Effects of Elevated Iodine in Milk Replacer on Calf Performance 1 K. J. JENKINS and M. HIDIROGLOU Animal Research Center, Research Branch Agriculture Canada Ottawa. ON. Canada K1A DCB ABSTRACT
generous supplementation, calves can receive excessive dietary iodine from errors in formulation or preparation of milk replacers. Apparently, no iodine tolerance data are available for preruminant calves. Iodine toxicity studies have been either with young ruminants or lactating cows (8). This study was conducted to estimate the concentration of iodine in milk replacer that would adversely affect calf performance and feed efficiency and to determine the effect of increasing dietary iodine on concentrations of iodine in plasma and tissue.
Calves were fed milk replacer containing .57, 10, 50, 100, or 200 ppm iodine (from ethylenediaminedihydroiodide) in DM, from 3 to 38 d of age, to estimate the minimum toxic concentration of iodine. Only the 200 ppm iodine intake reduced weight gains, DM intake, feed efficiency, and DM digestibility. At the 100 and 200 ppm iodine intakes, protein digestibility was reduced, and calves showed typical symptoms of iodine toxicity (nasal discharge, excessive tear and saliva formation, and coughing from tracheal congestion). Thyroid iodine increased with every elevation in iodine intake. Iodine in plasma, bile, and nonthyroid tissues started to increase at the 50 ppm intake and, except for muscle, tended to increase again at the 100 and 200 ppm intakes. Thus, the preruminant calf tolerated up to 50 ppm iodine in milk replacer DM for 5 wk postpartum. However, as iodine concentrations in plasma and nonthyroid tissues started to increase at 50 ppm iodine, an upper limit of 10 ppm would be more preferable. (Key words: iodine, calf performance, milk replacer)
MATERIALS AND METHODS Calves, Diets, and Experimental Procedures
INTRODUCTION
The NRC recommendation for minimum iodine in milk replacers (DM) for calves is .25 ppm (7). Manufacturers of milk replacers commonly supplement their products with iodine compounds, such as ethylenediaminedihydroiodide (EDDI), or calcium iodate, to supply additional iodine at this concentration, or frequently at higher concentrations. In addition to over-
Received July 5. 19S9. Accepted September 25. 19S9. lContribution Number 1621. 1990 J Dairy Sci 73:804--807
The Animal Research Centre dairy cattle herd provided 35 male Holstein calves over an 8-wk period for this 5-wk feeding study. After receiving colostrum for the first 3 d, the calves were assigned in equal numbers to the five dietary treatments in a manner that provided similar average starting weight for each treatment. Housing consisted of individual pens with eltpanded metal floors in a heated, insulated forced-air ventilated room. Water was provided for ad libitum intake. When respiratory infection occurred, treatment was with Pen-Di-Strep (Rogar/STB Inc., London. ON); scours were not a problem in this study. Two calves died (lots 2 and 3) with respiratory infection early in the experiment and were replaced with 3-d-old calves at d 1. The basal milk replacer (without added iodine) contained .57 ppm iodine, DM basis (Table 1); this was used as the control treatment although it was higher than the NRC (7) allowance of .25 ppm. Ethylenediaminedihydroiodide (EDDI; Sigma Chemical Company, St. Louis, MO) was added to provide five iodine concentrations, .57, 10, 5(1.. 100, and 200 ppm in DM. Milk replacers were prepared as a 28% (DM) concentrate and stored at -IS·C. Prior to
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IODINE TOLERANCE OF PRERUMINANT CALF TABLE I. Composition of basal diet. 1 Ingredient Whey, sweet Skim milk powder Tallow Coconut oil Soy lecithin emulsifier Tween 80 2 MgS04·7 H20 CaC12 Micro mineral premix Vitamin premix Choline chloride Dry matter composition Protein (N x 6.25), % Lipid, % Iodine, ppm
(% of DM)
8.8 69.0 16.6
2.0 .9 .1
1.0 .7 .4 .4 .1 24.4
20.5 .57
lBasal diet, without mineral and vitamin supplements, was purchased from Mutual Products Ltd., Morrisburg, ON. Micro mineral premix. supplied (mg/kg of diet): ZOO 60; CuS04·5H20 40; MnS04·H20 120; Na2Mo04·2H20 2.5; FeS04·7H20 500; and Na2Se04·lOH20 .5. Vitamin premix supplied (mg/kg of diet) pyridoxine 30; nicotinic acid 20; riboflavin 2.0; vitamin B12 .04; pantothenic acid 10; folic acid 1.0; thiamine 5.0; d-biotin .5 and (per kg diet), vitamin A 10.000 IV; vitamin D3 2000 IV; and vitamin E 50 IV.
~ween 80 - Sorbitan monooleate polyoxyethylene.
feeding. the concentrate was thawed and diluted 1:1 with hot tap water to about 37"C. Calves were fed twice a day, limited to 2. a kg of diet per feeding for the first 3 d on experiment followed by 5% of live weight per feeding for the subsequent 4 d. Each feeding for the 2nd wk was at 6% live weight and at 7% for wk 3, 4, and 5. Feces were collected quantitatively from the first four calves in each treatment between 6 and 13 d on experiment to measure apparent digestibility of DM, N, lipid, and fecal excretion of iodine. sampling Methods and Analytical Procedures
Samples of blood were taken from the first four calves in each treatment before the last meal of the trial and centrifuged for packed cell volume and plasma (stored at -25°C). The same calves were killed at the end of the 5-wk experimental period. Samples were taken of spleen, liver, kidney, heart, thyroid, leg muscle (triceps crural), and gall bladder bile, and stored at -25°C. Iodine concentration in plasma, tissues,
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feed, and feces was determined by the method of Moxon and Dixon (6). Plasma total iodine was determined rather than thyroxine (T4) and triiodothyronine (T3) concentrations. as high iodine intakes have no consistent effect on plasma T4 and T3 concentrations (2, 5). Analyses of feed and feces for OM, lipid, and CP (N x 6.25) were according the standard methods of the AOAC (1). Data were analyzed statistically by ANOVA and Duncan's multiple range test using 5% probability (12). RESULTS AND DISCUSSION
Dietary iodine up to 100 ppm DM had no effect on average daily gain (ADG), DM intake, or feed efficiency for the 5-wk experiment (Table 2). However, the calves could not tolerate the 200 ppm iodine concentration, showing reduced weight gains, feed intake, and feed efficiency. Apparent digestibility of DM also was reduced for the 200 ppm iodine intake, as was digestible CP for the 100 and 200 ppm treatments. Lipid digestibility was not affected by iodine intake. We are not aware of any other studies on iodine toxicity conducted with preruminant calves fed milk replacer. Iodine toxicity studies with dairy cattle have been carried out either with young ruminants or with lactating cows (8). In several experiments, Newton et aI. (9) fed young ruminant calves (80 to 100 kg, mean body weight) iodine intakes of 1.6, 10, 125, 50, 100, or 200 ppm (as iodate, in OM). Responses of growth rate to excess dietary iodine were variable. In one experiment, ADG was depressed at 50 ppm iodine intake, but in two other experiments, gains were reduced only at 100 or 200 ppm. Feed intake always was reduced at 100 ppm iodine. Fish and Swanson (2) found that young ruminant calves (average weight 100 kg) tolerated 20, 42, and 86 ppm iodine (as EDDI, in DM), but weight gains were slightly, but not significantly, depressed at 174 ppm iodine, It would appear from these two studies that performance of the young ruminant calf can be reduced by dietary iodine as low as 50 ppm or as high as 200 ppm, depending upon modifying factors that have not yet been clarified. Our results seem to indicate that the preruminant calf is slightly more tolerant of excess dietary iodine than the young ruminant, as both ADO and feed intake were not lowered with an intake of 200 ppm iodine. However, Journal of Dairy Science Vol. 73,
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JENKINS AND HlDIROGLOU
TABLE 2. Effect of dietary iodine concentration on calf weight gains. feed efficiency, nutrient digestibility, fecal e)(cretion of iodine, and blood hematocrit. 1 Dietary iodine treatment, ppm in OM Item
.57
10
50
100
200
SE
Starting weight, kg Average daily gain. kg/d OM intake. kg/d Feed:gain, kg/kg Apparent digestibility. % OM N Lipid Fecal iodine, % of intake Packed cell volume, %
42.4 .50" .86" l.72 b
43.3 .55"
41.g .4g" .84" 1.7Sb
43.0 ,4S" .S7" 1.81"b
42.S .3g b .7Sb 1.97"
1.2 ,03 .03 .06
93.3" 92.0" 94.1 IS.3 b 3g.9"b
94.0" 93.9" 95.5 22.g"b 40.5"
92.1" 91.S" 92.9 28.0" 39.8"
9O.8"b
88.2 b 84.6b 90.3 31.4" 34.3c
1.2 1.5 1.8 3.1 1.2
.90"
l.64b
87.0b
93.4 26.3"b 35.5 bc
".b,CMeans with different letters on same line differ (P<.OS). 1Starting weight. weight gains. feed intakes. and feed efficiencies are averages for seven calves per treatment from 3 to 38 d of age. Digestibility, fecal iodine, and packed cell volume are averages for the first 4 calves put on treatment. For digestibility, feces were collected quantitatively between 6 and 13 d of age. Packed cell volume data are for 38 d of age.
this may not be so, as our treatment period was only for 5 wk, whereas the studies on young ruminants (2, 9) were from 12 to 21 wk. The percentage of dietary iodine excreted in the feces tended to increase with elevated iodine intakes (Table 2). Dietary iodine is extensively absorbed in most animals (14). It is mainly excreted in the urine, but appreciable amounts are also lost in the feces due to excretion via bile and stomach secretions (14). The increased fecal iodine for our iodine-supplemented calves may have resulted from saturation of absorption mechanisms or, alternatively, from increased abomasal and bile iodine (3, 14) secreted into the gastrointestinal tract. Blood packed cell volume was reduced for the 200 ppm intake (Table 2). This concurs with findings by Newton et al, (9), who showed reduced blood hemoglobin concentrations in ruminant calves fed 200 ppm iodine. Newton and Clawson (10) also found that high intakes of iodine by pigs reduced blood hemoglobin concentrations and related this to impaired iron availability for hemoglobin synthesis. None of our calves fed ,57, 10, or 50 ppm iodine showed any symptoms of iodine toxicity. However, typical signs of iodism (II, 13, 14) were apparent in 5 of 7 calves receiving 100 ppm iodine and in all seven calves given the 200 ppm treatment. The signs included nasal discharge, excessive tear and saliva formation, and coughing from tracheal congestion. Newton et al. (9) also found that feeding either 100 or 200 ppm iodine to young ruminant Journal of Dairy Science Vol. 73.
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calves produced severe symptoms of iodine toxicity. However, in their study, the symptoms also appeared in 1 of 8 calves fed 25 ppm iodine and was severe in 2 of 8 calves provided a 50 ppm iodine diet indicating, again, that the preruminant calf may be slightly more tolerant of excess dietary iodine than the young ruminant. As expected, thyroid showed very large increases in iodine content with each elevation in dietary iodine concentration (Table 3). Thyroid concentrates most of the ingested iodine and contains 70 to 80% of the total body iodine; muscle contains 10 to 12%, bile 3 to 4%, skeleton 3%, and other organs 5 to 10% (3). Iodine concentrations in plasma, bile, and the nonthyroid tissues were unaltered by 10 ppm iodine relative to controls (Table 3). At 50 ppm, plasma, bile, and all tissue iodine concentrations were higher than controls. There was a tendency for these iodine concentrations to be raised again at the 100 and 200 ppm intakes, except for muscle iodine, which leveled off at the 50 ppm treatment. Of the nonthyroid tissues analyzed, kidney concentrated iodine the most at the higher intakes, likely because of its role in urinary excretion of iodine. The increase in bile iodine with higher intakes showed that the preruminant calf, as previously noted for ruminant calves and cows (3), can excrete iodine by this route. There are very few published data on the iodine content of tissues in farm animals. Our iodine data (controls) for thyroid tissue were
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IODINE TOLERANCE OF PRERUMINANT CALF TABLE 3. Effect of dietary iodine concentration on iodine content of blood plasma, bile. and tissues. l Dietary iodine treatment, ppm in DM Tissue
.57
Blood plasma Bile. gall bladder Muscle, triceps crural Spleen He an Kidney Liver Thyroid
10 .14 d .26c .074b .093c .11 c .16 d
.l7 d
361 e
50
.0SOb .lSbc .26c .51 ed .32 00 804d
100 .S9c 3.4b .26" .32 b .47 b
.32d .90c
I.I c .46 c 1627c
I.I b 5.0b 29 a 1.0a .56 b 2.g b 1.4b 23 lOb
200 4.0" 8.2 a .30" 1.2a .93 a 5.5 a 1.7" 4095"
SE .08 .64 .02 .07 .06 .27 .10 138
a,b.c.d.eMeans WIth different letters on same line differ (P<.05). 1Values are averages for the first four calves placed on dietary treatment. Blood plasma and bile data in micrograms iodine per milliliter: muscle, spleen. hean. kidney. liver. and thyroid in micrograms iodine per gram fresh tissue. All samples taken at end of experiment when calves were 38 d of age (except blood was sampled before the last meal of trial).
similar to those reponed by Georgievskii (3) for ruminant calves fed a recommended intake of iodine but were about twice his values for plasma, liver, and kidneys. Our control calf data were similar, however, to iodine concentrations reported by Groppel et aI. (4) for goat liver, spleen, kidneys, heart, and skeletal muscle. In conclusion, preruminant calves (given .57, 10, 50, 100, or 200 ppm iodine in milk replacer OM) tolerated up to 50 ppm iodine from 5 wk postpartum. Only at the 200 ppm iodine intake did calves show reduced weight gains, OM intake, feed efficiency, blood hematocrit, and OM digestibility. At both the 100 and 200 ppm iodine intakes, there was reduced protein digestibility, and development of typical symptoms of iodine toxicity. Iodine concentration for plasma, bile, and for the nonthyroid tissues samples started to increase at the 50 ppm iodine intake. Because of these iodine increases, it would appear preferable to set the upper limit for iodine in milk replacer at 10 rather than 50 ppm. ACKNOWLEDGMENTS
The authors grateful1y acknowledge the technical assistance of G. Griffith, post-monem examinations and blood and tissue sampling by K. Harrin and staff, and care of the calves by O. Featherston and staff. REFERENCES 1 Association of Official Analytical Chemists. 1970. Official methods of analysis. II th ed. Assoc. Oflic. Anal.
Chern.. Washington. DC. 2 Fish. R. E.. and E. W. Swanson. 1982. Effects of excessive intakes of iodine upon growth and thyroid function of growing Holstein heifers. 1. Dairy Sci. 65: 605. 3 Georgievskii. V. 1. 1981. The physiological role of microelements. Mineral nutrition of animals. V, microelemems. V. 1. Georgievskii, B. N. Annenkov. and V. T. Samokhin. ed. Butterworths. London, UK. 4 Groppel, B.• B. Kohler. E. Scholz, M. Anke, K. Korber. and G. Jahreis. 1986. The effect of different iodine supply on the iodine content of blood serum, hair, milk and several extrathyroidal organs and tissues. Spurenelement-Symposium. M. Anke. W. Baumann. H. Braunlich, C. BrlIckner, and B. Groppel. ed. Karl-Marx Univ., Leipzig, GDR. 5 Hillman. D., and A. R. Curtis. 1980. Chronic iodine toxicity in dairy cattle: blood chemistry. leukocytes. and milk iodide. J. Dairy Sci. 63:55. 6 Moxon, R.E.D., and E. J. Dixon. 1980. Semi-automatic method fOT the determination of total iodine in food. Analyst 105:344. 7 National Research Council. 1978. Nutrient requirements of dairy cattle. 5th rev. ed. Natl. Acad, Acad. Sci., Washington. DC. 8 National Research Council. 1980. Mineral tolerances of dorr:estic animals. Natl. Acad. Sci .• Washington. DC. 9 Newton, G. L., E. R. Barrick, R. W. Harvey, and M. B. Wise. 1974, 1974. Iodine toxicity. Physiological effects of elevated dietary iodine on calves. 1. Arum. Sci. 38:449. 10 Newton. G. L.. and A. J. Clawson. 1974. Iodine toxicity: physiological effects of elevated dietary iodine on pigs. J. Anim. Sci. 39:879. 11 Schwink. A. L. 1981. Toxicology of ethy1enediaminedihydroiodi
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