Please assess the relevance of each in vivo study to assess the mutagenic potential for 1,3-D in humans?

1) I consider the Mouse bone marrow micronucleus test (Gollapudi, 1985) of limited relevance in the context because no clear demonstration of target tissue exposure (no reduction of %PCE) and a limited statistical sample (1000 PCE/animal). However, despite the observed shortcomings, the limited relevance of this study for 1,3 D mainly rests on the observation that IARC carcinogen haloalkanes and haloakenes including 1,3 D are poor or no inducer of micronuclei as shown by Morita et al. (1997), Mutation Research 389,3–122.
2) I consider the Dominant lethal assay (Gollapudi, 1998) of limited relevance because its generally recognised low sensitivity and also because the general negative effects at somatic level.
3) The Big Blue mouse assay (Gollapudi, 1997) is slightly relevant since it partially rules out the in vitro mutagenicity concern generated by the positive findings obtained in the Ames test, due to the previous mentioned shortcomings related to the administration period of 14 days instead of 28 days requested for slow proliferating tissues/organs (e.g. liver).
4) The 32P Post-labelling assay (Stott, 1997) is of questionable relevance because the low dosages of 1,3-D both by inhalation (30 and 60 ppm) and by oral gavage (12.5 and 25 mg/kg/day), compared to the other available in vivo studies (e.g Gollapudi 1998; Young 2018). In addition, the 32P-postlabeling method is less sensitive for the detection of non-aromatic DNA adducts than aromatic adducts because of analytical difficulties in the separation of non-aromatic adducts from unmodified (normal) nucleotides (Phillips et al., 2000).
5) The Big Blue rat assay via oral route (Young, 2018) is clearly relevant since it rules out the in vitro mutagenicity concern generated by the positive findings obtained in the Ames test.

The post-labelling assay has undergone improvements since 1997, so it is not sufficient to ensure that no DNA adducts were produced. Also I believe the correct reference for this report is Reddy (see Zeiger report). The big blue assay by Gallapudi was not sensitive enough .to detect a low level of mutagenesis as it had a high background and used relatively few animals. The big blue assay by Young was only carried out using dietary exposure, inhalation exposure would have been preferable as it avoids the "firstpass" effect and is likely more relevant to exposure. The assay might have been more sensitive if the mice were euthanized 28 days after the last dose, so that sufficient time elapsed to fix all of the potential mutations. The dominant lethal assay is not very sensitive and I would not expect it to detect changes induced by a weak genotoxic agent. The bone micronucleus test suffers from a lack of data that the test compound or its metabolites reaches the target tissue. Several technical issues have been pointed out by the other reviewers.
My opinion of the possible mutagenicity of 1,3-D is that it is not likely to be mutagenic in humans, as it is a very weak mutagen at best, and human exposure is so low that even if it was mutagenic, the total mutagenic burden is probably well below background rates.

Gollapudi 1985 is not in copliance with current OECD 474 (not enough cells scored), and also shows a large vareability between dose groups.
As described above, without further info, I don't see the DL assay as a clean neg. Also I am would not give it much weight within the genotoxicity assessment since this is not a direct indication of germ or somatic cell genotoxicity.
Gollapudi 1997 is not compliant with current guideline (plus there are newer data available for the same endopoint -Young 2018)
Scott 1997 is difficult to judge without further detail.