Kinetic and steady-state effects of illumination on defects in hydrogenated amorphous silicon

Abstract

Nine recombination-driven mechanisms are possible in principle for the kinetics and steady-state effects of illumination on defects in hydrogenated amorphous silicon. By comparing the different mechanisms, and making choices based on the experimental observation that the carrier lifetime varies inversely with the metastable defect (dangling bond) density, these nine are reduced to three. They correspond to recombination that generates metastable defects (1) taking place at metastable defects, (2) being associated with direct electron-hole recombination, or (3) taking place at other specific defect sites in the material. Each of these three models is considered under the assumptions that (a) the rate constants involved are not functions of time, and (b) the rate constants involved are functions of time in a way similar to that observed for the decay of thermally induced defects, described by a stretched exponential formulation. Comparison with experimental data on kinetics as a function of time and light intensity indicates that both models 2a and 1b are capable of describing the reported results. If, however, it is maintained that all defect-related kinetics in amorphous silicon should exhibit the dispersive behavior leading to the stretched exponential description, then only model 1b is acceptable. Experiments for distinguishing between models 2a and 1b are suggested.