The presence of Se in groundwater and surface water mainly depends upon the characteristics of soil, and anthropogenic factors relating to that area (Giri 2019). The underground water of a seleniferous region showed 2.54–69.53 μg/l of Se, whereas a non‐seleniferous region was characterized by 0.25–8.63 μg/l (Dhillon and Dhillon 1991). Soil is the main source for the higher accumulation of Se in forage (Lakin 1972; Wu et al. 1988; Harada et al. 1989; Stephen et al. 1989; McQuinn et al. 1991). Feed supplements also caused selenosis in livestock animals. Wahlstrom and Olson (1959) and Wilson et al. (1982) reported a focal symmetrical poliomyelomalacia after administration of a Se supplement in swine but chronic selenosis in cattle, sheep, and horse was rare after a Se supplement in feeds. Therefore, diagnosis of Se in soil, forages, and in livestock animals should be executed properly. The primary source of Se for plants is soil followed by water. Se uptake by plants mostly depends upon the soil’s physico‐chemical properties and basically the pH of the soil determines the Se uptake by plants. If a plant has the capability to uptake Se (i.e. seleniferous plants), then it will accumulate higher Se. The nature of the soil defines the Se availability to plants. It has been found that Se uptake is higher in heavier‐textured soils that in clay‐type soil. The heavier‐textured soils promote Se uptake by plants. The pH of the soil is also important for Se uptake by plants. A study reported that high soil pH will increase the leaching of Se toward the sub‐soil from the top soil. Therefore, when examining Se availability in the soil, it has been well documented that soil should be tested for pH level and the soil samples should be taken at different depths according to the pH (Davis et al. 2000).
Higher levels of Se exposure triggered alkali disease and the effect of selenium toxicity was blind staggers (National Research Council [NRC] 1983). The higher Se level triggered three forms of toxicity primarily: acute, sub‐acute, and chronic toxicity. Animal poisoning is described as being acute, sub‐chronic, or chronic (National Research Council [NRC] 1983). A lot of factors control the selenosis in an animal’s body, such as the properties of Se and animal health properties. It was also found that selenosis varies from species to species of livestock animals (horses > cattle) (Ehlig et al. 1968; Rosenfeld and Beath 2013). Sub‐chronic and chronic Se toxicity causes pathological changes mainly in skeletal muscle, heart, liver, spleen, and kidney as Se is mostly accumulated at a higher level in these organs (Rosenfeld and Beath 2013). Therefore, some preventive measurement like agricultural field management, the feeding of high protein‐rich feed, dietary sulfate, methionine supplement, linseed meal, spraying sulfur‐containing materials on fodders grown in selenium‐rich soil, clean water, phyto‐remediation etc. are being implemented to maintain the health and higher productivity of domestic animals (Dhillon and Dhillon 1991). Therefore, this book chapter discusses in detail the sources and mechanism of Se toxicity in the bodies of livestock animal, as well as the probable preventive measures to attenuate Se toxicity leading to better health and higher production of the livestock animals and reduction of selenium in the human food chain through milk and meat intake.
4.2 Sources of Selenium to Domestic Animals
Following various studies, it has been found that the sources of Se toxicity in domestic animals are soil, water, feed supplements, fodders grown on selenium‐rich soil, etc. The Se levels in different food sources of different country are shown in Table 4.1.
Table 4.1 Presence of Se (mg/kg) in different foods of different countries.
| Food | ||||
|---|---|---|---|---|
| Country | Cereals (mg/kg) | Meat (mg/kg) | Dairy food (mg/kg) | Vegetables (mg/kg) |
| India | 0.23–1.64a | – | 0.01–0.09b | 0.92–1.34a |
| Australiac | 0.01−/0.31 | 0.06–0.34 | </0.001–0.11 | </0.001–0.022 |
| U.K.d | 0.11 | 0.12–0.6 | 0.01–0.085 | 0.005–0.01 |
| U.S.d | 0.3–0.56 | 0.06–1.33 | 0.006–0.3 | 0.004–0.07 |
| Canadad | 0.01 | 0.06–1.22 | 0.005–0.01 | 0.005–0.01 |
| Finlandd | 0.02 | 0.05–0.48 | 0.002–0.025 | 0.002 |
| New Zealandd | 0.035 | 0.03–0.38 | 0.004–0.025 | 0.003 |
a Dhillon and Dhillon (1991).
b Giri (2019).
c Australia (Tinggi et al. 1992; Tinggi 1999; Tinggi and Conor Reilly 2001).
d Combs (1988).
4.2.1 Soil
Weathering is the primary natural process to release Se in the soil. In different forms, Se present in the soil like elemental selenium, calcium selenate, basic ferric selenite, and organic selenium compounds after the decomposing of animal and plant materials. The coal‐mining region mainly contains a higher level of Se due to the presence of pyrite oxidation (Dreher and Finkelman 1992). The level of Se varies from states to states, country to country (Dhillon and Dhillon 2003; Lenz and Lens 2009). Usually, the soil contains 0.1–2 mg Se/kg (Fishbein 1983). It was found that soil in the US, India, and Ireland has a higher level of Se (100 mg Se/kg), while soil in Brazil and Argentina has a relatively lower level of Se (< 0.1 mg/kg) (Dhillon and Dhillon 2003; Lenz and Lens 2009). Depending on the higher and lower levels, one region may recognize each as a region that is seleniferous and nonseleniferous. Soil which contains 5 mg/kg Se is very toxic (Rogers et al. 1990).
4.2.2 Water
Se's presence in groundwater and surface water depends largely on soil characteristics, and anthropogenic factors relating to that area (Giri 2019). Underground water of a seleniferous region showed 2.54–69.53 μg/l of Se, whereas a nonseleniferous region was characterized by 0.25–8.63 μg/l (Dhillon and Dhillon 1991). Freshwater showed