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Description of key information

Human data on cyanide exposures are available from industrial exposures, cigarette smoking and dietary intake of cyanogenic glycosides.

Additional information

The occurrence of toxic effects after exposure to subacute levels of cyanide are assessed in humans by examining selected populations exposed to cyanide compounds in various ways. El Ghawabi et al, 1975 and Banerjee et al., 1997 studied self-reported adverse health effects and serum thiocyanate levels in workers in the electroplating industry. Serum thiocyanate levels and the incidence of goiter were found to be increased among cigarette smokers (ECETOC, 2007). Populations consuming cassava, a root vegetable high in cyanogenic glycosides, were investigated by Cliff et al, 1986, who found that the incidence of goiter was low. Iodine insufficiency is recognised as an important factor for development of thyroid disease after cyanide exposure (Hennart, et al., 1982). The mechanism of goitrogenic action of cyanide involves blocking the uptake of iodine into the thyroid gland and decreasing the synthesis of thyroid hormones. Data of Barrere et al., 2000 and Knudsen et al., 2002, support this mechanism, as they described adverse effects on the thyroid gland among iodine-deficient European populations exposed to cyanide primarily through cigarette smoking.

The conclusion of the ECETOC expert group is that background and lifestyle exposures to cyanogenic sources and dietary levels of iodine are important factors in the development of adverse effects on the thyroid gland. ECETOC identifies cyanide exposure which results in serum thiocyanate levels of 15 µg SCN-/ml, in the general iodine-sufficient population, to be a threshold for development of adverse health effects (goiter).