Cadmium, mercury, and lead are toxic to humans and animals. Although cadmium and inorganic mercury toxicities occur in humans, they have not been observed in domestic livestock under practical conditions. In contrast, cattle, especially young calves, are extremely susceptible to lead toxicity. Apparently, cattle are more tolerant of cadmium than are other animal species. Due partially to higher absorption and longer retention times in the body, the alkyl mercuries, especially methyl mercury, are more toxic than inorganic mercury compounds. Inorganic forms of cadmium, mercury, and lead are poorly absorbed from the intestine. However, due to lack of effective homeostasis, after absorption retention time is long. Injected cadmium, mercury, and lead are metabolized differently from that naturally absorbed. Most cadmium and mercury are in kidney and liver (50 and 23% of total body in goats); but highest total load of methyl mercury is in muscle (72% in cows). With low to moderate body burden, most lead is retained in the skeleton. However, beyond a certain point, the kidney accumulates large quantities. Only minute amounts of cadmium and mercury are secreted into milk, but milk is only moderately well protected from dietary lead. Likewise, little cadmium and inorganic mercury pass the placental barrier whereas lead and methyl mercury pass more readily.

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Thirty dairy cows, fed a control diet consisting of silage and concentrates, were given either 0, 1000, or 2000 ppm of supplemental Zn (DM basis), from zinc sulfate monohydrate (ZnSO4.H2O) for most of a lactation. Feeding 2000 ppm Zn decreased milk yield and feed intake after several weeks. Some cows were affected more severely than others. Generally, primiparous animals were more tolerant of the high Zn diet than multiparous cows. Milk Zn was materially higher for cows fed 1000 ppm added Zn than controls. With 2000 ppm Zn, milk Zn was elevated further but returned to control values when the high Zn diet was discontinued. Plasma Zn was higher in cows fed supplemental Zn with the increase from 1000 to 2000 greater than that for the first addition. Plasma Cu was lower in cows feed 2000 ppm Zn but milk Cu was not reduced. Milk fat content was not affected, but protein and SNF were reduced by the 12th wk with the 2000 ppm Zn diet. There was no apparent effect on long-term health or performance after the cows were removed from the 2000 ppm Zn diet. Except for lower calf weights with 2000 ppm Zn, reproductive performance was not measurably affected by the dietary treatments. The 1000 ppm added Zn diet had no adverse effect on the cows in any parameter measured.

Sixteen intact male Holstein calves averaging 86 kg and 63 d of age were assigned randomly to four treatment groups. The four treatment diets contained .17, .67, 1.31, and 2.35% Ca on an as-fed basis. The resulting Ca:P ratios with P held constant at about .34% were .47:1, 1.92:1, 3.83:1, and 7.20:1. Calves were fed diets at 3% of their body weights for 4 wk. Magnesium in the bone ash and serum was lowered by the 2.35% Ca treatment. Serum inorganic P was also reduced by the highest Ca diet during the last 2 wk of the experiment. Liver had the highest concentration of Zn in calves fed .67% Ca, and the muscle from calves fed 1.31% Ca diet had the lowest amount of Zn. Copper was reduced in pancreas for 1.31% Ca diet, but Ca was highest in the muscle and heart at the .67% Ca treatment. Weight gains and feed efficiencies were not affected by Ca. Fecal pH was different among treatments and increased as Ca intake increased. Young growing dairy calves can adapt to a wide range of Ca intakes and Ca:P ratios and maintain a moderate growth rate for 4 wk. It appears that excessive dietary Ca may affect concentrations of Zn, Fe, Cu, and Mn in some body tissues, but the magnitude of the effect is relatively small.

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Twelve intact male Holstein calves averaging 90 kg and 12 wk of age were fed one of three dietary treatments for 28 d. The diets were A) control, B) control plus 1000 ppm iron as ferrous carbonate, and C) control plus 1000 ppm iron as ferrous sulfate monohydrate. Calves were dosed orally on d 15 of the treatment period with 1 mCi of iron-59. Neither source of added iron had a significant effect on weight gains, feed consumption, hemoglobin, packed cell volume, serum total iron, serum total iron-binding capacity, unbound iron-binding capacity, serum copper, tissue copper, fecal dry matter, or a consistent effect on fecal pH. The ferrous carbonate had no significant effect on stable zinc or stable iron in any tissue studied. Calves fed ferrous sulfate had higher average stable iron in most tissues and significantly more in the small intestine. Tissue zinc was lower in spleen and pancreas of ferrous sulfate-fed calves. Both sources of added iron sharply reduced iron-59 in serum, whole blood, and body tissues. The reduction was substantially greater in calves fed the ferrous sulfate iron. Iron in ferrous sulfate had a higher biological availability than that in the ferrous carbonate; however, bioavailability of the ferrous carbonate iron appeared to be substantial and considerably more than that noted in previous studies in which a different source of ferrous carbonate was used. The maximum safe level of dietary iron is materially influenced by the source of iron with a higher tolerance indicated for ferrous carbonated than ferrous sulfate monohydrate.

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Sixteen male intact Holstein calves averaging 72 kg and 64 d of age were used to study the effects of high dietary Al on calf performance and P bioavailability. The main effects were two concentrations of added aluminum (0 and .20% Al) and two of added P (0 and .22% P). The basal diet contained, by analysis, .132% P, .74% Ca, and .021% Al. The calves were assigned to four treatment groups balanced according to body weight. The four treatments were 1) normal P, low Al; 2) low P, low Al; 3) low P, high Al; and 4) normal P, high Al. Calved had ad libitum access to their respective diets for 7 wk. Metabolism of a single oral 32P dose was determined during wk 6. The adverse effects of high dietary Al include a 17% reduction in feed intake and a 47% reduction in body weight gains. Alkaline phosphatase and plasma glutamic oxaloacetate transaminase activities increased in calves receiving the high Al diets. A negative balance of P and Ca was noted in the calves fed high concentrations of Al. Apparent absorption of 32P was reduced (37%) in calved fed diets high in Al (44% of dose vs. 69%). Urinary excretion of 32P was not affected by dietary Al concentrations. Calves fed the low P (deficient) diet showed significant reductions in feed intake, weight gain, serum inorganic P, bone ash, and P content of bone. Dietary P did not significantly affect 32P absorption. Adding .20% dietary Al severely affects P metabolism and performance of young growing calves.