Toxicity Profiles
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
|
