mg Se/l) (Schutz and Turekian 1965; Höghberg 1986). At high altitudes, groundwater contains 0.03–0.12 and 0.00–0.11 mg/l Se in summer and winter, respectively. During summer and winter, river water contains 0.06–0.32 and 0.28–0.46 mg/l Se (Giri 2019).
4.2.3 Forage
A positive correlation was found between the presence of Se in the soil and Se level in forage. In plants, the amount of Se in the seeds is higher than in any other part of the crop. Specific levels of Se in different plants are due in particular to the plants’ genetic composition (Harada et al. 1989; Stephen et al. 1989; McQuinn et al. 1991). Se in forage varies between 0.02–0.05 mg Se/kg DM in poisonous areas for Se (Whelan et al. 1994).
4.2.4 Feed Supplements
An enriched feed supplement is the second way to in which domestic animals can develop toxic levels, after Se‐enriched forage is consumed. Following different cases of Se toxicity in domestic animals in the US, the FDA has specified that selenosis causing all forms of Se should be within 0.3 mgSe/kgDM (FDA 1987).
Wahlstrom and Olson (1959) and Wilson et al. (1982) reported focal symmetric poliomyelomalacia following administration of a Se supplement in swine but chronic selenosis in cattle, goats, and horses was rare after a Se supplement in feeds. Knott et al. (1958) reported the severe hair loss caused by the administration of 13.3 g Se for 82 days in pigs. Dietary Se dose in horses between 17 and 24 mg/l induced hair loss, inappetence, emaciation, and hoof lesions (Miller and Williams 1940). Oral application of Na2SeO3 along with a diet of 0.25–0.5 mg Se/kg BW grain‐hay molasses induced animal mortality with many other characteristics such as depression, polioencephalomalacia, vomiting, gastrointestinal hazards, etc. (Maag et al. 1960). Many studies have shown that Se feed supplement within the seleniferous range has hindered growth rate, caused broken hooves, and decreased calving in cattle (Dinkel et al. 1963; Olson et al. 1973).
4.2.5 Diagnosis of Se in Soil, Forages, and in Livestock Animals
Soil followed by water are the primary sources of Se for plants. The amount of Se plant uptake not only depends upon the amount of Se present in the soil but also upon the soil’s physico‐chemical properties. Na2SeO4 is the most available form of Se for plant uptake (Hawrylak‐Nowak 2013). Soil nature defines plant availability of Se. Se uptake has been found to be higher in the more heavily‐textured soils than in softer soil. The heavier‐textured soils are promoting plants to take up Se. Soil pH also has the value of plants taking up Se.
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. Seleniferous soil, water, and plants respectively showed >2 ppm, >50 ppb, and >1.0 ppm. Planting should be scheduled taking into account the presence of Se in top soil or sub‐soil (Davis et al. 2000).
The overall allowable amounts for Se in human drinking water, livestock drinking water, and irrigation water are 0.01, 0.05, and 0.02 ppm, Therefore it is mandatory to diagnose the Se level in all water sources before using the water for drinking and cultivation (WHO 1987).
Plants with 5 ppm of accumulated Se caused livestock health hazards. A study reported that seleniferous plants may accumulate 15 000 ppm of Se (Rosenfeld 1964). However, seleniferous plants are not always responsible for selenosis in livestock animals. Plants grown in seleniferous soil may or may not accumulate the Se in their tissue. Plants which accumulate Se in their tissue are called obligatory seleniferous plants. Milk‐vetches, poison‐vetches and prince's plume are the some of the more common obligatory seleniferous plants (Davis et al. 2000). Livestock animals do not consume these plants because of their non‐palatability but sometimes sheep consume these plants. Other plants accumulate Se in their tissue by normal processes. These types of plant are called facultative selenium accumulators. These plants are unpalatable to the livestock animals and emit a garlic‐sulfur odor. Saltbushes, curlycup gumweed, broom snakeweed, and asters are plants in this group. If they are forage‐deprived, cattle and horses consume these plants (Davis et al. 2000). The non‐accumulator plants are also responsible for evoking selenosis in animals. Therefore, the presence of such plant species may categorize the grazing land (Davis et al. 2000).
Se is a necessary element for normal growth and fertility in livestock animals. Where there is Se deficiency or toxic Se levels, normal growth has reportedly been stunted in livestock animals, even causing death. The Se‐deficient level in grazing cattle is 0.10 ppm, and 0.03 ppm in sheep. The toxic level is 1–5 ppm in cattle, sheep, and horses. This minute gap between Se deficiency and toxicosis has to be maintained by a livestock feeding and management system. Selenosis in livestock animals produces three types of toxicosis: chronic, acute, and sub‐acute toxicity. In livestock animals there are some general diagnosed signs such as hunger and thirst, abdominal discomfort, excessive salivation, respiratory failure, dental grating, blindness, and paralysis, etc. In livestock selenosis results in hematological changes, alteration of blood biochemical parameters, reduced antioxidant enzymatic activity, etc. (Rosenfeld and Beath 1964; Davis et al. 2000).
4.3 Toxicopathology of Selenium in Different Domestic Animals
It is well‐known that all animals are susceptible to selenium poisoning. Grazing activity of sheep, cattle, horses that increases the rate of selenosis might be due to the consumption of forage of seleniferous grasses or shrubs, whereas poisoning that occurs in poultry or swine and other domestic animals is as a result of being given seleniferous grain or some other seleniferous food. Subtypes of toxicity to selenium are:i
i Acute intoxication:
This results from the ingestion of a lethal amount of primary‐indicator or other plants which contains high levels of selenium (several hundred ppm Se). As plants containing high levels of selenium are unpalatable, acute selenium intoxication is uncommon. However, it is usually associated with hungry animals that might eat these seleniferous plants.ii
ii Chronic intoxication:
Chronic selenium poisoning is a consequence of the consumption of toxic levels of selenium (5–40 ppm) in plants such as grass or grain where selenium is bound in plant protein and is fairly insoluble in water. However, it has been shown that this condition can be caused by feeding the element's inorganic salts. The seleniferous feed must be eaten for weeks or months to have its effect. The key symptoms of poisoning in cattle and horses include hair loss, emaciation, hoof malformations, and lameness. Perhaps the worst economic impact arising from seleniferous forage intake is lower reproduction.
Blind stagger type chronic selenium poisoning is said to be induced by organic selenium compounds. To show evidence of poisoning the animals will need to ingest highly toxic amounts of these plants over a significant period of time. The condition of blind staggers is described in three stages. The animal has some vision loss in the first stage, and wanders in circles, disregarding objects along its way. In the second stage, the signs in stage one reach extreme severity and the forelegs of the animal are weak and give way. In the third stage, oral activity is arrested. The mechanism of the tongue and swallowing becomes paralyzed, respiration is staggered and quickened, abdominal pain is evident, and the cornea becomes cloudy. The third stage occurs unexpectedly and death frequently follows within a couple of hours, usually due to respiratory arrest.
Toxicopathology relies on the concentration of selenium in blood and organs ranging from 1 to 5 ppm across the entire livestock in the seleniferous zone (O'Toole and Raisbeck 1995). The sub‐chronic and chronic toxicity of the Se causes pathological changes in the skeletal muscle, heart, liver, spleen, and kidney, as they are mostly accumulated at a higher level in these organs (Rosenfeld and Beath 2013). There are reports of histopathological changes such as disrupted endocardium layer, diffuse lung hemorrhages,