Following chronic oral exposure to excessive amounts of the organic selenium compounds in food, the two principal clinical conditions observed in humans are dermal and neurological effects, as described most completely in the epidemiological study of endemic selenosis in the People's Republic of China. The dermal manifestations of selenosis include loss of hair, deformation and loss of nails, and discoloration and excessive decay of teeth, while neurological effects include numbness, paralysis, and occasional hemiplegia.
The average dietary intake of selenium associated with selenosis in these people has been estimated to be 1,270 µg/day (~0.02 mg/kg/day, or 10–20 times higher than normal daily intake).
Loss of hair and malformation of hooves in pigs, horses, and cattle, and poliomyelomalacia in pigs have been reported to occur following long-term exposure to excessive amounts (more than 30 times the normal dietary amount of selenium) of the organic selenium compounds found in seleniferous plants. Histologically, swine with selenium-induced neurological signs exhibit bilateral macroscopic lesions of the ventral horn of the spinal cord.
The selenium in the selenium-accumulating plant Astragalus bisulcatus appears to be a more potent neurotoxicant than D,L-selenomethionine or selenate. The form of selenium in A. bisulcatus is unknown, although it is apparently nonprotein. Myocardial degeneration has been experimentally produced in cattle, sheep, and swine (as well as in laboratory mammals) by acute and longer-term exposures to inorganic salts of selenium, but it is unclear whether seleniferous grains or forages, or other natural sources of selenium, cause the same cardiomyopathy.
The determination of selenium in a variety of biological materials requires careful sample preparation. Diagnosing selenium intoxication can be done with ablood or urine test, which indicates recent selenium intake. Hair or nail samples can be taken to evaluate the long-term selenium status.