PNNL

Abstract

Molecular dynamics (MD) simulations with a modified Tersoff potential have been used to investigate cascade overlap, damage accumulation and amorphization processes in 3C-SiC over dose levels comparable to experimental conditions. A large number of 10 keV displacement cascades were randomly generated in a model crystal to produce damage and cause amorphization. At low dose, the damage state is dominated by point defects and small clusters, and their concentration increases sigmoidally with increasing dose. The coalescence and growth of clusters at intermediate and higher doses is an important mechanism leading to amorphization in SiC. The homogenous nucleation of small clusters at low dose underpins the homogenous-like amorphization observed in SiC. A large increase in the number of antisite defects at higher dose indicates that both interstitials and antisite defects play an important role in producing high-energy states that lead to amorphization in SiC. The topologies (such as total pair correlation function, bond-angle and bond-length distributions) of damage accumulation in the crystal suggest that a crystalline-to-amorphous (c-a) transition occurs at about 0.28 dpa, which is in reasonable agreement with the experimental value of 0.27 dpa under similar irradiation conditions. After the model crystal transforms to the fully amorphous state, the long-range order is completely lost, while the short-range order parameter saturates at a value of about 0.43.