MRS 2000 Spring Meeting
Symposium B: Si Front End Processing - Physics and Technology of Dopant-Defect-Interactions

ION IMPLANTATION EFFECT ON DISLOCATION PROPAGATION IN PSEUDOMORPHICALLAY STRAINED P/P+ SILICON

P. Feichtinger, H. Fukuto, R. Sandhu, B. Poust, and M.S. Goorsky, Dept of Materials Science and Engineering, University of California, Los Angeles; D. Oster, S.F. Rickborn, and J. Moreland, Wacker Siltronic Corporation, Portland, OR.

We studied damage evolution and influence on defect interactions as a function of Si self implantation in p/p+ silicon wafers. Si-28 (doses 1 x 10¹² and 1 x 10¹⁴ cm^-2 at 100 keV) was implanted into nominally un-doped p-type epitaxial layers. We employed highly boron doped 150 mm diameter silicon substrate wafers with a 2 mm thick pseudomorphic epitaxial layer (p/p+). Due to the misfit strain, misfit dislocations formed during the epitaxial growth process around the wafer edges. This non-uniform dislocation distribution was utilized to study the role of the implant on both the nucleation and growth of the misfit segments. The silicon self implantation was performed at room temperature. A simulation program was used to study the point defect distribution during the implantation process. Triple axis x-ray diffraction was used to determine that the layer was not amorphous at any point. Double axis x-ray topography combined with rapid thermal annealing was used to measure the evolution and nucleation of the misfit segments after annealing. SRP measurements were done in both implanted and un-implanted regions before and after ion implantation in order to characterize the carrier concentration profile. SIMS measurements confirmed that transient enhanced diffusion of boron was not appreciably different in the two regions. The implanted regions exhibited neither growth nor nucleation of misfit dislocation segments, in marked contrast to the growth and nucleation of misfits observed in the non-implanted regions. This comparison indicated that the excess point defects and crystallographic damage act to impede both dislocation motion and dislocation nucleation.