Modeling of Dopant Defect Interactions

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Modeling of Dopant Defect Interactions C. Camarce2, L. Radic2, P.Keys1, R. Brindos1, K.S. Jones1, and M. E. Law2 1 Department of Materials Science and Engineering 2 Department of Electrical and Computer Engineering University of Florida, Gainesville, FL 32611 ABSTRACT This paper presents a model for {311} defects based on in-situ experiments. The model fits the 311 dependence on silicon implant energy and doses. The surface dependence of the model is described in detail, and compared to previous literature data. New data is presented on the surface effect on {311} dissolution and the model is compared to that data. In addition, the model is also used to explain the effects of doping on {311} defect behavior. Doping does not influence the dissolution of {311} defects, but only influences their nucleation behavior. INTRODUCTION Transient Enhanced Diffusion (TED) has been the primary modeling challenge of the process simulation community. Qualitatively, the damage from the implant creates an enhanced level of point defects which substantially increases the diffusion of dopants for a short time until the implant damage is fully annealed. This qualitative explanation of the phenomena has been accepted for some time. Quantitative explanations, however, have been difficult to develop. The standard model of TED requires that the Frenkel pair distribution generated by the implant recombines very quickly. This leaves behind the excess atoms that were implanted - the “+1” model. This dose of interstitials quickly forms extended defects, which in turn dissolve relatively more slowly and create the enhanced diffusion of dopants that is observed. Rafferty et al.[1] have suggested that the dissolution is controlled by a strong surface sink. The surface annihilation is responsible for eliminating the excess defects. The rate of surface recombination, therefore, becomes a critical component of the model. Quantitative Transmission Electron Microscopy (TEM) has been used to help investigate and quantify this model. Eaglesham, et.al, [2]have suggested that for low dose silicon implants, interstitials are stored in {311} defects. This defect slowly dissolves and maintains an interstitial excess. Initial investigations have shown that this defect dissolves with a time constant approximately the same as for TED, and that this defect is "the source of the interstitials”[2]. This confirms the first part of the standard model, that roughly a “+1” of defects is contained in the {311}’s and that this defect dissolves slowly with a time constant similar to that of TED. Because of this work, we now have confirmation of part of the standard model. In this paper, a model is presented and compared to a variety of data showing the dependence of dissolution of the {311} defects on the surface. We also compare the model to dissolution studies performed in heavily doped backgrounds, and show that the model can explain these phenomena as well.

J9.1.1

Figure 1 – Left picture is the start of the in-situ annealing. The right picture is after 15minutes a

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