The Risk Assessment Information System

Toxicity Profiles

Condensed Toxicity Summary for CYANIDE

NOTE: Although the toxicity values presented in these toxicity profiles were correct at the time they were produced, these values are subject to change. Users should always refer to the Toxicity Value Database for the current toxicity values.

February 1994

Prepared by Rosmarie A. Faust, Ph.D., Chemical Hazard Evaluation and Communication Group, Biomedical and Environmental Information Analysis Section, Health and Safety Research Division, *, Oak Ridge, Tennessee. Prepared for OAK RIDGE RESERVATION ENVIRONMENTAL RESTORATION PROGRAM

*Managed by Martin Marietta Energy Systems, Inc., for the U.S. Department of Energy under Contract No. DE-AC05-84OR21400

Cyanide most commonly occurs as hydrogen cyanide and its salts--sodium and potassium cyanide. Cyanides are both man-made and naturally occurring substances. They are found in several plant species as cyanogenic glycosides and are produced by certain bacteria, fungi, and algae. In very small amounts, cyanide is a necessary requirement in the human diet. Cyanides are released to the environment from industrial sources and car emissions (ATSDR, 1989).

Cyanides are readily absorbed by the inhalation, oral, and dermal routes of exposure. The central nervous system (CNS) is the primary target organ for cyanide toxicity. Neurotoxicity has been observed in humans and animals following ingestion and inhalation of cyanides. Cardiac and respiratory effects, possibly CNS-mediated, have also been reported. Short-term exposure to high concentrations produces almost immediate collapse, respiratory arrest, and death (Hartung, 1982; EPA, 1985). Symptoms resulting from occupational exposure to lower concentrations include breathing difficulties, nervousness, vertigo, headache, nausea, vomiting, precordial pain, and electrocardiogram (EKG) abnormalities (Carmelo, 1955; El Ghawabi et al., 1975; Sandberg, 1967; Wuthrich, 1954). Thyroid toxicity has been observed in humans and animals following oral and inhalation exposure to cyanides (Philbrick et al., 1979; EPA, 1984). In animal studies, cyanides have produced fetotoxicity and teratogenic effects, including exencephaly, encephalocele, and rib abnormalities (Doherty et al., 1982; Frakes et al., 1986; Tewe and Maner, 1981b; Willhite, 1982).

Reference doses (RfDs) have been calculated for subchronic and chronic oral exposure to cyanide and several cyanide compounds (EPA, 1990a-e; 1991a-e). The values, derived from a single study, are based on a no-observed-adverse-effect level (NOAEL) of 10.8 mg/kg/day for cyanide in a 2-year dietary study with rats (Howard and Hanzal, 1955). The subchronic and chronic oral RfDs are 0.02 mg/kg/day for cyanide; 0.04 mg/kg/day for sodium cyanide, calcium cyanide, and cyanogen; 0.05 mg/kg/day for potassium cyanide, chlorine cyanide, and zinc cyanide; 0.1 mg/kg/day for silver cyanide; and 0.2 mg/kg/day for potassium silver cyanide. Data were insufficient to derive a reference concentration (RfC) for cyanide.

No suitable cancer bioassays or epidemiological studies are available to assess the carcinogenicity of cyanide. Therefore, EPA (1991b) has placed cyanide in weight-of-evidence group D, not classifiable as to human carcinogenicity. Retrieve Toxicity Profiles Formal Version

Last Updated 10/07/97

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