Light-induced defect creation in amorphous silicon: Single carrier versus excitonic mechanisms

Abstract

A quantitative explanation is derived for the light-induced degradation of compensated amorphous silicon. The analysis suggests that donor levels in compensated hydrogenated amorphous silicon (a-Si:H) lead to an efficient spatial separation of trapped electrons and holes, thereby preventing excitonic tail-to-tail recombination thought to be responsible for metastable defect creation during illumination. This confirms the original defect creation model which has recently been challenged by single carrier mechanisms invoking dispersive hydrogen motion as the rate-limiting step.