The role of selenium in health was first recognized as a toxic one, by the recognition of its adverse effects. Being a trace element, only a minute amount is needed to maintain its important physiological roles. The recommended dietary allowance is 55 mcg per day, based on a reference dose of 0.005 mg/kg body weight/day. The following table shows the upper levels fixed by the FDA. It is important to note that infants should not receive selenium supplementation.
Table 1: Upper Intake Levels for Selenium
As of now, selenium toxicity is diagnosed based upon the presence of features of selenosis in humans, since there are no accurate biochemical or preclinical parameters.
Selenium toxicity in animals was detected by the occurrence of neurological and muscular symptoms in cattle during the 1930’s. This was variously called alkali disease, or blind staggers, and is today thought to represent different stages of the same condition.
The clinical features of blind staggers include vision loss or impairment, random walking, poor feeding and paralysis. In alkali disease, there is loss of hair, deformed and sloughing hooves, joint erosion, anemia, and cardiovascular, hepatic and renal effects.
In animals, selenium toxicity has also been associated with abnormal fetal development in cattle, swine and sheep, but with infertility and a higher proportion of runt offspring and fetal deaths.
The symptoms of toxicity depend on the route of exposure.
The inhalation of selenium compounds causes respiratory membrane irritation, pulmonary edema, bronchial inflammation and pneumonia. Elemental selenium dust exposure also produces mucous membrane irritation, bleeding from the nose, and coughing, besides the other symptoms.
Other features include vomiting and nausea, cardiovascular effects, headaches and malaise, and ophthalmic irritation.
The long-term intake of excessive selenium may involve either organic or inorganic forms in food or water. The symptoms of chronic selenium toxicity or selenosis first appear as a garlicky odor in the breath, and a metallic taste in the mouth. This is followed by gastrointestinal symptoms such as nausea or diarrhea, tiredness and irritability, and joint pain, in more than 70-75% of patients.
Other characteristic features include loss of mentation, paresthesia, hyperreflexia, nail changes resulting in brittleness, deformation and loss of nails, alopecia, discoloration and loss of teeth, and skin rashes. These are seen in more than 60-65% of patients.
Acute toxicity presents with acute respiratory distress syndrome, myocardial infarction, renal failure, vascular symptoms such as tachycardia and flushing of the face, neurological features including tremors, irritability, and myalgia. ECG abnormalities such as T-wave inversion and QT prolongation are often seen, and death is due to refractory hypotension
Causes of selenosis range from ingestion of excessive selenium, as in the case of regular snacking on Brazil nuts which could contain up to 90 mcg of selenium per nut. There are also many other plants which have the capability to concentrate selenium that is taken up from the soil, and they are termed selenium accumulators.
In contrast to the normal plant’s selenium content of 10 ppm, even when they grow on selenium-rich soil, selenium accumulators may have concentrations in thousands of ppm. Astragalus racemosus was reported to have a concentration of almost 15,000 ppm of selenium.
These plants are able to grow only on seleniferous soils, and are called primary selenium indicators. While found largely in North America, some species do grow in Canda. Other selenium accumulators also exist, which can grow on selenium-poor soils, and these are secondary soil accumulators.
The most toxic compound of selenium following inhalation is hydrogen selenide. Other toxic compounds are selenium dioxide, sodium selenite and selenium sulfide. Sodium selenite is the most toxic compound on oral ingestion.
Selenium sulfide has been linked with the occurrence of liver and lung tumors in mice and rats following oral exposure, and is a Group B2 carcinogen as per EPA classification. Elemental selenium has low toxicity following oral administration.
EPA has classified elemental selenium as a Group D, not classifiable as to human carcinogenicity, and selenium sulfide as a Group B2, probable human carcinogen.
Exposure to selenium is primarily through food, and in some areas with seleniferous soils, through drinking water. Airborne exposure is rare, but occupational exposure is possible with the chemical processes for recovery of selenium, painting trades and the metal industries. Gun-bluing chemicals contain a high concentration of selenium and are often involved in acute poisoning. Potential sources of toxic levels of selenium include Astragalus and copper ingestion.
Some agencies have put forward a chronic reference exposure level of 0.02 mg/m3 for selenium and its compounds, and of 0.00008 mg/m3 for hydrogen selenide, based on findings in humans with selenosis and guinea pigs with selenium inhalation toxicity.
Selenium may exacerbate the effect of:
Selenium may impair the effects of: