1. Exposure Data

1.1. Chemical and physical data

1.1.1. Nomenclature

• Chem. Abstr. Serv. Reg. No.: 3252-43-5
• Chem. Abstr. Name: Dibromoacetonitrile

1.1.2. Structural and molecular formulae and relative molecular mass

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

• (a) Boiling point: 169–170°C
• (b) Conversion factor: mg/m³ = 8.1 × ppm

2. Studies of Cancer in Humans

No data were available to the Working Group.

3. Studies of Cancer in Experimental Animals

Dibromoacetonitrile 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. In the initiation/promotion study, in which dibromoacetonitrile 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, there was a dose-related increase in the number of mice with skin tumours except in the highest-dose group: control, 9/105; low dose (total dose 1200 mg/kg bw), 8/36 (p < 0.05); mid dose (total dose 2400 mg/kg bw), 33/70 (p < 0.01); high dose (total dose 4800 mg/kg bw), 10/74 (not significant). There was no increase in either the proportion of mice with lung tumours or the number of lung tumours per mouse (IARC, 1991).

4. Other Data Relevant to an Evaluation of 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 dibromoacetonitrile.

Dibromoacetonitrile induced DNA damage but not mutations in bacteria. 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 dibromoacetonitrile were available.

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

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. Study of the genotoxic activity of six halogenated acetonitriles, using the SOS chromotest, the Ames-fluctuation test and the newt micronucleus test. Mutat. Res. 1995;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]
• Valencia R., Mason J.M., Woodruff R.C., Zimmering S. Chemical mutagenesis testing in Drosophila. III. Results of 48 coded compounds tested for the National Toxicology Program. Environ. Mutag. 1985;7:325–348. [PubMed: 3930234]