Controlling defect passivation in polycrystalline silicon through hydrogen–dopant interactions during MW-ECR plasma treatment

Abstract

Hydrogen–dopant interactions play a crucial role in controlling the electrical properties of polycrystalline silicon during plasma processing. In this work, the interplay between dopant deactivation, hydrogen diffusion, and defect passivation in polycrystalline silicon is systematically investigated using microwave electron cyclotron resonance (MW-ECR) hydrogen plasma treatment. Defect passivation was evaluated from the evolution of the open-circuit voltage of n+pp.+ polycrystalline silicon structures, while dopant deactivation was independently examined by capacitance–voltage profiling of well-defined crystalline silicon junctions. Increasing the microwave plasma power markedly improved the open-circuit voltage of polycrystalline silicon, followed by saturation at high power. The electrical measurements reveal that boron deactivation in the p-type region generates active-dopant concentration gradients that favor deeper hydrogen penetration and enhance bulk and grain-boundary defect passivation. In contrast, phosphorus deactivation in the n+ region promotes the formation of electrically inactive P-H complexes, consuming mobile hydrogen and limiting its diffusion toward the bulk. Hydrogen diffusion coefficients increased from approximately 1.48 × 10–12 to 2.0 × 10–11 cm2/s as the microwave power increased from 150 to 650 W. At excessive hydrogen concentrations, molecular hydrogen accumulation and platelet formation, together with plasma-induced surface modifications, restrict further hydrogen transport and account for the observed saturation of passivation. These results demonstrate that dopant deactivation is not merely a parasitic consequence of hydrogenation but a key factor governing hydrogen transport and defect passivation in silicon. The findings provide a materials-processing framework for optimizing plasma hydrogenation conditions while preserving dopant activity and improving the electrical quality of polycrystalline silicon. The assignments to P-H complexes, molecular H₂/platelet formation, and plasma-induced defects should therefore be understood as literature-supported mechanistic interpretations of the electrical trends rather than as direct structural observations in the present samples.