Special Article Endemic selenium intoxication of humans in

prevalence, from 1961 to 1964, the morbidity was almost 50 % in the 248 inhabitants of the five most heavily affected villages; its cause was determined to be selenium intoxication. The most common sign of the poisoning was loss of hair and nails. In areas of high incidence, lesions of the skin, nervous system, and possibly teeth may have been involved. A case is reported of a middle-aged, female hemiplegic, whose illness and death apparently were related to selenosis. Daily dietary intakes of selenium, estimated after the peak prevalence had subsided, averaged 4.99 (range 3.20 to 6.69) mg and hair and blood selenium levels averaged 32.2 and 3.2 pg/ml, respectively. Up to l000x differences occurred when selenium contents of vegetables, cereals, scalp hair, blcod, and urine from the selenosis areas were compared with those from Keshan disease (selenium deficiency) areas. The ultimate environmental source of selenium was a stony coal of very high selenium content (average more than 300 xg/g; one sample exceeded 80,000 j.tg/g). Selenium from the coal entered the soil by weathering and was available for uptake by crops because of the traditional use oflime as fertilizer in that region. This particular outbreak of human selenosis was due to a drought that caused failure of the rice crop, forcing the villagers to eat more high-selenium vegetables and maize and fewer protein foods. Am J Cliii Nutr 1983;37:872-881. KEY WORDS Selenium toxicity in man, human selenosis, seleniferous foods, endemic sele-nium poisonin