First off let's define some concepts.
* DNAse hypersensitive regions are DNA regions which are in an open chromatin conformation (i.e. euchromatin). This means that those regions are more active at the genomic level (i.e. higher gene expression, gene regulation and higher TF binding) and are less prone to form nucleosomes.
* Histone mark sites are DNA regions known to bind certain type of histones and therefore also influences the chromatin conformation leading to the same effects described previously. The critical point is that the histones you are listing do not primarily bind a specific DNA sequence (as described by @mdperry) but rather DNA sequence marked by epigenetic modifications such as methylation and acetylation.
Now for your first questions, SNPs in DNAse hypersensitive regions might influence the chromatin state and therefore yes might influence gene expression and gene regulation. Will those SNPs also influence TF binding? Well they might indirectly via chromatin modifications. They will not directly act on TF binding if not located in a sequence known to bind TFs (TFBS). 29
DNAse hypersensitivity is not a synonym for transcription factor binding regions/sequences.
For your second question, SNPs in histone mark sites are a little bit more difficult to interpret. They might, or might not, provoke chromatin changes by influencing the binding of histones but not in a direct way. CpG islands are, for example, DNA regions known to be greatly under the influence of epigenetic marks and therefore mutations in those specific regions (e.g. a C -> T mutation) might influence the relative methylation/acetylation state and therefore the binding of histones. SNPs might therefore influence gene expression via chromatin changes which leads to higher/lower TF binding but again not in a direct way. Here again a SNP would influence TF binding directly only if the mutation is located in a TFBS.
As you can see my answer is full of "might" and the reason is that it is very difficult, at the current state-of-the-art, to determine the exact impact of a SNP on the 3D conformation of the chromatin and therefore predict the effect on specific gene expressions.
An advice would be to try to co-localize your SNPs with known TFBS either predicted In-silico or measured via CHiP-SEQ experiments and merge that with the information about DNAse hyperactivity and histone marks you already gathered. For example a SNP in a TFBS in a DNAse hyperactive region is very likely to have a greater impact than a SNP in a TFBS in a non active region.
I am sorry I cannot be more specific but this is a very active research area in genetics and there is still a lot to understand, especially for the interactions between all the players influencing the chromatin conformation. 29