Selenium was discovered by Jöns Berzelius in 1817 as a contaminant of sulfuric acid vats that caused illness in Swedish factory workers. He originally believed it to be the element tellurium (from the Latin tellus, "earth"), but on finding it to be an entirely new, yet similar, element, he named it from the Greek selene, "moon." Selenium has unusual light-sensitive electrical conductive properties, leading to its widespread use in industry. It is both an essential component of the human diet and a deadly poison.
Much of what is known about selenium centers around its role as an essential trace element required in the diet of most living things, not around its toxic properties. In the 1970s, it was discovered to be an essential cofactor of the enzymeglutathione peroxidase. Keshan disease, an endemic cardiomyopathy associated with multifocal myonecrosis, periacinar pancreatic fibrosis, and mitochondrial disruption, was described in 1979 in Chinese women and children who chronically consumed a selenium-poor diet.9 Kashin-Beck disease, a disease causing shortened stature from chondrocyte necrosis, is described in young children in Russia, China, and Korea; although other factors are also likely involved, partial improvement results from with selenium supplementation.2
These observations prompted the establishment, in 1980, of the United States' recommended daily allowance (RDA) of selenium. Taking into account the level of supplementation required to achieve optimal glutathione peroxidase activity in selenium-deficient study populations, as well as the amounts required to cause toxicity, the recommendation calls for 55 μg/d. Deficiency occurs when daily intake falls below 20 μg/d.9
Chronic selenium toxicity, or selenosis, has occurred throughout history. Described first in animals, the acute syndrome of "blind staggers" and the more chronic "alkali disease" affected livestock eating highly seleniferous plants. Findings included blindness, walking in circles, anorexia, weight loss, ataxia, and dystrophic hooves. Humans in seleniferous areas of China and Venezuela develop similar integumentary symptoms (dermatitis, hair loss, and nail changes) at an intake of approximately 6000 μg/d, which is more than 100 times the RDA.4,36 In recent years, there have been several outbreaks of chronic selenium toxicity related to improperly packaged dietary supplements.14,35,42
Selenium is widely distributed throughout the earth's crust, usually substituting for sulfur in sulfide ores such as marcasite (FeS2), arsenopyrite (FeAsS), and chalcopyrite (CuFeS2). It is found in the soil where it has leeched from bedrock, in groundwater, and in volcanic gas. The highest soil concentrations of selenium in the United States are in the Midwest and West. Dietary selenium is easily obtained through meats, grains, and cereals. Brazil nuts, grown in the foothills of the highly seleniferous Andes Mountains, contain the highest concentration measured in food, but chronic selenium toxicity from Brazil nuts has not been reported.2
In industry, selenium is generated primarily as a byproduct of electrolytic copper refining and in the combustion of rubber, ...