CYANIDE
Studies by Philbrick et al. (1979) showed decreased weight gain and thyroxin levels and myelin degeneration in
rats at 30 mg/kg/day CN. Other chronic studies either gave higher effect levels or used the subcutaneous route
(Crampton et al., 1979; Lessell, 1971; Hertting et al., 1960). Human data do not provide adequate information from
which to derive an RfD because effective dose levels of chronically ingested CN are not documented. Therefore,
the study of Howard and Hanzel (1955) provides the highest NOAEL, 10.8 mg/kg/day for CN, and is chosen for the
derivation of an RfD for CN of 1.5 mg/day or 0.02 mg/kg/day.
Cyanide is metabolized extensively in the liver, indicating that the only relevant route of administration for
quantitative risk assessment in the derivation of an oral RfD is the oral route of administration.
Decreased protein efficiency ratio was produced by dietary cyanide treatment of rats during gestation, lactation
and postweaning growth phase in the Tewe and Maner (1981a) experiment: the dose level of cyanide (10.6 mg/kg/
day) producing that effect is slightly lower than the currently accepted NOAEL of 10.8 mg/kg/day (U.S. EPA, 1985).
Furthermore, Tewe and Maner (1981b) tested sows. Possible effects observed at about 9.45 mg/kg/day were
proliferation of glomerular cells of the kidneys and reduced activity of the thyroid glands in the gilts. However, the
number of animals in this experiment was very small. A Japanese study (Amo, 1973) indicated that 0.05 mg/ kg/day
of cyanide obtained from drinking water decreased the fertility rate and survival rate in the F1 generation and
produced 100% mortality in the F2 generation in mice. However, these data are not consistent with the body of
available literature.
Classification — D; not classifiable as a human carcinogen.
Basis — Pertinent data regarding carcinogenicity have not been located in the available literature.
http://www.epa.gov/IRIS/subst/0031.htm