Molybdenum is a trace element that plays a part in various biological processes across many life forms. It functions as a component of several enzymes, including sulfite oxidase, xanthine oxidase, and aldehyde oxidase, which are involved in metabolism. While necessary for these functions, an excessive accumulation of molybdenum can lead to adverse health effects, a condition known as molybdenum toxicity.
How Molybdenum Toxicity Develops
Molybdenum toxicity can arise from various sources, ranging from natural environmental factors to human activities and dietary choices. Soils naturally rich in molybdenum can lead to higher concentrations of the element in plants grown there. Animals consuming these plants can then accumulate excessive levels of molybdenum, as seen in grazing animals like cattle and sheep.
Industrial processes, such as mining and metallurgy, also pose a risk of exposure. Workers in these environments may inhale or ingest molybdenum-containing dust, leading to elevated levels in their bodies. Dietary intake, particularly from supplements or certain foods consumed in very large quantities, can also contribute to excessive molybdenum levels. Once ingested, molybdenum is absorbed into the bloodstream, with absorption rates in humans ranging from 28% to 77% of the total dose.
Molybdenum is then distributed throughout the body, primarily excreted through urine, with excretion rates between 17% and 80%. In ruminant animals, the digestive process in the rumen allows molybdenum to react with sulfides, forming compounds called thiomolybdates. These thiomolybdates can then bind with copper, creating insoluble complexes that hinder copper absorption and utilization, thus leading to copper deficiency. This interaction is a primary pathway to toxicity in these animals, explaining their heightened susceptibility compared to monogastric animals or humans.
Recognizing Molybdenum Toxicity
The signs of molybdenum toxicity differ between humans and animals. In animals, especially cattle and sheep, molybdenum toxicity often manifests as a secondary copper deficiency. Symptoms include chronic, often greenish, diarrhea, poor growth, and changes in coat color, such as a “spectacle-like” depigmentation around the eyes in cattle.
Affected animals may also experience weight loss, infertility, lameness, and neurological disturbances like ataxia, which is a lack of coordination. In young lambs, a condition called “swayback” can occur, characterized by stiffness and difficulty rising. These clinical signs typically appear within one to two weeks of exposure to high molybdenum levels.
In humans, molybdenum toxicity is less common and usually linked to extreme occupational exposure or specific metabolic conditions. Symptoms reported in cases of high exposure include aching joints, gout-like symptoms due to elevated uric acid levels, and hyperuricosuria. There has been an isolated report of acute toxicity from molybdenum supplements, with a person experiencing hallucinations and seizures from daily doses between 300 and 800 micrograms over 18 days.
Managing and Preventing Molybdenum Toxicity
Diagnosing molybdenum toxicity often involves assessing the copper-molybdenum balance in feed, particularly for animals. A normal copper-to-molybdenum ratio in feed typically ranges from 6:1 to 10:1, while a ratio of 2:1 is consistent with a diagnosis of molybdenum toxicosis. Post-mortem analysis of liver tissue is the preferred method for assessing copper and molybdenum concentrations, although blood tests can also provide valuable information. For humans, molybdenum blood tests are generally reserved for individuals with suspected occupational exposure, with normal whole blood levels typically below 3.3 nanograms per milliliter.
Treatment for molybdenum toxicity primarily focuses on reducing exposure and counteracting the induced copper deficiency, especially in animals. For livestock, supplementing with copper is a common approach. This can involve adding copper sulfate to the feed or salt supplements, which helps to reduce molybdenum’s bioavailability in the gastrointestinal tract and enhance copper absorption. In cases of high molybdenum in feed, such as over 5 milligrams per kilogram, copper sulfate supplementation might be increased to as much as 5% in the salt supplement.
Preventing molybdenum toxicity in animals includes monitoring dietary intake, particularly the copper and molybdenum content of forage. For humans, prevention involves avoiding contaminated water or soil and adhering to appropriate industrial hygiene practices in high-risk occupations. While molybdenum toxicity in humans is rare, being aware of potential sources and symptoms can help in early detection and management.