate (Davies et al., 1977~. The yeast supplied all
of the dietary protein, whereas with zinc sulfate the diet was milk.
Numerous investigators have reported improvements in response to
toxic levels of zinc with a wide range of dietary supplements in addi-
tion to those described above. These include calcium and phosphorus
(Stewart and Magee, 1964; Hsu et al., 1975), liver extract (Smith
and Larsen, 1946; Magee and Matrone, 1960), distiller s dried solubles
(Magee and Spahr, 1964), and ethylenediaminetetraacetic acid (Vohra
and Kratzer, 19681. It is possible that dietary phytate and other food
components, which can decrease the bioavailability of required levels
of zinc, may also decrease the toxicity of zinc.
The effect of feeding low levels of three pesticides (P,P-DDT, 2.4
ppm; parathion, 0.33 ppm; and carbaryl' 2.3 ppm) with or without 7,000
ppm zinc was studied in female rats for a 4-month period that included
a pregnancy (Feaster et al., 19721. The pesticides alone had no adverse
effects. High zinc alone did not affect hemoglobin, but when combined
with pesticides there was a significant decline of hemoglobin in both
maternal and fetal blood. The high zinc level caused increased concen-
OCR for page 561
Zinc 561
"rations of one or more of the pesticides In maternal abdominal fat and
liver and in the fetal liver.
The recognition of chronic zinc poisoning in animals should be fol-
lowed by prompt removal of the source of exposure. Ott et al. (1966c)
fed calves 2,100 ppm zinc as the oxide for 12 weeks and then with no
zinc supplement for 6 weeks. Serum zinc declined rapidly during the
first 2 weeks after excess zinc removal; however, by 6 weeks it was still
slightly above the normal range. The high concentrations of zinc and
iron in the liver at 12 weeks declined when zinc was removed. At the
end of the Week period liver zinc was approximately 4 times normal
and liver iron approximately twice normal levels.
Johnson et al. (1962) fed chicks graded levels of zinc from hatching
to 10 weeks of age; the excess zinc was deleted between 10 and 16
weeks of age. Birds fed the levels of zinc that depressed growth, 3,000,
4,000, and 5,000 ppm; gained as much weight between 10 and 16 weeks
as birds that were unaffected by the initiad supplemental zinc. Although
some of the initial supplements of zinc increased liver zinc concentra-
tions several-fold, the values were normal by 16 weeks.
Attempts to reduce zinc toxicosis in turkey poults by feeding ethyI-
enediaminetetraacetic acid (EDTA) with very high levels of zinc were
unsuccessful (Vohra and Kratzer, 1968~. Addition of 15.4 or 30.8 milli-
moles of EDTA per kilogram of diet did not affect the growth of either
controls or zinc-fed birds.
TISSUE LEVELS
The most sensitive responses to excess dietary zinc were increases in
zinc concentrations in serum, liver, kidney, pancreas, and small in-
testine with bone almost as responsive. Sometimes zinc was higher in
the heart, but always remained unchanged in skeletal muscle. Increases
of zinc levels in one or more tissues have been observed with dietary
zinc levels of 200 and 500 ppm fed to cattle (Miller et al., 1970; Ott et
al., 1966c, respectively), 1,000 ppm fed to sheep (Ott e! al., 19666),
2,000 ppm fed to chicks (Johnson et al., 1962), and 125 ppm fed to
Japanese quail (Hamilton et al., 1979~. In general, tissue concentrations
are related to dose level. The wide variations in diet composition and
levels of zinc tested preclude precise comparisons to establish dif-
ferences between species. Murphy et al. (1975) summarized data on
human foods. Doyle and Spaulding (1978) compiled data on zinc in
liver, kidney, heart, and muscle of normal cattle, sheep, swine, and
chickens.
OCR for page 562
562 MINERAL TOLERANCE OF DOMESTIC ANIMALS
MAXIMUM TOLERABLE LEVELS
The data in Table 41 and the discussion of factors that can either
increase or decrease the severity of zinc toxicosis emphasize the diff~-
culty of establishing a maximum safe level. The types of diets of con-
cern here are practical diets composed primarily of natural ingredients.
With this type of diet, usually containing most or all nutrients in at least
modest excess of requirements, one would not expect any adverse
physiological effects of zinc at 500 to 600 ppm. Since a marked decline
in the homeostatic control of zinc occurred in cattle fed 600 ppm zinc,
it would seem desirable to limit zinc levels to no more than 500 ppm.
Sheep fed 750 ppm zinc during pregnancy produced almost no viable
young, whereas 150 ppm zinc had no adverse effect. The maximum
tolerable level for sheep was set at 300 ppm. Swine, turkeys, and
chickens performed normally with 1,000 ppm zinc in nonpurif~ed diets,
so this was set as the maximum tolerable level for swine and poultry.
With an adequate purified diet that contained most essential elements
at only required levels, 125 ppm zinc caused adverse effects in young
Japanese quail. Thus, caution is advised for pregnant animals and for
animals fed diets with essential nutrients at required levels only.
SUMMARY
Zinc is an important essential nutrient that is required at every stage of
the life cycle. It functions in a large number of zinc metalloenzymes.
For most species, overt toxicosis of zinc first appears when levels
around 1,000 ppm are incorporated into a natural-ingredient diet with
many nutrients above required levels. Lower levels of excess zinc
overwhelm the body's mechanism for regulating zinc metabolism and
effect changes in tissue concentrations of zinc and several other
minerals. With diets containing marginal levels of some minerals, much
less zinc produces adverse health effects. Signs of zinc toxicosis may
include gastrointestinal distress, emesis, decreased food consumption,
pica, decreased growth, anemia, poor bone mineralization, damage to
the pancreas, arthritis, white muscle disease, internal hemorrhaging,
and nonviable newborn. From considerations of deranged control of
zinc metabolism and overt toxicosis, maximum tolerable levels from
300 to 1,000 ppm zinc in the diet appear to be safe, depending on
species.
OCR for page 563
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Representative terms from entire chapter:
dietary zinc
574 MINERAL TOLERANCE OF DOMESTIC ANIMALS
TABLE 42 Acute Oral Toxicity of Zinc as Various Saltsa b
Species Salt TD~oC LDcoC =mc
Rat Zinc acetate, — 733
dibydrate
Rat Zinc chloride 168
Mouse Zinc chloride - 168
Hamster Zinc chloride 24
Guinea pig Zinc chloride — - 96
Hamster Zinc oxide -- 400
Hamster Zinc stearate -- 52
Rabbit Zinc sulfate — 810
Rat Zinc sulfate 891
Hamster Zinc sulfate 43 20
Rabbit Zinc sulfate, 436
heptahydrate
Rat Zinc sulfate. 502
heptahydrate
aPairchild et al., 1977.
lowest published toxic dose; ~Dco' lowest published lethal dose; ~D50, lethal dose,
505
zinc
575
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576 MINERAL TOLERANCE OF DOMESTIC ANIMALS
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