|
Items in cart [0] |
Questions? Call 888-624-8373 |
| Copyright © 2009. National Academy of Sciences. All rights reserved. Terms of Use and Privacy Statement |
Below are the first 10 and last 10 pages of uncorrected machine-read text (when available) of this chapter, followed by the top 30 algorithmically extracted key phrases from the chapter as a whole.
Intended to provide our own search engines and external engines with highly rich, chapter-representative searchable text on the opening pages of each chapter.
Because it is UNCORRECTED material, please consider the following text as a useful but insufficient proxy for the authoritative book pages.
Do not use for reproduction, copying, pasting, or reading; exclusively for search engines.
OCR for page 227
Todine
It is believed that the Chinese, many centuries B.C., had learned by trial
and error that substances in certain marine products exerted beneficial
effects upon the thyroid. Burnt sponges and seaweed were added to the
diet during the time of Hippocrates (46~370 B.C.) to relieve enlarged
thyroids. It was not known until discovered by Davy in 1815 that the
efficacy of burnt sponges and other marine products were due to the
presence of iodine (I), an element discovered by Courtois in 1811.
Probably the first to recommend the use of iodine in salt as a means of
preventing goiter was Koestl, who in 1895 began its use in Austria. The
view that iodine is an essential component of a protein molecule synthe-
sized by the thyroid began to take form shortly before 1900. By 1914
Kendall had isolated crystalline thyroxine from thyroid tissue. The
empirical formula for thyroxine was established in 1926 by Harrington,
who estimated that 40 percent of the total iodine present in the thyroid
is contained in thyroxine.
The use of iodine in livestock production is not limited to its role as
a nutrient in feed. Iodine in the form of ethylenediaminedihydriodide
(EDDI) is used at relatively high levels to prevent or treat foot rot and soft
tissue lumpy jaw in cattle (Miller and Tillapaugh, 1966~. Iodine-
containing products such as iodophors are widely used in the dairy
industry as teat dips and udder washes. Iodophor solutions are also
used as sanitizing agents for cleansing equipment.
227
OCR for page 228
228 MINERAL TOLERANCE OF DOMESTIC ANIMALS
ESSENTIALITY
Iodine is an essential element for animals and man. Although nearly
every cell in the body contains iodine, the thyroid gland is the main
location of iodine reserve. The thyroid hormones, which contain
iodine, are known to have a role in thermoregulation, intermediary
metabolism, reproduction, growth and development, hematopoiesis
and circulation, and neuromuscular functioning. The role. of iodine in
thyroid function and the manifestation of iodine deficiency in various
species have been described by Evvard (1928), Riggs (1952), and Ber-
son (1956~.
METABOLISM
Iodine occurs in foods largely as inorganic iodide and is absorbed in this
form from all levels of the gastrointestinal tract (Underwood, 19771. In
the ruminant the rumen is the major site of absorption of iodine and the
abomasum the major site of endogenous secretion (Barua e' al., 19641.
After absorption the iodide is rapidly distributed throughout the body.
The major sites of iodine concentration are the thyroid and the kidney.
In addition, iodine is concentrated by the salivary glands, stomach, skin
and hair, mammary gland, placenta, and ovary (Gross, 19621. The
iodide trapped by the thyroid is rapidly oxidized and converted to
organic iodine by combination with tyrosine. This process also occurs
in the lactating mammary gland and to a very small extent in the ovum
within the ovary. In the other sites the element remains in the form of
iodide. The iodide pool is replenished continuously, exogenously from
the diet and endogenously from the saliva, the gastric juice, and the
breakdown of hormones produced by the thyroid. Iodine is lost from
the iodide pool by the activities of the thyroid, kidneys, salivary glands,
and gastric glands, which compete for the available iodine. Iodine is
lost from the body mainly in urine and milk, with smaller amounts
appearing in the feces and sweat.
SOURCES
Iodine is widely distributed in nature, but it is present in both organic
and inorganic substances in very small amounts. Only in a few sub-
stances, such as the saltpeter deposits of Chile and some marine prod-
ucts, do concentrations of up to 1,000 to 2,000 ppm occur. Iodine is
OCR for page 229
iodine
229
present in soil, air, and water and becomes a constituent of plants and
animals used for food. The iodine content of water reflects the iodine
content of the rocks and soils of the region. Plants vary widely in iodine
content, depending on the species of plant and the iodine content of the
soil. Hemken et al. (1972), in a study of milk iodine and dairy cattle
performance, collected feed samples from Maryland and Illinois farms.
Samples of hay from Maryland farms contained 1.31 to 2.54 ppm
iodine, while those from Illinois contained 0.62 to 1.02 ppm iodine. The
Chilean Iodine Educational Bureau (1952) reported that oilseed meals
(soybean, cottonseed, linseed, and peanut) contained 0.11 to 0.2 ppm
iodine. Products of animal origin, other than fish meal, do not contain
significant levels of iodine, unless animals from which they were ob-
tained ingested large amounts of the element. Iodine sources permitted
as feed additives include calcium iodate, calcium iodobehenate, cup-
rous iodide, 3,5-diiodosalicylic acid, ethylenediaminedihydriodide
(EDD~) pentacalcium orthoperiodate, potassium iodate, potassium
iodide, sodium iodate, sodium iodide, and thymol iodide. A review of
the biological availability of some iodine compounds is presented by
Ammerman and Miller (1972~.
TOXICOSIS
More than a century ago, in practically all of the goiter areas of Europe
there occurred a wave of enthusiasm for the use of some form of
inorganic iodine in the treatment and prevention of goiter. It appears
that indiscriminate use of various iodine preparations was practiced
with many cases of poisoning. In 1860 Rillet presented to the French
Academy of Medicine a classical description of the toxic symptoms that
follow overdosage of iodine. Iodine toxicity has been studied in many
laboratory animals, dogs, poultry, swine, and cattle. Significant species
differences exist in tolerance to high levels of iodine. Prolonged ad-
ministration of large doses of iodine markedly reduces iodine uptake by
the thyroid, thus causing antithyroidal or goitrogenic effects. All
species appear to have a wide margin of safety for this element.
LOW LEVELS
In a series of trials, Newton et al. (1974) fed graded levels of calcium
iodate to give iodine levels ranging from 10 to 200 ppm iodine to calves
having an initial weight of about 100 kg. Elevated levels of dietary
iodine depressed growth rate and feed intake, with the depression being
OCR for page 230
230 MINERAL TOLERANCE OF DOMESTIC ANIMALS
significant for diets containing 50, 100, or 200 ppm added iodine. The
feeding of either 100 or 200 ppm iodine, and in some cases lower levels,
produced toxic signs that included coughing and nasal discharge. All
levels of added iodine increased serum iodine, and calves fed 200 ppm
had significantly lower blood hemoglobin and serum calcium. Calves
fed diets with added iodine tended to have heavier adrenal glands, but
there was no consistent iodine effect on the weight of the thyroid
Bands. Based on trends in growth rate and adrenal weights, Newton et
al. (1974) concluded that 25 ppm iodine was undesirable, and 50 ppm
appeared to be the minimum toxic level for calves.
Fish and Swanson (1977) found that calves weighing about 100 kg
tolerated 20 and 40 ppm iodine (from EDDY) with no untoward effects, but
daily gains were slightly depressed at 86 and 174 ppm. Iodine levels of
71, 140, and 283 ppm had no effect, but a level of 435 ppm depressed
daily gains in yearling (320 kg) heifers (Fish and Swanson, 19771. These
authors fed lactating dairy cows levels of iodine as high as 314 ppm for
12 weeks and found no adverse effect on milk production. Convey et at.
(1978) showed that lactating cows receiving about 200 ppm iodine (from
EDDIE for 49 weeks exhibited no aberrations in thyroid or pituitary func-
tion. When EDDY supplied iodine at levels of 2.5 mg/kg body weight and
below to pregnant cows, there was no significant effect on cows or their
calves. Levels of EDD' that supplied 5.0 and 7.5 mg iodine per kilogram
of body weight increased the incidence of premature calving, weals or
abnormal calves at birth, and stillborn calves (E. W. Swanson, Uni-
versity of Tennessee, personal communication).
Calves having an initial weight of 120 kg were given doses of 0' 50,
250, and 1,250 me iodine (as Emit per head per day for 6 months
(Haggard, 1978~. Determinations included titers to brucellosis, lepto-
spirosis, and infectious bovine rhinotracheitis (IBR) vaccinations. This
author found that the brucellosis and leptospirosis titers of calves in the
control and two lower levels of iodine were significantly higher than
those of calves given 1,250 mg iodine per day. The levels of iodine had
no effect on IBR titers. Hayed (1978) also showed that the white blood
cells with plasma and without plasma from calves of the control group
demonstrated greater in vitro phagocytic activity than white blood cells
from calves on all iodine levels. The white blood cell counts of calves
dosed with either 250 or 1,250 mg iodine per day were less than control
calves and calves dosed with 50 mg iodine per day. Rosiles e' al. (1975)
found that calves (192 kg) fed 500 mg EcD' per day coughed more, had
greater nasal discharge, and exhibited greater lacrimation than those
fed a daily dose of 50 ma. Neither the 5~ nor 500-mg level of EDD! had
any eject on growth rate of the calves.
OCR for page 231
Lorraine
231
McCauley et al. (1973) administered by capsule iodine, either in the
form of potassium iodide or EDIT, to lambs weighing about 30 kg. Iodine
was given daily for 22 days at levels of 150, 300, 450, and 600 mg per
lamb per day. Coughing was observed in lambs given large doses of
iodide, and these animals had higher mean rectal temperatures. Body
weight gains were depressed by daily intakes of 393 mg potassium
iodide (300 mg iodine) or 562 mg EDDY (450 mg iodine) per lamb per day.
Pigs are more tolerant of excess iodine than cattle. Newton and
CIawson (1974) fed levels of iodine ranging from 10 to 1,600 ppm to
growin~finishing pigs and found that the minimum toxic level was
between 400 and 800 ppm. Growth rate, feed intake, and hemoglobin
levels were depressed at 800 and 1,600 ppm iodine, and liver iron levels
were significantly depressed at 400 ppm. Arrington et al. (1965) fed
pregnant sows either 1,500 or 2,500 ppm iodine for 30 days before
Harrowing. These levels of iodine did not adversely affect reproductive
performance.
Using potassium iodide as the iodine source, Wilgus et al. (1953)
found no adverse effect on the performance of chicks fed 500 ppm
iodine up to 6 weeks of age followed by 180 ppm from 6 weeks through
maturity and the laying period. These workers found that 50 ppm in the
breeder ration caused a reduction and delay in hatchability. Excessive
levels of dietary iodine were shown to have a profound effect on egg
production and hatchability (Perdomo et al., 1966; Arrington et al.,
1967; Marcilese et al., 1968~. When laying hens were fed 625 to 5,000
ppm iodine, egg production varied inversely with level of iodine and
ceased with intakes of 5,000 ppm (Arrington et al., 1967~. The fertility
of the eggs was not affected, but early embryonic death, reduced hatch-
ability, and delayed hatching resulted. Egg production commenced
within 1 week after cessation of iodine feeding. Roland et al. (1977)
reported that serum calcium was significantly increased in laying hens
that received diets containing 5,000 ppm iodine. This level of iodine
caused a marked reduction in egg production and in the size of ovaries
and oviducts.
A high incidence (3 to 50 percent) of goiter was reported in thorough-
bred foals born on two farms in Maryland and on one farm in central
Ontario, Canada (Baker and Lindsey, 1968~. The dietary intake of
iodine by mares bearing goitrous foals ranged from 48 to 432 midday.
Plasma iodine levels were elevated in the goitrous foals as well as in the
mares fed rations containing high levels of iodine. Enlarged thyroids
and leg weakness were reported in four foals born to mares fed 83 mg
iodine daily (Drew et al., 1975~.
Marked differences exist between rabbits, hamsters, and rats in their
OCR for page 232
232 MINERAL TOLERANCE OF DOMESTIC ANIMALS
tolerance to high intakes of iodine. Mortality was high in the offspring
of rabbits fed 250 ppm iodine in late gestation. On the other hand, the
feeding of diets containing 2,500 ppm iodine to hamsters during gesta-
tion did not affect death loss in the offspring (Arlington et al., 19651.
The survival of the offspring of rats was not affected by feeding gestat-
~ng female rats 500 ppm of iodine, but high mortality of the young was
found when the gestation diets contained 1,000 ppm iodine (Ammerman
et al., 1964~. Webster et al. (1959) found no gross lesions or abnormali-
ties in mice or guinea pigs that received 5,000 ppm of potassium iodate
in their drinking water for several weeks. Microscopic examination,
however, showed hemosiderin deposits in the renal convoluted tubules
of nearly all the mice.
HIGH LEVELS
Webster et al. (1966) determined the minimum lethal dose and the
maximum allowable dose of potassium iodate for dogs. The iodine was
administered in gelatin capsules in single doses supplying either 100,
200, or 250 mg potassium iodate per kilogram of body weight. The 100
mg/kg level caused brief anorexia and occasional vomiting but all dogs
lived. The effects of feeding the 200 and 250 mg/kg doses were very
pronounced, and death preceded by anorexia, prostration, and coma
occurred at these levels. Fatty changes in the viscera and necrotic
lesions in the liver, kidney, and mucosa of the gastrointestinal tract
were sometimes present. Retinal changes were noted in one dog given
the intermediate level of iodine. Highman et al. (1955) reported severe
retinal degenerative changes in rabbits and guinea pigs injected ir~tra-
peritoneally with potassium iodate, but no such retinal changes were
observed in guinea pigs given potassium iodate in the drinking water.
FACTORS INFLUENCING TOXICITY
Many plants and plant products used for animal feeds or for forage are
known to contain substances that can induce goiter in animals. More
than 300 natural or synthetic chemicals possess goitrogenic properties
that may have an effect on iodine bioavailability (Talbot et al., 1976~.
Among the naturally occurring goitrogens, the best characterized are
the glucosinolate derivatives isolated from the Brassica species. The
occurrence of a potent goitrogen in soybean products is well docu-
mented. Thiocyanates, perchlorates, and rubidium salts are known to
interfere with iodine uptake by the thyroid, and high levels of arsenic
can induce goiter in rats (Underwood, 1977~. Bromide, fluoride, cobalt,
OCR for page 233
Iodine
233
manganese, and nitrate may also inhibit normal iodine uptake (Talbot
et al., 1976~.
Few studies have been conducted comparing the relative toxicity of
the various iodine compounds. Arrington et al. (1965) reported no
difference in toxicity to rats between sodium and potassium iodide.
Using white Swiss mice, Webster et al. (1957) compared the toxicity of
single doses of sodium iodide, sodium iodate, potassium iodide, and
potassium iodate given either orally, intraperitoneally, or intrave-
nously. In these studies the iodate salts were more toxic than the iodide
salts. Miller and Swanson (1973) found that ethylenedianunedihydn~
dide was absorbed at least as well as sodium or potassium iodide by
dairy cows. Also, the iodine from EDDI was retained in most organs and
tissues longer than iodine from sodium iodide.
Webster et al. (1959) showed that the daily consumption of potassium
iodate in the drinking water by mice and guinea pigs at times exceeded
the estimated oral LD50 values for single doses of iodate given by
stomach tube. This suggests a marked increase in tolerance to iodine
when it is given in divided, small doses. These same workers reported
that the presence of food in the stomach greatly decreased the acute
toxic effects of orally administered iodine.
TISSUE LEVELS
The level of iodine in milk is influenced by iodine intake, season, level
of milk production, and the use of iodine-containing disinfectants.
Hemken et al. (1972) reported that daily supplementation of the diet of
lactating dairy cows with either 0, 6.8, or 68.0 mg potassium iodide
resulted in milk containing 0.008, 0.081, and 0.694 ppm iodine, respec-
tively. In the same study, Hemken et al. (1972) reported that the iodine
content of milk from 13 Illinois farms averaged 0.425 ppm and that from
8 Maryland farms averaged 0.457 ppm. The range in iodine content
within each location was wide and could be explained largely by the
level of supplemental iodine used in the diets of the lactating cows.
Miller and Swanson (1973) fed dairy cows daily doses of either 106 mg
potassium iodide or 100 mg EDD] and obtained iodine levels in the milk
of 0.379 and 0.895 ppm, respectively. Feeding a level of 500 mg EDDI per
day caused the iodine content of the milk to reach 2.036 ppm. Feeding
16 and 164 mg iodine per head per day to cows resulted in milk iodine
levels of 0.370 and 2.2 ppm, respectively (Convey et al., 1977~. The
average iodine content of milk from 111 herds was 0.646 ppm, with a
range of 0.04 to 4.84 ppm (Hemken, 1978~. The high iodine levels in
OCR for page 234
234 MINERAL TOLERANCE OF DOMESTIC ANIMALS
milk were the result of either feeding high levels of dietary iodine or the
use of iodine as a sanitizing agent. Hemken (1978) reported that iodine
as udder washes caused the iodine content of milk to increase by 0.035
ppm.
Fisher and Carr (1974) reported that the iodine content of beef, pork,
and mutton was low (0.027 to 0.045 ppm). The studies by Miller et al.
(1975) showed that of the nonthyroid tissues skeletal muscle is the
poorest concentrator of radioiocline. Eggs from hens fecI 0.022 ppm
dietary iodine had O.001-ppm of iodine in the liquid egg, whereas those
from hens fed 5 ppm `dietary incline had 5 ppm incline in the liquid egg
Gus et al., 1953~. Marcilese et at. (1968) fed high concentrations of
incline (100 mg/day) to laying hens and found that the iodine content of
the egg increased linearly for 10 days and reached a plateau of approxi-
mately 3 mg/egg at that time. The iodine concentration in the eggs from
hens fed 500 mg/day increased rapidly to an average of 7 mg/egg by 8
days, at which time egg protiaction in most hens ceased.
MAXIMUM TOLERABLE LEVELS
Newton et al. (1974) showed that 50 ppm iodine significantly reduced
growth rate and feed intake of calves weighing about 100 kg. Fish and
Swanson (1977) found that calves weighing about 100 kg tolerated 20
and 40 ppm iodine (from ENDS) with no untoward effects. Yearling
heifers weighing about 320 kg were not affected by iodine levels of 71,
140, and 283 ppm (Fish and Swanson, 1977~. McCauley et al. (1973)
showed that daily iodine intakes of 300 me (from EDDY) or 150 mg (from
potassium iodide) depressed growth rate of lambs. Based on available
information, the maximum tolerable level of iodine for cattle and sheep
is 50 ppm. Although cattle can tolerate 50 ppm iodine, it should be
understood that this level in the diet may result in undesirably high
levels of iodine in the milk. Fish and Swanson (1977) showed that dairy
cows receiving 47 ppm iodine produced milk containing 2.4 ppm iodine.
The Food and Nutrition Board of the National Research Council (1970)
has stated that iodine intakes between 50 and 1,000 ,ug/day are esti-
mated as safe, but intakes between 100 and 300 ,ug/day are desirable.
Newton and CIawson (1974) reported that 400 ppm iodine had no
adverse effect on the performance of pigs weighing about 17 kg. Be-
cause 625 ppm iodine reduced egg production and hatchability, the
maximum tolerable level for iodine in poultry diets appears to be about
300 ppm.
Horses are less tolerant of excess iodine than cattle, sheep, swine,
OCR for page 235
Iodine
235
and poultry. A high incidence of goiter was found in the offspring of
mares consuming 48 to 432 mg iodine per day. Assuming that mares
consume 10 kg dry matter daily, the maximum tolerable level for iodine
in horse diets is 5 ppm.
SUMMARY
Iodine is an essential element for all animals. Its only known function
in the body is in the synthesis of the thyroid hormones. Species differ
widely in their susceptibility to iodine toxicity, but all animals can
tolerate iodine levels far in excess of their requirements for this ele-
ment. Feeding excessive levels of iodine has resulted in decreased egg
production in hens, inhibition of lactation in rats, decreased hemoglo-
bin levels in pigs, necrotic lesions in the liver of dogs, and goiter and
reduced thyroid hormone synthesis in several species. Increasing the
iodine intake of lactating cows and laying hens increases the levels of
iodine in milk and eggs.
OCR for page 236
is
~
ct
· -
s:
o
· -
em
·
·
·
o
-
o
In
-
m
Ed
o
._
-
Ct
-
C~
._
~ ~ C
_ C
is 3 3
_ v' ~
e ~ E
In
-
-
c,
A)
_,
o
o
._
-
ct
a
~ e O i, ~ E g~ ~ ~ _ _ 0 ~ o _ E ~ E E E E E
~ ·- ~ .- 04 so ~ ~ ~ i-' ~ ~ ~ c: ~ c sol c ~
~ -° ~ ~ ~ ~ ~ ~ c ~ ~ ~ ~ .= ~ ~ ·~ ~, ·_ ~, ._ ~,,
C ~ C ~ ~ C ~ ~ ~ O ~ O ~ O ~
O ~ ~ ~ ._ C ~ ._ O O O O O . ." ~ 0 0 ~ O ~ O ~ O
Z ~ ~ c) c) Z Z Z ~Q Z Z :Z Z Z
_ _ _ _
.O .L} .~ .O
a a ~ ~
-
~:
~ 3
.
CQ _ _
o
.~ c
t: ~
. -
(L) ·—
3
.E
ct ~ ~
C) Z ~
E ~ E ~ E E E ~ ~ ~~ ~,
=- ~ c~. c~ ~. c~~ =, c~. c:. E E ~ ~ EE
0 0 0 'l 0 0 0 ~ ~ ~ 0 0 0 0 0
— 0 0 ~ ', 0 ~ ~ oo ~ ~ x oo ~ 0
~ oo
~ ~ o
x - o
-
-
ct
~o
~ ~ l.=
~ ~ ~> ~
- - - ~
_ — tt, G
236
OCR for page 237
~ o ~
o - ~ 15 -
3 ~ .° ~ is
s on . ~ C o
U. _ ~ V — ~ —
·~ ~ lo ~ 3
~ Y ,_ _ _ _
_- ~ ~ ee sE ~
_ ~ ~^ ~ _ ~ ^
V
. ~ ~ ~ ~ ~ Do ~ o
· Cal · ~ · - ;
C
cat ~ ~ ~ In
e <~ c ,,,.~ V.= v c
~ — et ~ ~ > Cal ~ Ce
0 ° 0 ~ 0 ~ 0 ~ 0
~ 0 ~ 0 ~ 0 ~ 0 ~
~ ~ ~ Z
In U. ~ ~
E E :~, ~ ~ E 2 ~ ~ 2
C\S C~ tV ~ C 04 o ~ —V
O s-4 I.4 ~ Ce ~ 01) 08 ,_ C Ct ~ U~ ~, ~ U)
~ c ~ ~ ~ 2 ~ ~ ~ ~ C ~ C 3 .~° ~ ° o 2 o 2 o
Z Z~ ~ Z ~ ~ Z Z
-
_ ~ _ _ _
._ et ._ ._ ._
a ~ a a a
~ - ~:
3 ~o ~ ~ ~ 3
~ t_ o o `°
_ ~ ~ ~ r~
A ~ .C
E ~ ~ Ct. C~ E ~ ~ ~ E ~ ~ ~
8 ~ os os ~ ~ °^ 8 ° ° 8 ° ~ 8 8 8 8
oo — - \ — - , ~ _ - . ~ oo ~ V~ '.
_ ~
oe oo so
~ Y ~ ~ ao
o o ~ :' ~
O ~ — —~ 3
\0 ~ ^0
~ O
,, .c ~ | ~ ~ r
u' ~ cn ~ ~
237
OCR for page 238
c)
9#
-
-
:e
·~
S:
-
m
c
I:
£
at.
.
~ ^. ~ ~
,
_ I_ 4~,) _ lo
Cal UP _
_ ~ _
_ _ _] ~ _
~ IS ~ _
O o.3 ~5 C on
.t ~ - _ k 3
-
o os
· _ · _
~ .3
o .=
L. O
_ ~ ~
I.
'A B.e
Ad. ~
Ha ~
C 04
~ C
8 , ~ ~ ~
4- _ ~ ~ ._
o so _ .—
' ~~ ~ e ~ ~ :~ a ~ ~
_ ,, ._ A- ~ ~ ~ ~ ~ ~
.
be
,)
C—° Eo
O cn
'2
4, ~ £
._ ._ ._
a ~ ~ 0
55 ~ ~ ~ E ~ E D ~ 8 ~ 5; C ]. E
1 ~ - v~ c~~ c%l ~ v~
E o ~6 .° y >4 ~ ~ ~ ~ ~s ~ tts :~ O
so
E E o E E E E E ~ G D.
O~ . ~
~ —
o S
.O
3
a.£
a, ~ 1
=: ~ oo
3 4, 3 4, ~ ~ ~:
, ,
e y ~ ~ ~ D
c~ ~ ~ :r x ~: ~ ~
238
.
OCR for page 239
u~ ~
ON c,\
- - - ~
~ - -
~ - -
E ~ D D .C
~— ~ ~ ~
3 3
:^
_ _
_ ~ ~ ~ ._ oo
~ r: -~' ~ a
3 o o o o
_ ~ ~ ~ ~ — ~ ~ ~
.C _ C G ~ G ~ ~ ~ .5 C |
o 3~-B y, ~o ~ ° ~ g o
C ~ Y ~ O Y ~ G ~ O r Y C ~ O C O C
_> ,~,~ ~ O C G ~ O ~ ~ O C G ~ O tg, ~ O ~ ~ O C)
~ ~4
D C
C
~ _ ~ ~ ~
_ _ _ _
E E E G C C C E ~ E E c
oo oo o o o o oo ~ o o o
_ q" o o o o o~
_ _ ', o ~ o
_ _ ~ _ _
(~) oo ~ o
~ ~ o o o ~
- ~ - -
o ~ -
I ~ , o , c L E
239
-
3
C~
o
es
o
-
._
U)
-
cn
Ct
o
c
. o
._
=
._
. r.
_ L~
as ~
cn
cn
.E
e
C~
t_
0 ~
~ _
e 3C
Z ~
~ ~o
OCR for page 240
241) MINERAL TOLERANCE OF DOMESTIC ANIMALS
REFERENCES
Ammerman, C. B., and S. M. Miller. 1972. Biological availability of minor mineral ions:
A review. J. Anim. Sci. 35:681.
Ammerman, C. B.? L. R. Arrington, A. C. Warnick, J. L. Edwards, R. L. Shirley, and
G. K. Davis. 1964. Reproduction and lactation in rats fed excessive iodine. J. Nutr.
84:108.
Arrington, L. R., R. N. Taylor, Jr., C. B. Ammerman, and R. L. Shirley. 1965. Effects
of excess dietary iodine upon rabbits, hamsters, rats and swine. J. Nub. 87:394.
Arlington, L. R., R. A. Santa Cruz, R. H. Harms, and H. R. Wilson. 1967. Effects of
excess dietary iodine upon pullets and laying hens. J. Nutr. 92:325.
Baker, H. J., and J. R. Lindsey. 1968. Equine goiter due to excess dietary iodide. J. Am.
Vet. Med. Assoc. 153:1618.
Barua, J., R. G. Gragle, and J. K. Miller. 1964. Sites of gastrointestinal-blood passage of
iodide and thyroxine in young cattle. J. Dairy Sci. 47:539.
Berson, S. A. 1956. Pathways of iodine metabolism. Am. J. Med. 20:653.
Chilean Iodine Educational Bureau. 1952. Iodine Content of Foods: Annotated Bibliogra-
phy 182~1951, with Review Tables. Chilean Iodine Educational Bureau, London.
Convey, E. M., L. Chapin, J. S. Kesner, D. Hillman, and A. R. Curtis. 1977. Serum
thyrotropin and thyroxine after thyrotropin releasing hormone in dairy cows fed
varying amounts of iodine. J. Dairy Sci. 60:975.
Convey, E. M., L. T. Chapin, J. W. Thomas, K. Leung, and E. W. Swanson. 1978.
Serum thyrotropin, thyroxine and tri-iodothyronine in dairy cows fed varying
amounts of iodine. J. Dairy Sci. 61:771.
Drew, B., W. P. Barber, and D. G. Williams. 1975. The effect of excess iodine on
pregnant mares and foals. Vet. Rec. 97:93.
Evvard, J. M. 1928. Iodine deficiency symptoms and their significance in animal nutrition
and pathology. Endocrinology 12:529.
Fish, R. E., and E. W. Swanson. 1977. Iodine tolerance of calves, yearlings, dry cows,
and lactating cows. J. Dairy Sci. 60 (Suppl. 1):151.
Fisher, K. D., and C. J. Carr. 1974. Iodine in Foods: Chemical Methodology and Sources
of Iodine in the Human Diet. Life Sciences Research Office, Federation of American
Societies for Experimental Biology, Bethesda, Md. PB-233 599. National Technical
Information Service, Springfield, Va.
Gross, J. 1962. Iodine and bromine. In C. L. Comar and Felix Bronner, eds. Mineral
Metabolism. Academic Press, New York.
Haggard, D. L. 1978. Immunologic effects of experimental iodine toxicity in cattle.
M. S. thesis. Michigan State University, East Lansing.
Hemken, R. W. 1978. Factors that influence the iodine content of milk and meat: A
review. J. Anim. Sci. 48:981.
Hemken, R. W., J. H. Vandersall, M. A. Oskarsson, and L. R. Fryman. 1972. Iodine
intake related to milk iodine and performance of dairy cattle. J. Dairy Sci. 55: 931.
Highman, B., S. H. Webster, and M. E. Rice. 1955. Degeneration of retina and gastric
parietal cells and other pathologic changes following administration of iodates. Fed.
Proc. 14:407. (Abstr.)
Marcilese, N. A., R. H. Harms, R. M. Valsechhi, and L. R. Arrington. 1968. Iodine
uptake by ova of hens given excess iodine and effect upon ova development. J. Nutr.
94:117.
McCauley, E. H., J. G. Linn, and R. D. Goodrich. 1973. Experimentally induced iodine
toxicosis in lambs. Am. J. Vet. Res. 34:65.
.
OCR for page 241
Iodine
241
Miller, J. I., and K. Tillapaugh. 1966. Iodide Medicated Salt for Beef Cattle. Cornell Feed
Service No. 62. Cooperative Extension Service, Cornell University, Ithaca, N.Y.
Miller, J. K., and E. W. Swanson. 1973. Metabolism of ethylenediaminedihydriodide and
sodium or potassium iodide by dairy cows. J. Dairy Sci. 56:378.
Miller, J. K., E. W. Swanson, and G. E. Spalding. 1975. Iodine absorption, excretion,
recycling and tissue distribution in the dairy cow. J. Dairy Sci. 58:1578.
National Research Council (NRC), For and Nutrition Bond (FIB). 1970. Iodine Nutrition
in the United States. National Academy of Sciences, Washington, D.C.
Newton, G. L., and A. J. Clawson. 1974. Iodine toxicity: Physiological effects of elevated
dietary iodine on pigs. J. Anim. Sci. 39:879.
Newton, G. L., E. R. Barrick, R. W. Harvey, and M. B. Wise. 1974. Iodine toxicity.
Physiological effects of elevated dietary iodine on calves. J. Anim. Sci. 38:449.
Perdomo, J. T., R. H. Harms, and L. R. Arrington. 1966. Effect of dietary iodine upon
egg production, fertility and hatchability. Proc. Soc. Exp. Biol. Med. 122:758.
Riggs, D. S. 1952. Quantitative aspects of iodine metabolism in man. Pharmacol. Rev.
4:284.
Roland, D. A., S. T. McGready, R. H. Stonerock, and R. H. Harms. 1977. Hypercal-
cemic effect of potassium iodide on serum calcium in domestic fowl. Poult. Sci.
56:1310.
Rosiles, R., W. B. Buck, and L. N. Brown. 1975. Clinical infectious bovine rhinotra-
cheitis in cattle fed organic iodine and urea. Am. J. Vet. Res. 36:1447.
Talbot, J. M., K. D. Fisher, and C. J. Carr. 1976. A Review of the Effects of Dietary
Iodine on Certain Thyroid Disorders. Life Sciences Research Office, Federation of
American Societies for Experimental Biology, Bethesda, Md.
Underwood, E. J. 1977. Trace Elements in Human and Animal Nutrition, 4th ed. Acade-
mic Press, New York.
Webster, S. H., M. E. Rice, B. Highman, and W. F. Von Oettingen. 1957. The toxicology
of potassium and sodium iodate: Acute toxicity in mice. J. Pharmacol. Exp. Ther.
120:171.
Webster, S. H., M. E. Rice, B. Highman, and E. F. Stohlman. 1959. The toxicology of
potassium and sodium iodate. II. Subacute toxicity of potassium iodate in mice and
guinea pigs. Toxicol. Appl. Pharmacol. 1:87.
Webster, R. H., E. F. Stohlman, and B. Highman, 1966. The toxicology of potassium and
sodium iodate. III. Acute and subacute oral toxicology of potassium iodate in dogs.
Toxicol. Appl. Pharmacol. 8:185.
Wilgus, H. F., F. X. Gassner, A. P. Patton, and G. S. Harshfield. 1953. The Iodine
Requirements of Chickens. Colo. Agric. Exp. Stn. Tech. Bull. 49. Fort Collins, Colo.
Representative terms from entire chapter:
iodine content
