GENOTOXICITY TESTING OF THE HALON REPLACEMENT CANDIDATES TRIFLUOROIODOMETHANE (CF3I) AND 1,1,1,2,3,3,3-HEPTAFLUOROPROPANE (HFC-227EA) USINGTHE SALMONELLA-TYPHIMURIUM AND L5178Y MOUSE LYMPHOMA MUTATION ASSAYS AND THE MOUSE MICRONUCLEUS TEST

Trifluoroiodomethane (CF3I) and 1,1,1,2,3,3,3-heptafluoropropane (HFC- 227ea) are fluorocarbon replacement candidates for ozone depletion sub stances and were tested for genotoxicity using an exposure chamber mod ification of the Salmonella typhimurium histidine reversion mutagenesi s assay, a modification of the L5178Y/tk(+/-) mouse lymphoma cell muta genesis assay, and a mouse micronucleus rest in which exposures were b y nose-only inhalation. When tested without and with metabolic activat ion over a concentration range of 0.1-8.6% (v/v), CF3I was mutagenic i n S. typhimurium. In the mouse micronucleus test, CF3I induced dose-re lated toxicity and was genotoxic as evidenced by dose-related increase s in micronuclei in mice exposed to 5 or 7.5% CF3I. But in the mouse l ymphoma assay without and with activation, CF3I was negative for mutan t induction up to a concentration of approximately 50%. When tested wi thout and with metabolic activation over a concentration range of 43.9 -93.5%, HFC-227ea was toxic at the highest concentrations tested but n ot mutagenic in S. typhimurium. Neither toxicity nor mutagenicity was observed in the mouse lymphoma assay when HFC-227ea was tested to a co ncentration of 56.8%. Neither toxicity nor an increase in micronuclei was observed in mice exposed to 10.5% HFC-227ea. Thus, toxicity was ob served only in the Salmonella assay, and there was no evidence that HF C-227ea was capable of inducing gene or chromosomal mutations in vitro or chromosomal effects in vivo. Though CF3I was negative also for gen e and chromosomal mutations in the mouse lymphoma assay, it was positi ve for gene mutations in the Salmonella assay and positive for chromos omal effects in the mouse micronucleus test. More information is neede d to clarify these findings and to extrapolate the potential for CF3I to produce genotoxicity in additional mammalian systems.