Selenium is required by humans and animals but not by plants. Initial interest in selenium in soils centred around its presence inexcessive quantities. In the United States large areas were identified where animals suffered from selenium poisoning - known as "alkali disease" or "blind staggers” depending on severity - and similar areas were subsequently discovered in other countries, notably Australia, Canada China, Ireland, Israel, Mexico and South America.
In Ireland seleniferous soils (Fig, 7) are typically low lying, poorly drained, organic matter-rich, and mildly acid to alkaline in reaction ( Fleming, 1978 ). Carboniferous black shales and limestones are the main source of the element. Selenium leached from soil parent materials formed from these rocks reaches depressions filled by river flood plains and old lake-beds, and it is here that the most toxic soils occur. Selenium in these soils ranges from 5 to over 1000 mg/kg but the majority of toxic soils contain between 10 and 50 mg/kg. The soils occur most extensively in Co. Meath and are typically found in relatively small pockets scattered mostly throughout the centre and south east of the county. Sizeable areas of selenium-toxic soils also occur in west Limerick, and smaller areas may be found in south Tipperary, and north Dublin. Because of the sporadic distribution of the soils they are not readily mapped at the scales usually employed. A tentative estimate of their area in the country would be of the order of 1000 hectares. Selenium-toxic soils are also enriched with molybdenum. From the practical farming aspect, seleniferous soils give rise to pastures which when consumed by livestock result in symptoms including loss of hair and cracking of hooves. Horses, cattle and sheep can all be affected. Selenosis can cause significant ill-thrift but recovery usually occurs when animals are removed to normal pastures.
Other areas exist in the country where the selenium levels are slightly elevated but give rise to no identifiable animal problems.Selenium addition to soils from atmospheric deposition is known. It is alleged that soils on the west coast of Norway have probably been enriched from industrial sources in the U.K. Hill-land areas particularly in the east of Ireland and also peatlands, could well be in receipt of "bonus” selenium in a similar way. Such hill-lands frequently have a skin of peat and, as shown in Table 4 (Fleming and Walsh, 1957), organic matter is capable of retaining selenium.
|Selenium and organic matter in a seleniferous soil profile
|Soil depth (cm)
|Organic matter (%)
|0 - 15
|15 - 30
|30 - 50
|50 - 60
|60 - 85
Selenium deficiency - low Se soils
Interest in selenium deficiency was triggered in the late 1950's by the discovery that a selenium-containing compound ("Factor 3") was capable of preventing a liver necrosis in rats (Schwartz and Foltz, 1957). This finding lead to investigations of certain livestock disorders in many countries and selenium-deficient soils are now widely recognized, e.g. in Australia, New Zealand, theU.S. and China. In Europe, selenium deficiency is especially important in Scandinavia where acid igneous rocks give rise to soils with extremely low levels of the element.
In Ireland, low-selenium soils are known to occur (Fig 7) in parts of Carlow, Wexford, Cork, Tipperary, Waterford and also in light-textured soils formed from clear water limestones in east Galway (Fleming, 1978). However, more intensive sampling is necessary before accurate delineation of low-selenium soil is possible.
Soil analysis for selenium
The occurrence of low-selenium soil, and the incidence of selenium deficiency in livestock must not be equated. The correlation between soil selenium analyses and plant uptake of Se is not good except where soil values are extremely low or very high. Herbage analyses are therefore preferable in endeavouring to identify areas of selenium deficiency in animals but, even here, problems exist as "selenium responsive" diseases of livestock which are conditioned by factors such as the vitamin E content of the diet.
Selenium and Irish Soils
Selenium (Se) is not essential for plant growth but is required for animal and human nutrition. At farm level, problems in animals may arise from either excess or deficiency of Se. Disorders due to Se excess have been known for a long time but those arising from a deficiency of the element have been highlighted only since the late 1950’s when the possible essentiality of Se for animals was shown by the researchers Schwartz and Foltz (1957).
|Table 1 Selenium and Organic Matter in a seleniferous soil profile
|Soil Depth (cm)
|Organic Matter (%)
Selenium in Irish soils
The early work in Ireland on Se was in relation to toxicity (Walsh et al., 1951; Walsh and Fleming, 1952; Fleming and Walsh, 1957; Fleming, 1962). During this period the general areas where toxicity occurred were delineated. These seleniferous soils are typically low lying, poorly drained and of high pH and organic matter status. The soils have been influenced to a large degree by percolating waters from Se-rich rocks where black shales are the predominant facies. These rocks are Namurian (mid Carboniferous) in age and are enriched in a number of elements including selenium, molybdenum and to a lesser degree copper, cobalt, vanadium and uranium.
Seleniferous areas are not extensive and occur mainly in Counties Limerick, Tipperary and Meath. Some small isolated areas also occur in Counties Dublin, Kilkenny, Carlow, Kildare, Offaly, Westmeath and Mayo. The toxic areas of Co. Meath were known in the last century, through the identification of the toxic element was not and early writings refer to “the poisoned lands of Meath” (Fream, 1890). Seleniferous soils can have selenium values as high as 200 mg/kg and those in excess of 5 mg/kg are considered to be toxic.
Geochemical considerations would suggest that soils of low Se status would be found on soils formed from sandstone, granite, the purer limestone and soils developed on glacial and fluvio-glacial sands and gravels. Blanket peats of the western seaboard, those on the sandstones of Co. Kerry, on the schists and gneiss of Co. Mayo and on the Dalriadans of Co. Donegal would also be suspect. Soils formed on the granite hills of Wicklow and the Leinster chain may well be the subject of atmospheric fallout mainly from the U.K. Fleming and Parle (unpublished) found 3 mg/kg Se in peat on the top of Mount Leinster. Enrichment from atmospheric deposition is one of the main sources of Se (Haygarth, 1994).
Selenium concentrations in Irish soils (excluding the seleniferous soils) range from 0.15-2.5 mg/kg and having a mean value of the order of 0.8 mg/kg. In a survey of some Irish stud farm soils Parle et al. (1995) found that 90 percent of soils from Tipperarystud farms had values which fell in the range 0.15-0.50 mg/kg. A delineation of the Se status of Irish soils is shown in Fig. 7. However, before a very accurate assessment can be made an intensive sampling scheme would be required.
Selenium in Irish pastures
In non-seleniferous Irish pasture the herbage Se content will generally be in the range 0.02- 0. 50 mg/kg. A review of the herbage analysed at Johnstown Castle in the period 1986-1995 showed that 76 percent of samples had values of <0.10 mg/kg Se, and 25 percent had values of <0.05 mg/kg.
Factors affecting the selenium content of pastures
Because of the chemical similarity of sulphur and selenium it is not unreasonable to expect that the addition of sulphur to soil will affect the uptake of Se by the plant. Ravikovitch and Margolin (1959) reduced the Se content of lucerne from 4.6 to 1.4 mg/kg using gypsum. Superphosphate has also been shown to reduce Se content of grass, resulting from the calcium sulphate component of this fertiliser. The authors, in a field trial reduced the uptake of applied and native Se by the addition of gypsum (Fleming, 1970b).
Applications of high amounts of nitrogen producing large responses in grass growth can reduce the Se content of the grass by a dilution effect.
Liming will increase the availability of soil Se and thus enhance Se uptake by herbage.
Long dry periods in summer can have the effect of increasing soil Se availability by the oxidation of some of the soil Se to the selenate form - a more soluble form of selenium.
Selenium toxicity is usually associated with cattle and horses with the latter being more prone to the disorder. Animals suffering from Se toxicity will lose hair from the body - in the case of horses the mane and tail are particularly affected - cracking of hooves is common and in severe cases the hooves will slough. Toxicity may be acute or chronic. Acute toxicity or “blind staggers” results from the consumption of plants capable of accumulating large quantities of Se whereas the chronic form (alkali disease) is caused by the prolonged ingestion of fodder containing lower but yet toxic quantities. Selenium-accumulating plants have been reported from the United States and from Australia. In the U.S. certain species of the genus Astragalus are among the better known Se accumulators. Amounts of Se in excess of 1000 mg/kg are frequently found in these plants. In Australia a native plant of Queensland Morinda reticulata is a selenium accumulator and has caused selenium poisoning in horses. True selenium accumulators are only found where seleniferous soils occur and their presence has been used as an aid in the mapping of such soils.
In Ireland true selenium accumulating plants do not occur and the acute form of poisoning in animals is unknown. The chronic type is known and is prevalent in pastures with Se levels ranging from 3 to 100 mg/kg. The variation in Se content can be quite large and outbreaks of selenium poisoning will depend on the length of time animals spend grazing toxic pastures. Soil ingestion may also contribute to the onset of the disorder.
Where farm size is small as in parts of Co. Limerick, the problem of selenium toxicity is serious, as stock must be removed to non-seleniferous pastures when symptoms of poisoning occur. In Co. Meath, Crinion (1980) has recorded a number of instances of selenium poisoning both in cattle and horses but because farm size is generally larger in this part of the country it is easier to take preventive measures. The levels of Se recorded (Fleming and Walsh, 1957) for some typical Irish seleniferous pastures are shown in Table 2.
|Table 2 Selenium contents of soil and plant materials from toxic areas (mg/kg)
The identification of seleniferous soils and pastures on a farm is obviously of primary importance and can be achieved by means of soil and/or herbage analysis. Frequently seleniferous pastures occupy only a fraction of the total farm area and in such cases they should be fenced off and, if practicable, used for cereal or sugar beet production. In such cases the dilution effect at mill or factory will be sufficient to remove any possibility of danger. If this is done it must be realised that tillage operations inevitably lead to increased surface soil aeration with possible oxidation of soil selenium to more available forms. When such land is ultimately returned to grass, hay should be made as its toxicity is less that of fresh grass. Toxicity can decrease with storage but even then forage should be fed only sparingly to stock and should be monitored for selenium content. Selenium values in excess of 5 mg/kg can be toxic to cattle and in the case of the horse values greater than 2 mg/kg should be viewed with extreme caution.
The spreading of river spoil in areas where Se is elevated will result in an increase in soil and herbage Se values. Material dredged from some rivers in Co. Meath has proven deleterious in this regard and the practice is not advisable.
The realisation that selenium might be capable of playing an essential role in animal nutrition arose from the work of Schwartz and Foltz (1957) which identified selenium as a component of a preparation capable of preventing liver necrosis in rats. In theUSA studies by Muth et al. (1958) indicated that supplementation of the diet of ewes with trace quantities of selenium was effective in preventing prenatal myopathy (muscle wastage) in lambs. Similar studies by a number of workers demonstrated the efficiency of selenium in the prevention of muscular dystrophy or white muscle disease (WMD) in livestock.
It is now recognised that the biochemical functions of selenium are intimately associated with those of vitamin E and the effects of selenium deficiency are often modified by changes in the dietary supply of this vitamin. Both are involved in processes protecting animal cells against oxidative damage to fats and other cellular components. Vitamin E and the selenium-containing enzyme glutathione peroxidase (SeGSHpx) act as antioxidants in destroying peroxides which cause muscle damage. The most commonly recognised clinical syndrome of selenium/vitamin E deficiency in cattle and sheep is a nutritional myopathy. Other selenium-responsive diseases such as “ill thrift” in cattle and reproductive disorders including infertility in ewes and retained placentae in cattle have been widely reported and are described by Levander (1986). There is also evidence to suggest that “tying up” in horses, which can occur following racing, training or heavy work is associated with low Se values (Cunha, 1991).
The most recent work on Se has been on the non-Se-GSHPx functions and in particular on the important relationships between Se and thyroid hormone metabolism. It has been shown that Se deficiency can increase some indicators of the hypothyroid stress associated with deficiency.
A dietary intake of 0.1 mg/kg Se is quoted by Levander (1986) as being satisfactory in providing a margin of safety against any dietary variable or environmental stresses likely to be encountered by grazing animals. However, requirements are greater when sulphate intakes are high and interfere with the conversion of Se to tissue SeGSHpx in animals (Mayland, 1994). Selenium utilisation varies depending on the form in the feed. The bio-availability of Se in animal by-products (including fish meal) can be as low as 9 percent, whereas that in plant products can be over 80 percent. Oldfield (1997) has reviewed the efficacy of various forms of selenium for livestock.
Increasing an animal’s Se status may be accomplished directly by injection or by the use of a selenium heavy pellet or indirectly by means of the soil-plant route. Using the latter method Culleton et al. (1997) maintained blood levels in a dairy herd at similar levels to that of a herd which was supplemented by Se injection. Attention must be drawn to the fact that under EU regulations the use of Se in fertilisers is not allowed at the present time.
Selenium deficiency in animals has been well characterized, but this is not so in the case of humans. A role for Se in preventing cardiovascular problems has been demonstrated in the Keshan province of China and by Keshin-Beck disease, an endemic osteo-arthropathy that occurs in eastern Asia. Both diseases are always located in low-Se eco-environments. There is no doubt that Keshan disease is Se-responsive, however it is clear from epidemiological features that the incidence of the disease suggests an infectious rather than a nutritional cause. It has now been shown that a certain benign human virus, which remains benign in Se-adequate mice become virulent in Se deficient mice (Beck et al., 1994; Beck et al., 1995). This is the first time that it has been shown that host nutritional status can influence the genetic make-up of a pathogen (Levander and Beck, 1996).
Plasma Se and GSHpx activity of people of low Se status in China were increased by supplementation with Se (Xia et al., 1989). In Finland where the incidence of cardiovascular diseases is high, all agricultural multinutrient fertilisers have been supplemented with Se since 1984 in order to increase the Se content of domestic foods and thus raise the population’s low Se intake (Eurola et al., 1991).