Well dothandar, the answer to your first question is "YES", because this phenomenon has been seen many times over many years. In those earlier years, experiments were performed to determine the immunoglobulin molecules present, and in every case there was a mixture of IgM and IgG. In the end, it was decided that performing such experiments was a waste of time and money, for very little return. Why reinvent the wheel now?
Turning to question two, all immune antibodies start off as IgM as a result of primary sensitisation, but then quickly change to IgG, even from the primary sensitisation (and almost always from a secondary sensitisation), and, undoubtedly, some IgG antibodies can cause agglutination when no potentiating agents are present (for example, IgG ABO antibodies), however, this is not true of Rh antibodies. In the case of Rh antibodies, it is not a function of the antibody, so much as a function of the number and proximity of the antigens. This can be seen with certain examples of human-derived IgG anti-D, which never cause "saline agglutination" at 37oC with red cells of "normal" Rh types, but do so with red cells exhibiting the exulted-D types (such as D--/D--, DCw-/DCw-. etc, because the number of D antigen sites available, particularly towards the outer layer of the sialic acid cloud, allow for Rh IgG immunoglobulins to come close enough between two (or more) different red cells to cause agglutination. However, even in such a situation, the incubation temperature needs to be 37oC, and not "room/ambient" temperature.