| Studies in vitroStudies in vivoBromoethane has been studied in a variety of mutagenicity tests
      employing various strains of Salmonella typhimurium, for which a dose-response and at least a doubling of scores formed the
      basis of a positive response. In two well conducted closed system assays,
      positive responses were recorded in strains TA1535 and TA100 with and without
      metabolic activation (Barber et al., 1981; Roycroft, 1989). A negative result was obtained with TA98 in both
      studies. Simmon (1981), using only TA100 in a closed system assay, also
      reported a positive response with bromoethane.
 Plate incorporation and preincubation studies produce results
      that are fairly consistent with those obtained from closed system assays.
      One plate incorporation study of bromoethane produced positive results
      with strains TA98, TA100, and TA104 in the presence of Aroclor 1254-induced
      rat liver S9 and with strain TA97 both with and without metabolic activation
      (Strobel & Grummt, 1987).
 An abstract reports positive results for TA100 and TA102 in
      a preincubation (60 min) study (Simmons et al., 1986). A second abstract also records a positive response in these two
      strains following a 10-min preincubation (Hughes et al., 1987). Haworth et al. (1983) obtained negative results following a 20-min preincubation of bromoethane
      with strains TA98, TA100, TA1535, and TA1537. The preincubation method
      they describe suggests that open vessels were used. This would allow bromoethane
      to escape and so reduce the actual exposure concentration, resulting in
      possibly false-negative results.
 The above data indicate that bromoethane is directly mutagenic
      to Salmonella strains.
 Only one in vitro mammalian cell genotoxicity study of bromoethane was available (Loveday et al., 1989). In this study, Chinese hamster ovary cells were used to study
      the clastogenicity and sister chromatid exchange (SCE)-inducing potential
      of bromoethane at concentrations of up to 1 mg/ml, the limit of solubility
      in dimethyl sulfoxide in this test system. No evidence of cell death was
      seen at this concentration.
 In the clastogenicity experiment, cells were exposed to bromoethane
      in the absence of an exogenous metabolic activation system for 8 h and
      harvested 2 h later. It is possible that the exposure times did not cover
      a complete cell cycle. In the presence of rat liver S9, cells were exposed
      for 2 h and harvested 10 h later. At concentrations of up to 1 mg/ml, bromoethane
      did not induce any increase in the incidence of chromosome aberrations
      in the cells under either of these test conditions.
 SCE-inducing potential was investigated by treating cells
      for 26 h in the absence of, or for 2 h in the presence of, Aroclor 1254-induced
      rat liver S9. Cells treated with S9 were then incubated for a further 24
      h so that both sets of cells were sampled 26 h after the experiment began.
      Dose-dependent increases were seen in both the number of SCEs per chromosome
      and the number of SCEs per cell in the absence or presence of S9. In the
      absence of metabolic activation, 1.75- to 3.7-fold increases in the number
      of SCEs per cell were seen when compared with solvent controls, whereas
      the increases seen with metabolic activation were not sufficiently large
      to be considered positive.
 Negative results were reported in a sex-linked recessive lethal
      test on Drosophila using Berlin K males for solutions containing bromoethane at concentrations
      up to 8.2 mmol/litre (0.9 mg/ml) (Vogel & Chandler 1974).
 No in vivo genotocxicity data in either animals or human were vailable.
 
 References
 EBarber E, Donish W, Mueller K (1981) Procedures for the quantitative
      measurement of the mutagenicity of volatile liquids in the Ames Salmonella/microsome 
assay. Mutation Research, 90: 31-48.
 ESimmon V (1981) Applications of the Salmonella/microsome assay. In: 
Stich HF, San RHC, eds. Short term tests for chemical carcinogens. New 
York, NY, Springer, pp. 120?126 (ISBN 0-387-90496-4).
 EStrobel K, Grummt T (1987) Aliphatic and aromatic halocarbons as potential mutagens in drinking water. 3. Halogenated ethanes and ethenes. Toxicology 
and Environmental Chemistry, 15: 101-128.
 EHughes T, Simmons D, Monteith L, Myer L, Claxton T (1987) Mutagenicity
      of 31 organic compounds in a modified preincubation Ames assay with Salmonella 
typhimurium strains TA 100 and TA 102. Environmental Mutagenesis, 9(Suppl. 8): 49.
 EHaworth S, Lawlar T, Mortelmans K, Speck W, Zeiger E (1983) Salmonella 
mutagenicity test results for 250 chemicals. Environmental Mutagenesis, 
5(Suppl. 1) :3-142.
 ELoveday K, Lugo M, Resnick M, Anderson B, Zeiger E (1989) Chromosome aberration and sister chromatid exchange tests in Chinese harnster ovary cells in vivo. 2. Results with 20 chemicals. Environmental and Molecular 
Mutagenesis, 13: 60-94.
 EVogel E, Chandler J (1974) Mutagenicity testing of cyclanate and some
      pesticides in Drosophila melanogaster. Experientia, 30: 612-623.
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