Molybdenum poisoning

Symptoms of molybdenum poisoning in cattle include emaciation, diarrhea, anemia, stiffness, and fading of hair color. Vegetation containing 230 mg/kg of this substance affects cattle. 

The element molybdenum (Mo) is found in all living organisms and is considered to be an essential or beneficial micronutrient. However, molybdenum poisoning of ruminants has been reported in at least 15 states and 8 foreign countries. Molybdenum is used primarily in the manufacture of steel alloys. Its residues tend to be elevated in plants and soils near molybdenum mining and reclamation sites, fossil-fuel power plants, and molybdenum disposal areas. Concentrations of molybdenum are usually lower in fish and wildlife than in terrestrial macrophytes. 

The improvement in diagnostic abilities to distinguish molybdenum poisoning from copper deficiency... 

Parada, R. 1981. Zinc deficiency in molybdenum poisoned cattle. Vet. Human Toxicol. 23 16-21. 

In livestock, chronic molybdenum poisoning, known as teart disease, is caused by a diet high in molybdenum and low in copper. Symptoms include anemia, gastrointestinal disturbances, bone disorders, and growth retardation. ... 

Sheep are more susceptible to copper poisoning than are cattle, but cattle are more sensitive to molybdenum poisoning than are sheep. The in vivo relationship between copper and molybdenum is well understood. Excess copper induces molybdenum deficiency and vice versa. The most frequent cause of copper poisoning in sheep is by uninformed farmers feeding cattle feed to sheep. Copper from different sources is additive. Copper is an essential element for cattle and is usually added to their feeds however, molybdenum is not considered essential and is therefore not added. Cattle feeds therefore have high copper concentrations and no molybdenum feeding this ration to sheep upsets the normal 6 1 copper molyb-denum ratio in vivo. 

One patient who consumed 300-800 pg Mo per day for about 19 days developed an acute psychosis with visual and auditory hallucinations, and a series of petit mal seizures with one life-threatening grand mal attack. At one year after the molybdenum poisoning, this patient was diagnosed as having toxic encephalopathy with executive deficiencies, learning disability, major depression, and post-traumatic stress disorder (Momcilovic 1999). 

Molybdenum chemistry is complex and inadequately known. Its toxicological properties in mammals are governed to a remarkable extent through interaction with copper and sulfur residues of molybdenum alone are not sufficient to diagnose molybdenum poisoning. 

Domestic mminants, especially cattle, are especially sensitive to molybdenum poisoning when copper and inorganic sulfate are deficient. Cattle are adversely affected - and die if not removed - when grazing on pastures where the ratio of copper to molybdenum is <3, or if they are fed low copper diets containing molybdenum at 2.0-20.0 mg/kg diet death usually occurs when tissue residues exceed 10.0 mg Mo/kg body weight. The resistance of other species of mammals tested, including domestic livestock, small laboratory animals, and wildlife, was at least tenfold higher than that of cattle. Mule deer (Odocoileus hemionus), for example, showed no adverse effects at dietary levels of 1000.0 mg/kg. 

Additional research is recommended in several areas the role of molybdenum on inhibition of carcinomas and dental caries the establishment of minimum, optimal, and upper daily requirements of molybdenum in aquatic and wildlife species of concern the improvement in diagnostic abilities to distinguish molybdenum poisoning from copper deficiency and the determination of sensitivity of early developmental stages of fishes to molybdenum insult. 

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