Selenium poisoning in people is reviewed from the perspective of the clinical laboratory and the evaluation of this condition is straightforward when the analytic results are markedly elevated and the patient is acutely symptomatic and the distinguishing of toxic from non – toxic elevation is a more frequent and more challenging issue. Selenium is a trace element, so only a minute amount is needed to maintain its important physiological roles.
The recommended daily allowance of selenium is 55 mcg per day and this is based on a reference dose of 0.005 mg/kg per body weight on daily basis. It is important to remember not to give selenium supplements to your infants. Hydrogen selenide is the most toxic compound of selenium following inhalation. Selenium sulfide, sodium selenite, and selenium dioxide are other toxic compounds. The most toxic compound on oral ingestion is sodium selenite.
History of Selenium Poisoning
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In the 1930s was firstly detected selenium toxicity in animals by the occurrence of neurological and muscular symptoms in cattle [1]. This was known as blind staggers or alkali disease and nowadays, it is thought that it represents different stages of the same condition. The clinical features of the blind staggers include paralysis, poor feeding, random walking, and vision loss or impairment, while in the alkali disease, there is anemia, joint erosion, deformed and sloughing hooves, loss of hair, and renal, hepatic, and cardiovascular effects.
Also, in animal studies, selenium toxicity has been associated with abnormal fetal development in the sheep, swine, and cattle, but with infertility and a higher proportion of runt offspring and fetal deaths. [2]
Selenium Poisoning: Causes
There are different causes for selenium poisoning and they can range from ingestion of excessive selenium, such as in the case of regular snacking on Brazil nuts, which could have up to 90 mcg of selenium per nut. Also, there are other plants that have the capability to concentrate the selenium that is taken up from the soil and they are termed, selenium accumulators. The normal plant selenium content is 10 ppm, even when they grow on selenium-rich soils, but the selenium accumulators may have concentrations in thousands of ppm.
There are some studies in which are reported that Astragalus racemosus has a concentration of almost 15,000 ppm of selenium [3]. These plants are able to grow only on seleniferous soils and they are primarily known as selenium indicators. They are largely found in North America, but some species grow in Australia too. Also, there are other selenium accumulators and they can grow on selenium–poor soils, so they are considered as secondary selenium accumulators.
Types of selenium poisoning
There are two types of selenium poisoning – acute and chronic.
Acute selenium poisoning: Acute selenium poisoning is known as short – term selenium poisoning and the effects of acute selenium poisoning are depending upon the route of exposure. The acute inhalation exposure to selenium (this is usually happening in the form of hydrogen selenide or selenium dioxide) is primarily resulting in respiratory effects with irritation of the mucous membranes in the throat and nose, producing chemical pneumonia, bronchitis, bronchial spasms, dyspnea, nosebleeds, and coughing.
Also, there may be gastrointestinal effects, including nausea and vomiting; irritation of the eyes; neurological effects, such as malaise and headaches; cardiovascular effects. The acute oral exposure to selenium results in lesions of the lung and pulmonary edema; gastrointestinal effects including diarrhea, vomiting, abdominal pain, and nausea; cardiovascular effects, such as tachycardia; effects of the liver; and neurological effects, such as tremors, chills, irritability, and aches. [4,5]
Chronic selenium poisoning:
Chronic selenium poisoning is known as long–term selenium poisoning. The chronic exposure to the high levels of selenium in food and water is resulting in discoloration, deformation and loss of nails, listlessness, lack of mental alertness, weakness, a garlic odor to the breath, excessive tooth decay and discoloration, and reversible loss of hair (baldness). [6,7]
References:
[1] Khanal DR, Knight AP. Selenium: Its role in livestock health and productivity. The Journal of Agriculture and Environment. 2010;11:101-6.
[2] Hosnedlova B, Kepinska M, Skalickova S, et al. A summary of new findings on the biological effects of selenium in selected animal species—A critical review. International Journal of Molecular Sciences. 2017;18(10):2209. doi:10.3390/ijms18102209
[3] Trelease SF, Trelease HM. Selenium as a stimulating and possibly essential element for indicator plants. American Journal of Botany. 1938;25(5):372-80.
[4] Hadrup N, Ravn-Haren G. Acute human toxicity and mortality after selenium ingestion: A review. Journal of Trace Elements in Medicine and Biology. 2020;58:126435.
[5] MacFarquhar JK, Broussard DL, Melstrom P, et al. Acute selenium toxicity associated with a dietary supplement. Archives of Internal Medicine. 2010 ;170(3):256–61.
doi:10.1001/archinternmed.2009.495
[6] Vinceti M, Filippini T, Cilloni S, et al. Health risk assessment of environmental selenium: Emerging evidence and challenges (Review). Molecular Medicine Reports. 2017;15(5):3323-35.
[7] Rhian M, Moxon Al. Chronic selenium poisoning in dogs and its prevention by arsenic. The Journal of Pharmacology and Experimental Therapeutics. 1943;78(3):249-64.
