GENOTOXICITY TESTING OF THE HALON REPLACEMENT CANDIDATES TRIFLUOROIODOMETHANE (CF I) 3 AND 1,1,1,2,3,3,3-HEPTAFLUOROPROPANE (HFC-227ea) USING THE SALMONELLA TYPHIMURIUM AND L5178Y MOUSE LYMN ASSAYS AND THE MOUSE MICRONUCLEUS TEST

Abstract

Trifluoroiodomethane (CF3I) and 1,1,1,2,3,3,3-heptafluoropropane (HFC-227ea) are fluorocarbon replacement candidates for ozone depletion substances and were tested for genotoxicity using an exposure chamber modification of the Salmonella typhimurium histidine +/reversion mutagenesis assay, a modification of the L5178Y/tk mouse lymphoma cell mutagenesis assay, and a mouse micronucleus test in which exposures were by nose-only inhalation. When tested without and with metabolic activation over a concentration range of 0.1-8.6% (v/v), CF3I was mutagenic in S. typhimurium. In the mouse micronucleus test, CF3I induced dose-related toxicity and was genotoxic as evidenced by dose-related increases in micronuclei in mice exposed to 5 or 7.5% CF3I. But in the mouse lymphoma assay without and with activation, CF3I was negative for mutant induction up to a conReceived centration of approximately 50%. When tested without and with metabolic activation over a concentration range of 43.9-93.5%, HFC-227ea was toxic at the highest concentrations tested but not mutagenic in S. typhimurium. Neither toxicity nor mutagenicity was observed in the mouse lymphoma assay when HFC-227ea was tested to a concentration of 56.8%. Neither toxicity nor an increase in micronuclei was observed in mice exposed to 10.5% HFC-227ea. Thus, toxicity was observed only in the Salmonella assay, and there was no evidence that HFC-227ea was capable of inducing gene or chromosomal mutations in vitro or chromosomal effects in vivo. Though CF3I was negative also for gene and chromosomal mutations in the mouse lymphoma assay, it was positive for gene mutations in the Salmonella assay and positive for chromosomal effects in the mouse micronucleus test. More information is needed to clarify these findings and to extrapolate the potential for CF3I to produce genotoxicity in additional mammalian systems.