Studies on the toxicology of acrylonitrile

Abstract

It was found that the toxicity of acrylonitrile was due not only to the hydrogen cyanide liberated from it but to acrylonitrile itself. A small amount of hydrogen cyanide appeared in the blood of animals after a single injection of acrylonitrile. Although when sodium thiosulfate was injected before the acrylonitrile there was a great reduction in the hydrogen cyanide concentration in the blood and a lessening of symptoms, animals were not protected effectively from poisoning. In contrast, L-cysteine greatly reduced both the acrylonitrile and hydrogen cyanide concentration in the blood and protected the animals from poisoning. L-Cysteine formed an addition compounds with acrylonitrile in the test tube. This compound caused neither acute nor delayed symptoms when injected into animals. About 15% of the acrylonitrile given was excreted unchanged in the expired air and urine and another 15% was excreted in the urine as thiocyanate. The fate of about two-thirds of the acrylonitrile given is not yet clear. Acrylonitrile had an inhibitory effect on K+-stimulated respiration of brain cortex slices at 10-3M, whereas it had little effect on respiration of the liver at the same concentration. Acrylonitrile was judged to have a strong anesthetic effect on peripheral nerves when its effect was compared with those of various anesthetics and organic solvents. Sulfhydrile (SH) and disulfide (S-S) compounds had good therapeutic effect on acute acrylonitrile poisoning in animals, especially in rabbits which received these compounds intravenously. © 1965, National Institute of Occupational Safety and Health. All rights reserved.