The effect of magnetic reconnection on ICME-related GCR modulation

The large-scale magnetic structure of interplanetary coronal mass ejections (ICMEs) has been shown to cause temporary decreases in the galactic cosmic ray (GCR) flux measured in situ by spacecraft, known as Forbush decreases (Fds). In some ICMEs, the magnetic ejecta exhibits a magnetic flux rope structure; the strong magnetic field strength and closed field line geometry of such ICME magnetic flux ropes has been proposed to act as a shield to GCR transport. However, as ICMEs propagate, they undergo many processes including interactions and magnetic reconnection with the interplanetary magnetic field (IMF) in large-scale solar wind structures and other solar transients. In this study, we investigate how ICME interaction and reconnection during propagation affects Fd size, shape, and duration. We hypothesize that the alteration of the ICME magnetic topology due to reconnection (specifically the opening of the closed magnetic field configuration in the ICME flux rope) will have a strong effect on the ICME’s ability to modulate GCRs. To test this hypothesis, we compare the Fds of ICMEs that likely underwent reconnection during propagation with ones that likely did not.

To this end, we identify ICMEs that exhibited open magnetic field line topologies (i.e., ones that likely underwent reconnection) and we compare their effects on GCRs with those of ICMEs that exhibited closed topologies (both ends connected to the Sun). We use magnetic field, solar wind plasma, and suprathermal electron pitch angle distribution data at ACE and Wind to select the ICMEs. Furthermore, we use data by the SOPO and McMurdo neutron monitors at Earth to investigate how the magnetic structure of the ICME ejecta modulates the GCRs by comparing the resulting Fds for the selected ICMEs. The results of our study yield new insights into how the modulation of GCRs is affected by ICME evolution and interaction during propagation and whether reconnection of the ICME flux rope weakens its modulation of GCRs.