Cadmium uptake from feed and its distribution to food products of livestock.

Distribution of cadmium (Cd) into the edible products of three species of food-producing animals was investigated during long-term dietary administration of supplemental cadmium chloride. Cows were exposed to 0.2 (control), 2.4, and 11.3 ppm Cd on whole ration basis for a period of three months followed by a three-month period on control ration. No accumulation of Cd occurred in milk, muscle, or bone at any of the time periods. A dose-related increase of Cd was observed in liver and kidney. The Cd concentration in these organs showed a gradual rise even when the animals were given control ration for three months after an initial three-month exposure to Cd; this observation suggests a mobilization and redistribution of this metal from other tissues. Dietary Cd levels in swine rations were 0.2, 2.4, and 10.1 ppm. The highest level of Cd produced a slightly reduced growth rate in swine. No accumulation of Cd was observed in muscle, bone, or brain. Liver and kidney showed a treatment and time-related increase in cadmium values at 6 and 12 weeks on experiment. During a three-month depletion phase after an initial three months of Cd administration, no further change in liver and kidney Cd levels was observed. White Leghorn chickens were treated by administering 0.3, 1.9, and 13.1 ppm Cd in their diets for up to 6 months. No accumulation of Cd occurred in eggs or bones. A slight increase of Cd level was observed in chicken muscle after six months of exposure. Liver and kidney had the highest levels of Cd, which showed a dose and time-related increase in these organs. No depletion of liver and kidney Cd was seen during seven weeks following a six-week treatment period. In all three species, the kidney Cd levels were severalfold higher than those of liver at all dietary levels. In swine, the renal cortex and medulla had similar Cd concentration in control animals but in all animals exposed to supplemental Cd, a dramatic rise in Cd levels in renal cortex was observed. Medullary Cd did not show a proportional time and dose-related increase in Cd levels, although the levels showed some increase. In kidney and liver of all three species the Cd levels showed a positive correlation with the amount of Cd-binding protein in these tissues. Induced levels of this metal-binding protein may explain accumulation and persistence of Cd-residues in these organs. In all three species, the concentrations of renal Cd-binding protein increased at a rate greater than those in liver. Although the food-producing animals may act as an effective filter of Cd in the case of an environmental increase of this metal, consumption of visceral organs from such animals may pose a hazard. This is particularly critical since the daily intake of Cd in human diet is already estimated to exceed the tolerance limits suggested by WHO/FAO.

Short term disposition of soluble vs. insoluble forms of cadmium in rat lung after intratracheal administration: an autoradiographic assessment.

An autoradiographic study was undertaken to compare the initial distribution patterns of soluble and less soluble forms of cadmium in the rat lung after intratracheal (i.t.) instillation. Male Sprague--Dawley rats were divided into 2 groups, each group received either soluble or a less soluble cadmium (109Cd) i.t. in 0.1 ml buffered saline. At 5, 30 and 90 min post-instillation, rats were sacrificed and processed for autoradiography, and radioactivity estimation of lung sections. 109Cd was unevenly distributed in the lungs at 5 min for both forms of Cd. At 90 min post-instillation, 109Cd was almost evenly distributed in the lung instilled with the soluble form; in case of the less soluble form a spotty distribution of 109Cd in the bronchi was observed. 109Cd was mainly translocated to the liver and stomach, followed by the kidney and intestine. It is apparent that the initial translocation of instilled 109Cd from the lung is relatively slow in the case of less soluble form as compared with the soluble form.

Lead, cadmium, and arsenic residues in animal tissues in relation to those in their surrounding habitat.

The relationships of the residues of lead, cadmium, and arsenic in animal tissues to those in surrounding vegetation and soil were determined in a natural habitat representing a wide range of such residues. The samples studied were selected from 18 different locations. Analyses were performed on a total of 113 animals, 332 plant specimens (representing 33 species), and 408 soil samples (taken at different depths). For the purpose of evaluating relationships, the samples from each location were averaged and reported as parts per million on a dry weight basis. The average lead residues from different locations ranged from 1.4-9.2 ppm in the liver, 45-195 in bones, 4-283 in vegetation, and 15-1399 in soil samples. The cadmium contents ranged from 1-27 ppm in the liver, 3-77 in bones, 0.5-5 in vegetation, and 1-10 in soil. The arsenic contents in different components of the ecosystem varied with an average of 1-9 ppm in liver, 0.6-94 in vegetation, and 7-655 in soil samples. The soil residues varied considerably according to the depth of sampling. Little variation was noted in different species of vegetation or in soil and vegetation samples according to the time and year of sampling. Statistical analyses performed on the averages indicated a significant correlation between vegetation and soil residues for all three elements, and also between animal to vegetation and animal to soil cadmium residues. Multiple linear correlations for all elements in soil, vegetation, and animal tissues were determined. The results indicated a possibility of an increase in cadmium in animal tissues depending upon the increased residues of this metal in the environment.

Clinicopathologic features of fluoride toxicosis in cattle.

Cattle normally ingest variable low-level amounts of fluorides with no known adverse effects, but when excessive amounts are ingested, adverse effects are induced. Several sources may contribute to the total fluoride intake. The many recognized factors that influence structural and functional responses of animals to fluorides are cited. Signs and lesions of fluoride toxicosis in cattle have been characterized. Major fluorotic lesions occur in the permanent teeth and in the bones. Dental lesions occur when excessive amounts of fluoride are ingested during the period of tooth formation and calcification. Bone effects can be induced at any time during an animal's life. A table relating structural changes and functional processes in cattle of various ages has been compiled as a guide for diagnosing and evaluating fluoride toxicosis. Recommended fluoride tolerance levels for cattle have been established. Prevention and control of fluoride toxicosis in cattle can be accomplished when the nature of the disease is realized; the symptomatology, lesions and pathogenesis are properly interpreted, correlated and evaluated; and the source(s) of excessive fluorides are eliminated.

Effect of excessive exposure to sodium fluoride on composition and crystallinity of equine bone tumors.

Sodium fluoride (5 mg/kg of body weight) was fed for 20 months to horses with hereditary multiple exostoses (HME), a skeletal disorder that primarily affects endochondral bones during skeletal development. Rib biopsies were performed on both HME horses not fed fluoride (control) and HME horses that were fed fluoride to obtain comparable specimens for chemical analyses and x-ray diffraction. Fluoride content of the rib from a horse fed fluoride for 20 months was approximately 20 to 30 times higher than that from a control horse. Fluoride content of the bone tumors was higher than those of normal bones in both control and fluoride-fed horses. The effect of fluoride uptake on the Ca/P ratio was slight. The Ca/P ratios did not differ significantly between tumorous and normal ribs. X-ray diffraction studies showed that the crystallinity (ie, crystal size/perfection) of the mineral apatite in tumor of the rib from the control horse was lower than that of normal bone from the same rib. Fluoride, however, induced a marked change in the crystallinity at both the tumorous and the normal bone sites. The crystallinity of the tumor apatite in the fluoride-fed horse exceeded that of normal bone in the control horse. Otherwise, there were not demonstrable fluoride-induced gross or radiographic changes in the bone tumors.

Clinical signs and bone changes associated with phosphorus deficiency in beef cattle.

For 10 years, 42 female Herefords (as they progressed from weanling calves to aged cows) were fed diets individually, with phosphorus (P) content being the only variable. During growth and the first 3 gestations, clinically evident differences were not associated with 2 dietary treatments (approx 12 and 38 g of P/day). During the next 2 gestations (2 years), half the cows from each original treatment group were fed less than 6 g of P (n = 21 cows, 11 from the group fed 12 g of P/day and 10 from the group fed 38 g of P/day) daily. The other half were fed diets supplying approximately 8 g of P (n = 11 cows fed 12 g of P/day) and 35 g of P (n = 10 cows fed 38 g of P/day) daily. During the last 3 years of the experiment, all remaining cows were fed diets containing 12 g (n = 19 cows originally fed 12 g) or 19 g (n = 17 cows originally fed 38 g) of P/day. Cows fed diets containing less than 6 g of P/day developed an insidious and subtle complex syndrome characterized by weight loss, rough hair coat, abnormal stance, and lameness. Spontaneous fractures occurred in the vertebrae, pelvis, and ribs. In severely affected cows, fractures did not heal properly. Some bones were demineralized markedly, and the cortical surfaces were porous, chalky white, soft, and fragile. Osteoid tissue was not properly mineralized. Radiography revealed diminished bone density (osteoporosis), cortical thinning, and resorption of trabeculae. Time-related availability of dietary P initiated excessive turnover of bone, with resultant structural changes and impaired function.(ABSTRACT TRUNCATED AT 250 WORDS)

Relationship of cheek tooth abrasion to fluoride-induced permanent incisor lesions in livestock.

Teeth from cattle, sheep, and horses that ingested various fluoride intakes and teeth from field studies of these species plus deer, elk, and bison were examined for abnormalities. Approximately 99,000 animals in 322 herds were examined for fluorosis. From field studies, 988 cattle of various ages and with different degrees of dental fluorosis were slaughtered and necropsied. The severity of fluoride-induced mottling, hypoplasia, and abnormal abrasion of paired permanent incisor teeth was correlated with abrasion of premolar and molar (cheek) teeth that form and mineralize at approximately the same age. Severe irregular wear of cheek teeth impaired mastication and resulted in poor utilization of feed and unthriftiness. Excessive amounts of fluoride during tooth formation and mineralization induce characteristic dental changes. Offspring from the fluoride-affected animals did not have discernible fluoride-induced lesions in the deciduous teeth.

Dietary phosphorus for beef cows.

Hereford heifers (48 initially) were individually fed variable amounts of dietary phosphorus (P) from weaning through their 8th gestation. During phase I, 2 groups (24 cows each) were given 20.6 to 38.1 g of P/day and 6.0 to 12.1 g of P/day (increasing as animals grew). During phase II (the 4th gestation), half of the animals from each group were maintained with the same respective diets, and the other half were given 5.1 to 6.6 g of P/day. Within 6 months, animals given 5.1 to 6.6 g of P/day gradually developed signs of P deficiency. Clinical signs of deficiency and lesions included general unthriftiness, body weight loss, reduced feed consumption, reluctance to move, abnormal stance, spontaneous bone fractures, and finally, impaired reproductive performance. Cows given 7.8 to 8.9 g of P/day in diet 2 during phase II did not develop discernible clinical signs of P deficiency. Cows that were given 5.1 to 6.6 g of P/day apparently regained their health and reproductive capability when fed 11.7 to 12.6 or 17.1 to 20.5 g of P/day. The data indicate that bones serve as an effective storage source of P and support and buffer body needs until there is serious depletion of skeletal P. These results indicate that common recommendations for dietary P, such as those outlined by the National Research Council (17.5 g of P/day over the entire year for cows weighing 450 kg), exceed the basic requirements for beef cattle; 12 g of P/day is adequate for 450-kg beef cows.

Nicotiana glauca-induced congenital deformities in calves: clinical and pathologic aspects.

Seven calves born to 7 cows fed Nicotiana glauca during portions of the 1st trimester of gestation were deformed at birth. Deformities increased in severity as the calves aged. At birth, calves typically had arthrogryposis of the forelimbs or curvature of the spine; severity varied among calves. In 4 calves necropsied at about 15 months of age, there was general malpositioning and misalignment of the distal ends of the radius and ulna and the proximal ends of the metacarpal bones. Carpal joints were severely affected, fetlock joints were moderately affected, and pastern joints were slightly affected, with lateral rotation of forelimbs common; severity varied among calves. In 1 of the 4 calves, there was moderate torticollis and scoliosis resulting from wedging of some of the cervical and thoracic vertebrae and abnormal cranial curvature of the left thoracic ribs. Histologic changes were not noticed in muscle, brain, spinal cord, or endocrine organs of the 4 calves.

Hereditary multiple exostoses: clinicopathologic features of a comparative study in horses and man.

Investigation of hereditary multiple exostoses in horses under controlled research conditions for 10 years and epidemiologic studies that have spanned up to five generations of human families contain notable similarities. The present study demonstrated that a single dominant autosomal gene is responsible for hereditary multiple exostoses in horses and man. Affected individuals transmit this trait to approximately 50% of their progeny, whereas nonaffected individuals do not transmit the condition to their offspring. The tumors in affected horses are most often present at birth. They tend to be bilaterally symmetrical and vary in size, shape, and texture. Those on the legs generally do not appear to enlarge as the animal matures, but others, notably those on the ribs and scapulae, enlarge until skeletal maturity, Histologically, the tumors appear as typical ostosteochondromas in both horse and man. Sarcomatous transformations have not yet been detected after 10 years in horses, although such changes are occasionally reported in the similar disease condition in man. The remarkable similarities of hereditary multiple exostoses in the horse to that in man provide an opportunity for comparative biomedical study.

Parainfluenza-3 virus exposure of beef heifers prior to natural breeding.

Ninety-six Hereford heifers (approximately 7 months of age) were randomly divided into 2 equal groups and housed 1.6 km apart (with 2 replications in time, 1 year apart). At 15 months of age, 1 group/replicate was inoculated with parainfluenza-3 virus, and the other group was given virus-free spent culture medium. Twenty-four hours later, 2 virgin bulls (2 years old) were placed with each group (24 cows) for natural breeding. Viral inoculation caused a twofold increase in parainfluenza-3 titer and a 0.3 C body temperature increase. There was no effect recognized from the virus on natural breeding efficiency.

Clinical effects of low dietary phosphorus concentrations in feed given to lactating dairy cows.

Thirty-four Holstein cows, pregnant with their second calf, were individually fed diets containing 3 concentrations of phosphorus (P): 24 cows for 12 months and 10 cows for 7.5 months of lactation. Cows were randomly allotted to the specific dietary groups 2 months before expected parturition. The 3 dietary concentrations of P were 0.24%, 0.32%, and 0.42% in diet. Cows given 0.24% P in diets produced significantly less milk than did cows in the other groups. Other clinical signs of P deficiency in the cows fed the diet with 0.24% P included loss of body weight, decreased feed consumption, and lower inorganic serum P concentration 2 to 10 weeks after parturition. There were no significant differences in the variables measured between cows given dietary P concentrations of 0.32% and 0.42%. There was no evidence of hemoglobinuria after parturition. Reproductive performance did not differ significantly, although the trend was in favor of the cows fed the diet with 0.24% P.

DNA polymorphism analysis of hereditary multiple exostoses in horses.

Genomic DNA polymorphisms obtained by restriction fragment-length polymorphism from healthy horses and horses with hereditary multiple exostoses were analyzed. These DNA were digested by 12 restriction enzymes and were hybridized against 6 isotopically labeled oncogene probes. Hybridization was not detected with the viral oncogene, v-ras, which indicated this oncogene was absent in the equine genome. Oncogenes (c-raf-1, c-fes, c-myb, c-myc, and c-sis) were present and had similar hybridization patterns and signal intensities in DNA from healthy horses and horses with hereditary multiple exostoses. Unique and distinct restriction fragment-length polymorphisms were detected with the c-raf-1 probe only in BamHI- and PstI-digested equine DNA.

Effects of diets containing sodium fluoride on mink.

Mink (Mustela vison) kits still nursing, and adult male mink were fed diets containing various levels of fluorine (as NaF) to determine the effects on health, growth and pelt quality. Different groups were fed diets containing 25.5 (control), 46.0, 111.5 or 287.0 ppm fluorine (on a wet basis) for 7-8 mo. Gross, radiographic and microscopic changes were seen in bones from some animals ingesting the higher levels of fluorine. Chemical analyses for fluorine generally reflected levels ingested. Fluorine caused no detectable differences in pelt quality. After data were evaluated, tolerance levels in the feed of not more than 50 ppm fluorine for breeding stock and 100 ppm fluorine for animals being raised only for pelts are recommended.

Fluoride toxicosis in wild ungulates.

To compare the occurrence of chronic fluoride toxicosis in wild and domestic animals in selected areas of Utah, Idaho, Montana, and Wyoming, deer, elk, and bison bones and teeth were collected for evaluation. Vegetation and drinking water samples also were collected, so that potential sources of fluoride could be evaluated. Deer, elk, and bison were found to be susceptible to the adverse effects of ingestion of excessive amounts of fluoride. Teeth and bones were primarily affected with characteristic lesions. Pathognomonic soft tissue changes were not observed. The animals had been exposed to a variety of sources of excessive fluoride, including water high in fluoride, forages contaminated by industrial effluents that were high in fluoride, vegetation contaminated with high fluoride-content soil by rain splash or wind, or a combination of these sources. Waters high in fluoride, especially from geothermal springs and wells, often contained appreciable amounts of various soluble salts. Evidence accumulated from specimens collected throughout the aforementioned states indicated that there are areas where chronic fluoride toxicosis is a problem for wildlife. These areas were where natural sources of fluorine (especially geothermal waters) provided amounts for ingestion that exceed species tolerance limits or were near certain industrial operations.