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Mineral Tolerance of Domestic Animals (1980)
Board on Agriculture (BOA)

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227
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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

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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

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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

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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.

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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

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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,

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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

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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,

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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.

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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. .

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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