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OCR for page 93
Cadmium
Cadmium (Cd) is a silvery white metal that resembles aluminum. Cad-
mium constitutes about 0.000011 percent of the earth's crust. It occurs
geologically in zinc ores and is a by-product of zinc production, either
as a vapor from roasting zinc ores or as a sludge from zinc sulfate
purification. Several cadmium salts possess commercially desirable
colors, ranging from yellow through oranges and reds. Their heat resis-
tance makes them useful for ceramics, enamelware, and plastics. Al-
though the metal oxidizes readily, it is highly resistant to corrosion and
is widely used to plate iron and steel. Cadmium is also used in solders,
nickel-cadmium batteries, and in stabilizers for polyvinyl chIonde. The
U.S. industrial uses (in metric tons) of cadmium in 1974 were as fol-
lows: batteries, 544; pigments, 997; stabilizers, 906; plating, 2,718; and
others (including alloys), 441 (Stubbs, 19781. Mining and smelting
operations represent point sources of environmental pollution; how-
ever, the widespread sources are corrosion of metal-plated iron, clis-
carded cadmium-containing consumer products, and losses from indus-
trial operations such as plating baths. Inorganic fertilizers contain some
cadmium; however, the use of urban sewage sludges to fertilize pas-
tures or food croplands represents a potentially serious source of cad-
mium access to animal and human foods. Various aspects of cadmium
flow in the United States were described by Yost (1979~.
Similarities in chemical reactivity of zinc and cadmium lead to similar
metabolic pathways in biological systems. Whereas zinc is an important
essential element, cadmium is best known for its toxicity and metabolic
93
OCR for page 94
94 MINERAL TOLERANCE OF DOMESTIC ANIMALS
antagonisms of zinc and other essential elements. Anemia, bone de-
mineralization, and kidney damage are the principal adverse effects of
cadmium ingested in "moderate,' amounts. Higher levels can lead to
death. As evidence of long-term adverse effects of cadmium in man has
accumulated, any cadmium pollution of the environment is recognized
as a potentially serious health hazard to man.
The biological importance of cadmium lies been considered from a
variety of aspects in several reviews (Schroeder and Balassa, 1961;
Schroeder et al., 1967; Flick et al., 1971; Fr~berg et al., 1971, 1974;
Fassett, 1972; Neathery and Miner, 1975; FIeischeret all, 1974; Under-
wood, 1977~.
ESSENTIALITY
Very limited data suggest that cadmium may be an essential element.
In rats fed a highly purified diet containing <0.004 ppm cadmium, a
growth depression was observed when they were maintained in a metal-
free environment but not under conventional laboratory conditions
(Schwarz and SpaBholz, 1978~. The dietary concentrations that in-
creased growth are less than those of present human diets.
In studies of hypertension, Perry et al. (1977) maintained their rats in
stainless steel cages in a room designed to exclude airborne contami-
nants. Their specially prepared rye-based diet contained 0.0137 +
0.0019 (SD) ppm cadmium. During the first 18 months, rats receiving 1
ppm cadmium in the drinking water consistently weighed at least S
percent more than rats fed the control diet; however, a statistical analy-
sis was not presented.
METABOLISM
In this review, primary consideration will be given to the metabolism
and effects of cadmium taken orally. An extensive literature deals with
injected cadmium; however, it is not clear how applicable many of
these findings are to the effects of dietary cadmium.
There appears to be no homeostatic control mechanism to limit cad-
mium absorption and retention below a nontoxic threshold. With t09Cd,
absorption of cadmium in mice occulted irrespective of the body bur-
den, and cadmium was not cleared from the body by subsequent cad-
mium dosing (Cotzias et al., 1961~.
The intestinal tract limits cadmium absorption as discussed below.
OCR for page 95
Cadmium
95
There was little transfer of cadmium across the placenta in mice (Berlin
and UBberg, 1963), rats (Lucis et al., 1972; Pietrzak-Flis et al., 1978),
and cows (Neathery e' al., 1974~. Sonawane et al. (1975) found a higher
proportion of an injected dose of t09Cd, as the chIonde, was transported
across the placenta of pregnant rats late in pregnancy. The mammary
gland markedly limited cadmium transport into the milk of rats (Lucis
eta)., 1972) and cows (MiDeret al., 1967; Neathery et al., 1974; Sharma
et at., 19791. Very little cadmium was transported into avian eggs (Sell,
1975; Leach et al., 19791.
Me duodenum of the young Japanese quad! was shown to take up a
high proportion of ingested cadmium (Jacobs et al., 1974~. The cad-
m~um retained by the gastrointestinal tract appears to represent pr~-
marily the fraction that is most rapidly cleared from the body. This
phase usually takes 4 to 12 days in rats (Moore et al., 1973a; Kello and
Kostial, 1977), cows (Miller et al., 1968), and goats (Miller et al., 1969~.
Small amounts of injected doses of cadmium were excreted via bile and
the intestinal tract wall (Berlin and UlIberg, 1963; Cikrt and Tichy,
1974; Havrdova et al., 1974; Homer and Smith, 1975; Stowe, 1976~.
Urinary excretion of cadmium is typically very small; however, data in
humans suggest that it may be an index of body burden (Kjellstrom,
1979).
Absorption of cadmium was approximately 0.3 to 2.5 percent of a
single oral dose in rats (Moore et al., 1973b; Kello and Kostial, 1977)
and 5 percent of cadmium fed in the diet for 1 week to Japanese quail
(Jacobs et al., 197Sb). Growing sheep fed 60 ppm cadmium excreted 95
percent of their cadmium intake in the feces (Doyle et al., 19741. Miller
et al. (1969) estimated that 0.3 to 0.4 percent was retained by young
goats 14 days after an oral dose of i°9CdCl2. The intestinal tract still
retained a significant amount of cadmium. Similar results were obtained
for dairy cows (Neathery et al., 1974~.
The biological half-life for whole-body retention of orally admin-
istered cadmium was reported to be 206 days for rats (Moore et al.,
1973b), less than 200 days for mice (Richmond et al., 1966), 99 days for
Chipping sparrows (Anderson and Von Hook, Jr., 1973), and 116 days
for young Japanese quad! (Jacobs et al., 1978b). Perry et al. (1977) gave
rats 0, 1.0, 2.5, 5.0, 10.0, 25.0, or 50.0 ppm cadmium in the drinking
water for 2 years; subsets of animals were killed at 6-month intervals.
Assuming that the liver and kidneys accounted for half of the absorbed
cadmium in the body (as estimated by Friberg et al., 1974), the rats
retained 1 percent of the ingested cadmium at the end of the first year
and 0.6 to 0.9 percent at the end of the second year. The proportions
retained were similar for all dose levels.
OCR for page 96
96 MINERAL TOLERANCE OF DOMESTIC ANIMALS
Berlin and Ullberg (1963) injected ~°9CdCl2 intravenously into mice
and made sagittal whole-body autoradiographs of animals killed at in-
tervals from 5 minutes to 16 days after injection. Cadmium left the
blood rapidly and accumulated in the liver, kidney, gastrointestinal
mucosa, salivary glands, pancreas, hypophysis, adrenal, thyroid,
spleen, lymph glands, testes, hair follicles, heart, and major blood
vessels. Nordberg and Nishiyama (1972) also prepared autoradiographs
from whole-body sections of mice. They observed high cadmium con-
centrations in the liver, kidney, salivary glands, testicle, and pancreas
112 days after injection. Homer and Smith (1975) injected t°9CdCl2 into
the femoral vein of rats and measured i09Cd in 27 tissues and body fluids
at intervals between 5 minutes and 60 days after injection. After 24
hours, the concentrations of cadmium in most tissues remained rela-
tiveiy constant; however, the t09Cd content of the kidney gradually in-
creased throughout the experimental period. Cadmium per gram of
three muscles amounted to 0.02 to 0.03 percent of the total body burden
between 1 and 60 days.
Young Japanese quail were fed a diet containing ~~5mCd as the chIo-
ride (total 1 ppm cadmium) for 1 week followed by basal diet for 50 days
(Jacobs et al., 197Sb). At the end of the experiment, 3.58 percent of the
cadmium remained in the whole bird. This was distributed as follows:
liver, 24.~; kidney, 24.5; intestinal tract, 11.9; skin and feathers, 6.8;
and carcass, 33.7 percent. Miller e! al. (1969) found that 14 days after
a single oral dose of ~09CdC 12 in young goats, the tissue concentrations
of t09Cd were in decreasing order as follows: kidney, liver, duodenum,
and abomasum. Under similar conditions for cows, Neathery et al.
(1974) found the following sequence: kidney, liver, and small intestine.
The bovine fetal tissues with the highest concentrations were kidney,
tibia, and liver. Numerous investigators have demonstrated the rapid
concentrating effect of cadmium in the liver and kidney and the gradual
shift of cadmium from other tissues to the kidney. Cross-sectional
studies of human populations in the United States, Sweden, and Japan
showed 2.7- to 5.~fold increases of cadmium in muscle between ado-
lescence and middle age (Kjellstrom, 1979~. The biological half-time of
cadmium-109 in muscle, 77 days, was longer than that for liver and
kidney, 65 days, in adult male Japanese quail (A. O. L. Jones, FDA,
Washington, D.C., 1979, personal communication).
Margoshes and Vallee (1957) were the first to isolate an unusual
protein with a high metal content from equine renal cortex. Isolation
procedures and characterization of the protein, metallothionein, have
been studied by several workers (Kagi and Vallee, 1960; Pulido et al.,
1966; Shanks and Lucis, 1971; Nordberg et al., 19721. In 1974 Kagi et
OCR for page 97
Cadmium
97
al (1974) described the isolation and properties of equine hepatic and
renal metaBothioneins. The molecular weight of each was about 6,600.
Both were high in cysteine (approximately one-third of the amino acid
residues), whereas phenylalanine, tyrosine, tryptophan, and histidine
were absent. Both proteins exhibited considerable microheterogeneity
even within tissues from the same animal. The total metal content
(cadmium, zinc, and copper) for each protein was 6 g atoms per mole,
or one metal atom per three cysteinyl residues. Zinc was the predomi-
nant metal in the liver protein, and cadmium predominated in the kid-
ney protein. Bremner (1978) reviewed information on the distribution
of metadothionein in various tissues and its involvement in cadmium
metabolism.
SOURCES
The industrial uses of cadmium provide the largest sources of environ-
mentaRy hazardous amounts of cadmium. The points at which pollution
is most apt to occur begin with mining and smelting, followed by manu-
facturing, loss from manufactured products during use and when dis-
carded, and the reclamation and use of waste products contaminated
with cadmium. The air, water, and soil provide pathways by which
cadmium may be dissipated and enter animals and man either directly
or via the food chain. Numerous aspects of these problems have been
reviewed (Fassett, 1972; FIeischer et al., 1974; and Faberg et al., 1971,
1974).
Underwood (1977) reviewed the effects of pollution on the cadmium
content of animal feeds. Pollution has been shown to increase the
cadmium content of mixed pasture herbage by more than Refold. A
considerable portion of the cadmium taken up is retained by the root
system. Some plants, such as clover, have a special capacity for con-
centrating cadmium from the soil. Parts of the seed containing highest
concentrations of cadmium may be removed during mining to produce
somewhat lower cadmium concentrations in products for human use;
however, many of the cadn~um-rich by-products may be used in animal
feeds. Urban sewage sludges contain significant amounts of cadmium.
Use of high-cadmium sludges for fertilizing either animal or human food
croplands has been shown to increase substantially the cadmium con-
tent of animal and human foods (Council for Agricultural Science and
Technology, 1976~. Superphosphate fertilizers contain some cadmium,
but they do not supply nearly as much cadmium as equivalent fertilizer
application of most sludges. There are great variations in the capacity
OCR for page 98
98 MINERAl TOLERANCE OF DOMESTIC ANIMALS
of different plant species, varieties, and tissues to take up cadmium. In
general, the leaves contain the highest amounts. Leafy vegetables can
contain over 100 ppm cadmium (dry weight) without evidence of toxi-
cosis in the plant (Chancy and Hornick, 1978~. It was shown that
cadmium taken up by Swiss chard and romaine lettuce from sludge was
available for absorption by guinea pigs (Furr et at., 1976) and mice
(Chancy et al., 1978b), respectively. The seeds of some plants, such as
corn, contain less cadmium than the leaves, whereas for others, such
as wheat or soybeans, the quantities are similar. Cadmium uptake is
greater at lower soil pH, at lower soil organic matter, and at higher soil
temperature. Most forages and plant materials fed to animals contain
levels of cadmium well below 0.5 ppm on a dry weight basis Cable 12;
Underwood, 1977; Baker et al., 1979; Chaney et al., 1978a).
Feed phosphates from FIorida deposits typically contain 6 to 7 ppm
cadmium (D. J. Thompson, International Minerals and Chemical Cor-
poration, 1979, personal communication). Since these phosphates are
present at levels of approximately 1 percent in finished feeds, they
contribute 0.06 to 0.07 ppm cadmium to the diet.
Kopp and Kroner (1968) reported relatively low values for cadmium
in 1,577 samples of surface waters collected throughout the United
States. The mean for the 40 positive samples was 9.5 Ago.
Information on tissue levels of cadmium is summarized in Table 12.
The cadmium content of the unpurified basal diets, which was similar
to commercial diets for domestic animals, ranged from 0.18 to 0.32
ppm. These were for cattle, swine, and chickens. The highest level, 0.7
ppm, was in a grass diet for sheep in Scotland and the lowest level was
in a purified soy isolate diet for chickens which contained 0.07 ppm.
TOXICOSIS
The effects of various oral intake levels of cadmium in animals are
summarized in Table 11.
LOW LEVELS
Most studies of cadmium have been designed to define the effects of
high intakes, generally in a short period of time, rather than to establish
no-effect levels. With an adequate diet, 5 ppm dietary cadmium is the
level at which gross adverse effects are most apt to begin.
Mills and Dalgarno (1972) fed sheep diets with 3.5 ppm cadmium
during the latter part of pregnancy and for 7.5 to 8.0 weeks following
OCR for page 99
Cadmium 99
parturition. The lambs had normal copper and zinc levels in the liver at
birth, but these elements were markedly depressed at the end of the
experiment.
Hansen and Hinesly (1979) observed decreased liver iron and kidney
manganese in swine fed 0.47 ppm cadmium in the form of corn grown
on sludge-fertilized land. Controls received 0.1 ppm cadmium, the
background dietary level. Hepatocyte m~crosomal protein and
o-dealkylation of p-n~trophenitole were increased. Decreased egg pros
auction was observed by Leach et al. (1979) in hens fed 3 ppm cadmium
in a soy isolate diet. A similar effect did not occur with a nonpurif~ed
diet. As little as 1 ppm cadmium in the diet of young Japanese quad]
produced acute degenerative damage to the absorptive cells of the
intestinal viDi (Mason et al., 1977~. These changes became less marked
after continuous exposure for 28 or 49 days.
With 0.5 or 2.5 ppm cadmium in the drinking water, dogs ate nor-
mally and had no adverse effects during 4 years; pathological changes
in the kidney occulted with 5 ppm (Anwar et al., 1961~. Shortened life
span, kidney damage, arteriosclerosis, and ventricular hypertrophy oc-
curred in rats receiving 5 ppm cadmium in their drinking water
(Schroeder et at., 1965; Kanisawa and Schroeder, 1969~. Increased
sodium and water retention occulted in rats receiving 5 ppm cadmium
in their drinking water (Doyle et al., 1975~.
With 1 ppm of cadmium in the~d~inking water of rats, Perry et al.
(1977) showed that the systolic by pressure was-elevated at 12 and
18 months of exposure, but not at earlier or later periods. With 2.5 ppm
cadmium in the drinking water, blood pressure was elevated at 6, 12,
and 18 months. Ohanian et al. (1978) reported that rats genetically
sensitive to hypertension developed increases in blood pressure, car-
diac hypertrophy, and kidney damage with 1 ppm cadmium in the
drinking water. This hypertension was most pronounced with high salt
intake. The liver and kidney cadmium concentrations were highest in
those rats with highest blood pressure. Similar effects of cadmium and
salt either did not occur or were much smaller in a line of rats resistant
to hypertension. The two lines were derived from the same pool of
Sprague-Dawley rats.
HIGH LEVELS
Details of conditions that caused cadmium toxicity are presented in
Table 1 1.
The higher levels of cadmium produced a wide range of changes in
metabolic measurements that have been observed in one or more spe-
OCR for page 100
100 MINERAL TOLERANCE OF DOMESTIC ANIMALS
cies. These include decreased serum ceruloplasmin, decreased renal
leuc~ne aminopeptidase, decreased bone ash, decreased serum albu-
n~n, increased serum ~2-, it-, and >-bobbins, =d increased transfer-
rin. Tissue mineral level changes include decreased iron and copper in
liver, increased zinc in the liver and kidney, increased copper in the
kidney, and decreased zinc and iron in the tibia. Decreased tissue levels
of zinc, copper, and iron have also been reported for the newborn.
In the young animal, cadmium can reduce growth rate. Cadmium can
cause anemia (decreased hemoglobin, hematocrit, and red blood cell
counts), neutrophilia, lymphocytopenia, enteropathy, renal tubular
damage, bone marrow hypoplasia, decreased granulation of the adrenal
medulla, hypertrophy of the heart ventricles, hypertension, and spleno-
megaly. Sheep fed cadmium have lost the crimp in their wool, a charac-
teristic of copper deficiency. Shortened life span was reported for
animals that were otherwise reasonably healthy.
Reproductive problems related to ingested cadmium have been pro-
duced in cattle, sheep, goats, and mice. These included abortions,
deformed young, atrophy of ovaries, testicular hypoplasia, decreased
egg production, decreased egg weight, and infertility (Table 111. At
very high levels cadmium can cause death. The oral ~D50 for four species
(dogs, rats, mice, guinea pigs) ranged from 39 to 107 mg/kg of body
weight.
FACTORS INFLUENCING TOXICITY
Since cadmium is retained in the body so long, factors that influence the
absorption of small amounts of cadmium are important as well as fac-
tors that modify overt cadmium toxicity. Several physiological consid-
erations have been shown to be important. Male rats retained less
cadmium than females (Kello et al., 1979~. Newborn rats had a very
high absorption of cadmium (Kello and Kostial, 1977; Sasser and Jar-
boe, 19771. The palatability of diets containing 40 ppm cadmium was
not involved in toxicosis in cattle (Powell et a]., 1964a). Cousins e! al.
(1977) found that inanition was not a factor in most of a large number
of toxic changes produced in rats by dietary cadmium.
Terhaar et al. (1965) reported that doses of cadmium as low as 0.01
mg/kg protected against 100 mg/kg given 24 hours later. Protection was
observed with pretreatments administered between 2 weeks and 7
hours prior to the large dose. The effects of cadmium and zinc on
induction of metallothionein synthesis have been studied by many in-
vestigators, including the relation of the preexisting metallothionein in
protecting against acute cadmium toxicity (Leber and Miya, 1976;
OCR for page 101
Cadmium
101
Webb and Verschoyle, 1976; Probst e! al., 19771. The relationships of
zinc and cadmium to metallothionein synthesis and degradation have
been reviewed (Cousins, 19791.
Valberg e' al. (1977) found that an oral dose of cadmium bound in
thionein was taken up by the intestinal mucosa to the same extent as
cadmium as the chloride. Less of the cadmium in thionein was trans-
ported out of the mucosa, and the cadmiu~thionein caused severe
mucosal lesions, whereas cadmium as the chloride caused little dam-
age. The bioavailability of cadmium in animal and plant products as
incorporated into feeds needs investigation.
With respect to interactions between cadmium and other nutrients,
many of these result from the effects of cadmium in markedly altering
tissue concentrations of several minerals. The relationships of specific
nutrients to the effects of cadmium have been reviewed (Fox, 1974,
1979a; Bremner, 1978~. In animals receiving marginal or deficient levels
of zinc, cadmium caused either the appearance or exacerbation of the
signs of zinc deficiency, including lower tissue levels of zinc. With
higher levels of dietary zinc, the effects of cadmium were lessened or
entirely counteracted. These studies have been earned out in turkeys
(Supplee, 1961), chicks (Supplee, 1963), calves (Powell e' al., 1964b,
1967), goats (Powellet al., 1967), and rats (petering et al., 19711.
Bunn and Matrone (1966) fed cadmium to copper-def~cient rats and
mice. The cadmium caused decreased weight gains and lowered hemo-
giobin; these effects were almost completely overcome by supplements
of copper and zinc. When Campbell and Mills (1974) fed only the
copper level required by the rat for growth and hemoglobin formation,
as little as 1.5 ppm of cadmium in the diet caused decreased plasma
ceruloplasmin. Under similar experimental conditions, Davies and
Campbell (1977) found that 4.4, 8.8, and 17.6 ppm of cadmium
markedly increased the uptake of 64Cu by the duodenal mucosa; how-
ever, 17.6 ppm of cadmium decreased the absorption of the 64Cu dose.
As dietary cadmium increased, there was an inverse relation between
the copper and cadmium concentrations in a low-molecular-weight pro-
tein fraction isolated from the intestinal mucosa.
Van Campen (1966) demonstrated that cadmium could interfere with
copper absorption from ligated intestinal loops in rats. Starcher (1969)
showed that oral administration of a very large dose of cadmium dis-
placed copper from a tow-molecular-weight mucosal protein. He sug-
gested that the protein was important in copper absorption. Evans et al.
(1970) reached similar conclusions from in vitro studies of the effect of
cadmium on copper binding to bovine low-molecular-weight proteins
isolated from the duodenum and liver.
OCR for page 102
102 MINERAL TOLERANCE OF DOMESTIC ANIMALS
HE et al. (1963) fed 25 to 400 ppm of cadmium to chicks in a copper-
and iron deficient diet. Supplements of copper, zinc, and iron each par-
tiaBy corrected the adverse effects of cadmium. Stowe et al. (1974)
found pyndox~ne deficiency to protect against the anemia causes! by
cadmium in rats. Banis et al. (1969) showed that supplements of iron
and zinc had marked protection against cadmium in the rat. Fox et al.
(1971) showed that iron (II) was much more protective against cadmium
than iron (III) anti that the cadmium antagonism was primarily that for
iron (IlI). Pond and Walker (1972) reported that injected iron prevented
the anemia associated with feeding cadmium to rats. Freeland and
Cousins (1973) found that cadmium decreased iron absorption in
chicks. Hamilton and Valberg (1974) found that low amounts of cad-
~um inhibited only mucosa] iron uptake, whereas larger amounts
diminished both uptake and transfer of iron. Dunng high iron absorp
tion by iron-deficient mice, the absorption of cadmium was greater than
in iron-replete animals absorbing less iron.
Vitamin C has been shown to decrease markedly the toxicoses pro-
duced by dietary cadmium in young Japanese quail as shown by im-
provements in the following responses: depressed growth, anemia,
decreased bone mineralization, depression of spermatogenesis, bone
marrow hyperplasia, and decreased granulation of the adrenal (Fox and
Fry, 1970; Fox et al., 1971; Richardson et al., 19741. Ascorbic acid
supplements normalized most of the changes in tissue- mineral concen-
trations produced by cadmium. It appears that the primary effect of
ascorbic acid was to improve iron absorption. Tissue cadmium concen-
trations were not affected.
Decreased bone mineralization resulting from oral cadmium intake is
noted in Table 11. Itokawa et al. (1973) observed a marked curvature
of the spinal column in rats fed cadmium in diets that were low in zinc,
calcium, and protein. In a subsequent experiment with rats fed calcium-
deficient diets, dietary cadmium caused renal hypertrophy, degenera-
tion of ~omeruli and tubules, thinning of cortical osseous tissue,
decreased osteocytes, and decreased acid mucopolysacchandes in epi-
physeal cartilage (Itokawa et al., 1974~.
Increased kidney and liver levels of cadmium have been found in
mice fed diets low in calcium, with cadmium supplied by polluted rice
(Kobayashi et al., 19711. Similar effects of a low-calcium diet on cad-
mium levels in the kidney cortex were obtained by Larsson and Pisca-
tor (1971) and Pond and Walker (l97S) in rats fed purified diets. Ando
et al. (1977) found a marked increase in the fecal and urinary excretion
of either an oral or an intravenous 47Ca dose by rats that had received
10 mg cadmium per day by Savage. The uptake of 47Ca by bone was
OCR for page 103
Cadmium 103
decreased in cadmium-exposed rats irrespective of the route by which
47Ca was administered.
Washko and Cousins (1976) gave a dose of ~09Cd by stomach tube to
calcium-def~cient rats and controls. The calcium-deficient rats had
greater amounts of the cadmium dose in the intestinal mucosa, serum,
lungs, liver, and unne, with less in the feces. Cadmium bound to a
low-molecuIar-weight protein in the intestinal mucosa was present in
greater amounts in calcium-deficient rats. Except for the lungs, they
found no effects of calcium deficiency on the distribution of an injected
dose of ~09Cd. Subsequently, Washko and Cousins (1977) found a simi-
lar distribution pattern in calcium-deficient and control rats that had
received cadmium in drinking water for ~ weeks. Rats fed a low-
calcium diet had a greater capacity to absorb either calcium or cad-
m~um. There was enhanced binding of 45Ca and itsmCd to intestinal
calcium-binding protein, and it was concluded that this was the factor
responsible for increased cadmium absorption in calcium deficiency.
The relationships between calcium and cadmium are especially im-
portant because the painful cadmium-induced disease, Itai-Itai Byo,
occurred in human beings consuming a low-calcium diet (Friberg et al.,
19711. The patients were postmenopausal women who had borne many
children. The primary features of the disease were kidney damage and
loss of bone mineral, which resulted in multiple fractures.
Because of its role in calcium metabolism, the effects of vitamin D on
cadmium metabolism and toxicosis have also been investigated. When
rachitic chicks were treated with vitamin D, Worker and Migicovsky
(1961) observed an increased cadmium uptake by the tibia. Cousins and
Feldman (1973) found no effect of vitamin D upon cadmium uptake in
liver and kidney when the vitamin was administered to vitamin D-
deficient chicks. In other experiments, they observed an in vitro effect
of cadmium in decreasing conversion of 25-hydroxycholecalciferol to
1,25-dihydroxycholecalciferol by kidney homogenates and isolated
mitochondria from vitamin D-deficient chicks. They also showed de-
creased conversion by kidney mitochondria from chicks that had
received 50 ppm cadmium in their drinking water (Feldman and
Cousins, 1973~.
Suzuki et al. (1969) produced a rapid effect on cadmium absorption
by feeding a low-protein diet to mice for 24 hours before and 24 hours
after an oral dose of ii5mCd. This treatment caused a significant increase
in the uptake of cadmium by the liver, kidneys, and whole body. In
Japanese quad! receiving 75 ppm cadmium, toxicosis was markedly less
with dried egg white as the protein source than with either soy isolate
or casein plus gelatin (Fox et al., 19731. With very low levels of dietary
OCR for page 120
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124 MINERAL TOLERANCE OF DOMESTIC ANIMALS
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Representative terms from entire chapter:
cadmium toxicity
