1. Exposure Data

1.1. Chemical and physical data

1.1.1. Nomenclature

• Chem. Abstr. Serv. Reg. No.: 545-06-2
• Systematic name: Trichloroacetonitrile

1.1.2. Structural and molecular formulae and relative molecular mass

1.1.3. Physical properties (for details, see IARC 1991)

• (a) Boiling point: 85.7°C
• (b) Melting-point: −42°C
• (c) Conversion factor: mg/m³ = 5.91 × ppm

2. Studies of Cancer in Humans

No data were available to the Working Group.

3. Studies of Cancer in Experimental Animals

Trichloroacetonitrile was tested in a limited carcinogenicity study in female SEN mice by skin application, in an initiation/promotion study in female SEN 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 after skin application in mice or in the initiation/promotion study, in which trichloroacetonitrile was applied topically as six equal doses over a two-week period, followed by repeated doses of 12-O-tetradecanoylphorbol 13-acetate for 20 weeks. A small, significant increase in the proportion of mice with lung tumours and in the number of tumours per mouse was observed: control, 3/31 and 0.1; treated group (10 mg/kg bw, three times per week, eight weeks), 9/32 and 0.38 (p < 0.05) (IARC, 1991).

4. Other Data Relevant to an Evaluation Carcinogenicity and its Mechanisms

4.4. Genetic and related effects

4.4.1. Humans

No data were available to the Working Group.

4.4.2. Experimental systems (see Table 1 for references)

Table 1

Genetic and related effects of trichloroacetonitrile.

Trichloroacetonitrile did not induce DNA damage in bacteria. Conflicting results were obtained in bacterial mutation studies. It induced sister chromatid exchanges and DNA strand breaks in mammalian cell lines. Micronuclei were induced in the erythrocytes of newt (Pleurodeles waltl) larvae exposed for 12 days, but in mice dosed for five days, neither micronuclei in bone marrow nor abnormal sperm morphology were induced.

5. Evaluation

No epidemiological data relevant to the carcinogenicity of trichloroacetonitrile were available.

There is inadequate evidence for the carcinogenicity of trichloroacetonitrile in experimental animals.

6. References

• Bull R.J., Meier J.R., Robinson M., Ringhand H.P., Laurie R.D., Stober J.A. Evaluation of mutagenic and carcinogenic properties of brominated and chlorinated acetonitriles: by-products of chlorination. Fundam. appl. Toxicol. 1985;5:1065–1074. [PubMed: 4092869]
• Daniel F.B., Schenck K.M., Mattox J.K., Lin E.L., Haas D.L., Pereira M.A. Genotoxic properties of haloacetonitriles: drinking water by-products of chlorine disinfection. Fundam. appl. Toxicol. 1986;6:447–453. [PubMed: 3699330]
• IARC (1991) IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, Vol. 52, Chlorinated Drinking-water; Chlorination By-products; Some Other Halogenated Compounds; Cobalt and Cobalt Compounds, Lyon, pp. 269–296. [PMC free article: PMC7681469] [PubMed: 1683674]
• Le Curieux F., Giller S., Gauthier L., Erb F., Marzin D.7 1995 Study of the genotoxic activity of six halogenated autonitriles, using the SOS chromotest, the Ames-fluctuation test and the newt micronucleus test. Mutat. Res. 341 289 302. [PubMed: 7531288]
• Meier J.R., Bull R.J., Stober J.A., Cimino M.C. Evaluation of chemicals used for drinking water disinfection for production of chromosomal damage and sperm-head abnormalities in mice. Environ. Mutag. 1985;7:201–211. [PubMed: 3971958]