Point defects and dopants of boron arsenide from first-principles calculations: donor compensation and doping asymmetry

TL;DR

This study uses first-principles calculations to analyze point defects and dopants in boron arsenide, revealing native defect dominance, p-type conduction tendencies, and the effects of impurities on doping asymmetry.

Contribution

It provides detailed formation energies and charge transition levels for native defects and dopants in boron arsenide, highlighting the mechanisms behind doping asymmetry and defect compensation.

Findings

Native boron-related defects dominate intrinsic defect landscape.

Certain impurities like Be_B, Si_As, and Ge_As are effective shallow acceptors.

Donor passivation is likely due to native defects and impurities.

Abstract

We apply hybrid density functional theory calculations to identify the formation energies and thermodynamic charge transition levels of native point defects, common impurities, and shallow dopants in BAs. We find that boron-related defects such as V_B, B_As, B_i-V_B complexes, and antisite pairs are the dominant intrinsic defects. Native BAs is expected to exhibit p-type conduction due to the acceptor-type characteristics of V_B and B_As. Among the common impurities we explored, we found that C substitutional defects and H interstitials have relatively low formation energies and are likely to contribute free holes. Interstitial hydrogen is surprisingly also found to be stable in the neutral charge state. Be_B, Si_As and Ge_As are predicted to be excellent shallow acceptors with low ionization energy (< 0.03 eV) and negligible compensation by other point defects considered here. On the other hand, donors such as Se_As, Te_As, Si_B, and Ge_B have a relatively large ionization energy (~0.15 eV) and are likely to be passivated by native defects such as B_As and V_B, as well as C_As, H_i, and H_B. The hole and electron doping asymmetry originates from the heavy effective mass of the conduction band due to its boron orbital character, as well as from boron-related intrinsic defects that compensate donors.