Is the rationale for suggesting that 1,3-d has some genotoxic potential (as indicated in some panel member responses) based on results that represent exceedances of the the KMD or is it just the limits and inherent uncertainty of the data that lead some to take that position?

The question of whether 1,3-d has some genotoxic potential doesn't specify in vivo , where exceeding KMD is an issue. Results from the Ames test (on purified 1,3-d) and several other cell culture and in vivo studies indicate a genotoxic potential exists - probably via the epoxide. In a real world situation this pathway only represents a very minor one and not likely significant, since detoxification via glutathione would greatly reduce the availability of the epoxide. However a number of aliphatic epoxides are mutagenic and genotoxic, and therefore a strict answer to the question of whether 1,3-d has genotoxic potential has to be yes. Whether the genotoxicity has any significant health effects (likely not), is a different question.

My rationale was based on some evidences of potential clastogenicity generated by the DNA breakage observed in the in vivo comet assay in different organs (Sasaki et al., 2000) and the concomitant absence of additional reliable in vivo assays relevant for clastogenicity (e.g. micronucleus test). In addition, the presence of obsolete in vitro assays relevant for clastogenicity and aneugenicity does not permit to rule out a general clastogenic concern.

I don't believe it has, but the data on the clastogenicity side is not clean so this leaves a vulnerability