For definition of Groups, see Preamble Evaluation.
VOL.: 52 (1991) (p. 269)
Halogenated acetonitriles are not produced on an industrial scale. Chloro- and trichloroacetonitriles have been used on a limited basis in the past as pesticides.
Several halogenated acetonitriles have been detected in chlorinated drinking-water in a number of countries as a consequence of the reaction of chlorine with natural organic substances (and bromine in the case of brominated acetonitriles) present in untreated water. The only known route of human exposure is through chlorinated drinking-water.
Halogenated acetonitriles (chloroacetonitrile, dichloroacetonitrile, trichloroacetonitrile, bromochloroacetonitrile and dibromoacetonitrile) were tested in a limited carcinogenicity study in female Sencar mice by skin application, in an initiation/promotion study in female Sencar mice by skin application and in a screening assay for lung tumours in female strain A mice by oral administration. No skin tumour was produced by any of the haloacetonitriles after skin application in mice. In the initiation/promotion study, reproducible, significant increases in the numbers of animals with skin tumours were seen only with dibromoacetonitrile; no dose-related increase in the incidence of skin tumours was observed. Marginal increases in the proportion of mice with lung tumours occurred with all of the halogenated acetonitriles, but the increases were significant only with chloroacetonitrile, trichloroacetonitrile and bromochloroacetonitrile.
No data were available to the Working Group.
In short-term screening studies in vivo, chloroacetonitrile, bromochloroacetonitrile and dibromoacetonitrile caused minimal developmental toxicity in the presence of significant maternal toxicity. In developmental toxicity studies, dichloroacetonitrile and trichloroacetonitrile caused malformations and embryolethality in the presence of maternal toxicity; with trichloroacetonitrile, embryolethality was also observed at lower dose levels in the absence of maternal toxicity.
Mutations were induced in bacteria by bromochloroacetonitrile and dichloroacetonitrile but not by chloroacetonitrile, dibromoacetonitrile or trichloroacetonitrile. Mutations were induced in insects by dichloroacetonitrile but not by dibromoacetonitrile.
Sister chromatid exchange was induced in cultured mammalian cells by all five halogenated acetonitriles. DNA strand breaks were induced in human lymphocytes in vitro by bromochloroacetonitrile, dibromoacetonitrile and trichloroacetonitrile.
In orally treated mice, neither micronuclei in bone-marrow cells nor sperm-head abnormalities were induced by any of the five halogenated acetonitriles.
There is inadequate evidence for the carcinogenicity of bromochloroacetonitrile in experimental animals.
There is inadequate evidence for the carcinogenicity of chloroacetonitrile in experimental animals.
There is inadequate evidence for the carcinogenicity of dibromoacetonitrile in experimental animals.
There is inadequate evidence for the carcinogenicity of dichloroacetonitrile in experimental animals.
There is inadequate evidence for the carcinogenicity of trichloroacetonitrile in experimental animals.
No data were available from studies in humans on the carcinogenicity of halogenated acetonitriles.
Bromochloroacetonitrile is not classifiable as to its carcinogenicity to humans (Group 3).
Chloroacetonitrile is not classifiable as to its carcinogenicity to humans (Group 3).
Dibromoacetonitrile is not classifiable as to its carcinogenicity to humans (Group 3).
Dichloroacetonitrile is not classifiable as to its carcinogenicity to humans (Group 3).
Trichloroacetonitrile is not classifiable as to its carcinogenicity to humans (Group 3).
For definition of the italicized terms, see Preamble Evaluation.
Subsequent evaluations: Vol. 71 (1999) (Bromochloroacetonitrile); (Chloroacetonitrile); (Dibromoacetonitrile); (Dichloroacetonitrile); (Trichloroacetonitrile)
See Also: Toxicological Abbreviations