Arianna Rivera1,Noel Kennedy2,Christopher Hatem2,Kevin S. Jones1
University of Florida1,Applied Materials, Inc.2
Arianna Rivera1,Noel Kennedy2,Christopher Hatem2,Kevin S. Jones1
University of Florida1,Applied Materials, Inc.2
As semiconductor devices continue to scale, ion implantation processes must follow suit to confine fabrication to nanosized structures. One such process is ion-beam induced amorphization, namely in silicon devices. Pre-amorphizing implants are known to increase dopant solid solubility once post-annealed, increasing the active carrier concentration within the recrystallized layer. Because of this, they are often incorporated during the processing of top-off implants, used to decrease contact resistance. The mechanism of silicon-substrate amorphization mechanism varies with ion mass but for heavier ions, it is associated with the overlap of damage cascades induced by nuclear stopping. As such, it should show little dependence on the surface. However, if the point defect accumulation mechanism associated with light ions is active, then the surface may play a role. To better understand the amorphization mechanism at ultra-low energies, the critical threshold for amorphization is investigated for different implant temperatures and energies. Silicon substrates were implanted with Si<sup>+</sup> ions at low energies between 1 keV to 10 keV and implant temperature was varied ranging between 25°C to 150°C. The dose is kept constant at 3×10<sup>14</sup> ions/cm<sup>2</sup> at a dose rate of 0.95 mA. The amorphous layer was studied by high resolution cross-sectional TEM and to SRIM simulations to determine the threshold damage density for amorphzation. By studying the amorphization extent at varying energies and implant temperatures, it was possible to observe how the amorphization layer thickness produced by the implant differs as the damage becomes closer to the surface. It was found that as the implant energy decreased, the threshold damage density for amorphization increased, suggesting a shift in the amorphization mechanism possibly induced by an increasing role of the surface. The role of implant temperature will also be presented.