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Description of key information

Cyanogen chloride is apparently converted to cyanide ion in vivo by a reaction with hemoglobin and glutathione, which eventually liberates the CN ion (1/2). The small quantity of cyanide always present in human tissues is metabolized at the approximate rate of 17 ug/kg x min, primarily by the hepatic enzyme rhodanese, which catalyzes the irreversible reaction of cyanide and a sulfane to produce thiocyanate, a relatively nontoxic compound excreted in the urine. The limiting factor under normalconditions is the availability of a sulfane as a substrate for rhodanese, and sulfur is administered therapeutically as sodium thiosulfate to accelerate this reaction. The lethal dose of cyanide is time dependent because of the ability of the body to detoxify small amounts of cyanide via the rhodanese-catalyzed reaction with sulfane. A given amount of cyanide absorbed slowly may cause no biological effects even though the same amount administered over a very short period of time may be lethal (3). Cyanogen chloride reacts rapidly with both serum and red cells, but cyanide is produced only from ther reaction with red cells. As would be expected, higher percentage conversions of cyanogen chloride to cyanide are obtained with washed red cells than with whole blood. Cyanogen chloride reacts rapidly with rat hemoglobin, no more than 1% of the original cyanogen chloride added being left after 5 sec from a mixtureof cyanogen chloride (17.3 ug/mL) and of hemoglobin (5-7 vol O2%). It would appear that the essential reactions in the production of of cyanide from cyanogen chloride and blood are an initial reaction with hemoglobin followed by liberation of cyanide by reaction with glutathione. However, cyanogen chloride reacts directly with glutathione. The rate of reaction is of the same order as with hemoglobin (4).

Key value for chemical safety assessment

Bioaccumulation potential:
no bioaccumulation potential

Additional information

References:

(1) Clayton, G. D. and F. E. Clayton (eds.). Patty's Industrial Hygiene and Toxicology: Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John Wiley Sons, 1981-1982., p. 4861

(2) NIOSH Pocket Guide to Chemical Hazards & Other Databases CD-ROM. Department of Health & Human Services, Centers for Disease Prevention & Control. National Institute for Occupational Safety & Health. DHHS (NIOSH) Publication No. 2005-151 (2005)

(3) U.S. Army Research Institute of Chemical Defense, Chemical Casualty Care Division; Medical Management of Chemical Casualties Handbook, 3rd Ed. Aberdeen Proving Ground, MD (July 2000)

(4) Aldridge WN; Biochem 48: 271-6 (1951)