Quick Facts...
- “Seleniferous” means high in selenium.
- Selenium is a nutrient that is required by livestock in small amounts, but can be toxic at high concentrations.
- Selenium poisoning occurs when livestock eat seleniferous vegetation growing in high pH soils in arid climates, typical of western states.
- Information on the treatment of selenium toxicity can be found in Fact Sheet 6.110 Preventing Selenium Toxicity.
Introduction
Selenium (Se) is an essential nutrient for the health of humans and animals. New claims that Se may reduce liver disease and prevent or even cure cancer have encouraged some people to look to Se to cure their ailments.
However, excess Se can be toxic to both humans and animals. Selenium from the soil is absorbed by plants, and when livestock eat those plants, Se toxicity may develop. Selenium toxicity was first reported in farm animals in China in the 13th century, but the first documented report in the United States occurred during the 1850s in South Dakota.
Se toxicity in livestock can occasionally be acute (one-time consumption of toxic Se levels) or more commonly chronic (consumption of lower, but elevated, Se levels over a long period). Acute selenium toxicity is often called “blind staggers,” although the affected livestock are not always blind nor staggering. Recent research has shown that blind staggers is sometimes associated with high sulfur intake and is not always due to Se toxicity. Typical symptoms of blind staggers include head pressing, perspiration, blindness, abdominal pain, colic, diarrhea, increased heart and respiration rates, and lethargy. Death can occur quickly.
Chronic Se toxicity is called “alkali disease” and is characterized by dullness and lack of vitality; roughness of coat; loss of hair (especially around the mane and tail of horses and the tail switch in cattle); hoof soreness, overgrown or deformed hooves, horizontal ridging, cracking and even sloughing of hooves or complete loss of the hoof wall; and stiffness and lameness.
Where do Se toxicities occur?
Se toxicity is most common in areas that have:
1) arid or semi-arid climates (less than 20 inches annual precipitation),
2) soils with pH levels above 7.0 (above neutral level), and
3) soils developed from shale.
Seleniferous soils are widespread in the Rocky Mountain and Great Plains regions of the western United States. Although these soils exist throughout Colorado, most Colorado soils are not seleniferous.
Where does the Se come from?
The primary source of Se is weathering of rocks that contain Se, especially shales. Excessive irrigation can lead to dissolution of these rocks and speed up weathering. In addition, mining increases the potential for Se toxicity through exposure of seleniferous rocks to air, which leads to the solubilization of the Se. Selenium may also enter soils through deposition from coal combustion and incineration of municipal wastes.
Is the Se problem getting worse?
Historically, remote desert areas where Se toxicity normally occurs have not been areas of high population. However, now that these areas are increasing in population, large ranches are being sub-divided. The shift from large to small acreage agriculture increases the use of high Se areas and increases potential for Se poisoning.
As population demographics in Western states change, three factors are contributing to increased problems with Se poisoning:
1) fewer land managers have a historical knowledge of the interaction between soil, plant, and animal dynamics,
2) people moving onto the landscape create disturbances which allow weeds that accumulate Se to spread, increasing the risk of poisoning, and
3) effective range management techniques that can minimize Se toxicity are new concepts to incoming land managers.
It is crucial that landowners have a clear understanding of how soils, plants, and animals interact with each other to cause a poisonous reaction so that Se poisoning can be prevented.
Diagnosis of Selenium Toxicity
Soil
Since most Se in soil is not available to plants, Se uptake by plants is not closely related to the total amount of Se in the soil. Therefore, a chemical procedure should be used that extracts only the Se that is available to plants.
Selenate, one of many forms of selenium, is the predominant form of Se in Colorado’s high pH, well-aerated soils. Selenate is the form of Se that is most soluble, most mobile in soils, and most readily taken up by plants. Seleniferous soils tend to be heavy-textured or clayey. However, clays fix Se in soils; therefore, at the same soil Se level, heavier-textured soils tend to support plants with lower Se levels than sandy soils.
Soil Se levels can be classified according to the Se levels of non-accumulator plants growing in that soil or the soil Se levels themselves.
| |
Total Soil Se |
Water Soluble Se (in soil) |
Plant Se Level Normal |
| Normal |
less than or equal 2 ppm |
less than 50 ppb |
less than 1.0 ppm |
| Seleniferous |
greater than 2 ppm |
greater than or equal 50 ppb |
greater than or equal 1.0 ppm |
| ppm=parts per million ppb=parts per billion |
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When soil is sampled for Se determination, it is important to sample both the subsoil (down to 3 feet deep) and the topsoil since Se levels are often higher in the subsoil. Many Colorado soils have higher pH in the subsoil than in the surface. This higher pH makes Se in the subsoil more available to plants, hence more dangerous to livestock. Deep-rooted plants extract Se from deep within the soil. Therefore, when a deep-rooted plant dies or drops its leaves and the Se which was extracted from the subsoil is re-deposited on the soil surface, shallow-rooted plants take it up.
Water
The maximum permissible limits for Se levels in water include:
| Drinking Water for Humans |
0.01 ppm |
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| Drinking Water for Livestock |
0.05 ppm |
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| Irrigation Water |
0.02 ppm |
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Avoid water with Se concentrations that exceed these limits, or dilute with another water source.
Plants
Poisonous effects of Se result when plants absorb it from soil or water in concentrations that are toxic to livestock. Some plants only grow on seleniferous soils and store Se in their tissues in greater concentrations than exist in the soil. These plants are referred to as obligate accumulators. Some of the more common and well known are milkvetches, poisonvetches and prince’s plume. Several of the woody asters and goldenweeds are also obligate Se accumulators.
Fortunately, most of these obligate accumulators are not readily consumed by grazing animals because they are unpalatable and emit a garlic-sulfur odor. Cattle and horses only eat obligate Se accumulators if forced to by overgrazing and near starvation. Sheep, however, may eat these plants more readily. Yet, accumulator plants are important indicators of seleniferous soils on rangeland and can be used to identify soils where Se poisoning may occur.
Other plants can grow on soils without a high Se content, but concentrate Se in their tissues when they grow on seleniferous soils. These plants are called facultative selenium accumulators. Often, these plants cause Se poisoning, because some are quite palatable. Among them are saltbushes, curlycup gumweed, broom snakeweed, and asters. Fortunately, with increasing amounts of Se, these plants become less palatable than they would be on soils containing low Se levels. Problem areas are distinguished by high Se levels over a wide area and restricting animals to areas with high Se levels.
Although most plants are non-accumulators (plants that do not accumulate Se), almost all plants will absorb Se until they are inhibited in their growth or killed as a result of abnormally high Se levels. Therefore, many non-accumulator plants can be toxic in seleniferous soils. In fact, most instances of chronic Se toxicity in livestock are due to consumption of non-accumulator forages grown on seleniferous soils.
In areas with marginal levels of Se, an accumulator plant may lead to a localized area of highly seleniferous soil because of its death and decay. When the accumulator plant dies, another plant may germinate and grow. Even non-accumulator plants that grow in these spaces may cause toxicity to livestock if consumed over a sufficient period of time or in sufficient quantities.
Livestock
Selenium is necessary for growth and fertility in animals and for the prevention of a variety of diseases. The minimum intake requirement of Se for a given species varies with the form of Se ingested and dietary composition. The Se requirement is 0.10 ppm for grazing cattle and horses and 0.03 ppm for sheep. The maximum tolerable concentrations for cattle, sheep, and horses range from 1 to 5 ppm. Therefore, there is a narrow gap between deficient and toxic Se levels in feed.
Acute Se toxicity has been associated with the one-time consumption of accumulator plants that contain 100 to more than 9,000 ppm of Se. Chronic toxicity is associated with consumption of grain or grass grown in seleniferous areas with lower forage Se levels, over a long period of time.
At the onset of acute poisoning (selenosis), the movement of the animal becomes abnormal. The animal is likely to walk a short distance with an uncertain gait and then stop and assume a characteristic stance, with head lowered and ears drooped. Animals receiving acutely toxic doses of Se develop a garlicky breath odor as well as vomiting, labored breathing, muscle tremors, and death from respiratory failure within a few hours to several days.
Subacute selenosis, a moderate form of acute selenosis, results from exposure to Se over a period of time (weeks or months). This condition is most frequently observed in grazing livestock that have consumed Se-accumulator plants. Cattle may exhibit blindness, abdominal pain, excessive salivation, teeth grating, paralysis, respiratory failure, and death. Death also results from starvation and thirst because, in addition to loss of appetite, the lameness and pain in the hooves are so severe that the animals are unwilling to move in order to consume food and water.
Alkali disease (chronic Se toxicity), the most common form of Se poisoning, can occur over a period of years, with abnormal hoof development in cattle, which becomes more pronounced as the animal ages. Alkali disease is not limited to grazing livestock, which usually accounts for the more acute forms of selenosis, but can occur from consumption of high Se feed.
Clinical signs of alkali disease in cattle and horses include hoof deformation, lameness, lack of thriftiness, and loss of hair, appetite and vitality. In prolonged Se toxicity, the hooves may be sloughed off. Selenium toxicity is evidenced by abnormal or malformed hooves in cattle and sheep, and there is some evidence of reproduction being adversely affected. Earlier studies have also associated Se toxicity with muscle degradation, cirrhosis of the liver, inflammation of the kidney, and heart degeneration. However, a recent study was unable to reproduce these later signs of Se toxicity, leading the researchers to suggest that other dietary factors may have been the cause of the liver, heart, and kidney damage.
Information on the treatment of Se toxicity can be found in Fact Sheet 6.110 Preventing Selenium Toxicity.
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