The transient supersaturation in a system undergoing Ostwald ripening is related to the cluster formation energy E fc as a function of cluster size n. We use this relation to study the energetics of self-interstitial clusters in Si. Measurements of transient enhanced diffusion of B in Si-implanted Si are used to determine S͑t͒, and inverse modeling is used to derive E fc ͑n͒. For clusters with n . 15, E fc ഠ 0.8 eV, close to the fault energy of ͕113͖ defects. For clusters with n , 10, E fc is typically 0.5 eV higher, but stabler clusters exist at n ഠ 4 (E fc ഠ 1.0 eV) and n ഠ 8 (E fc ഠ 0.6 eV). [S0031-9007(99)09311-4]
Copper centers in copper-diffused n-type silicon measured by photoluminescence and deep-level transient spectroscopy Appl. Phys. Lett. 101, 042113 (2012) Bonding and diffusion of nitrogen in the InSbN alloys fabricated by two-step ion implantation Appl. Phys. Lett. 101, 021905 (2012) Shift of Ag diffusion profiles in CdTe by metal/semiconductor interfaces Appl. Phys. Lett. 100, 171915 (2012) Diffusion of co-implanted carbon and boron in silicon and its effect on excess self-interstitials Implanted B and P dopants in Si exhibit transient enhanced diffusion ͑TED͒ during annealing which arises from the excess interstitials generated by the implant. In order to study the mechanisms of TED, transmission electron microscopy measurements of implantation damage were combined with B diffusion experiments using doping marker structures grown by molecular-beam epitaxy ͑MBE͒. Damage from nonamorphizing Si implants at doses ranging from 5ϫ10 12 to 1ϫ10 14 /cm 2 evolves into a distribution of ͕311͖ interstitial agglomerates during the initial annealing stages at 670-815°C. The excess interstitial concentration contained in these defects roughly equals the implanted ion dose, an observation that is corroborated by atomistic Monte Carlo simulations of implantation and annealing processes. The injection of interstitials from the damage region involves the dissolution of ͕311͖ defects during Ostwald ripening with an activation energy of 3.8Ϯ0.2 eV. The excess interstitials drive substitutional B into electrically inactive, metastable clusters of presumably two or three B atoms at concentrations below the solid solubility, thus explaining the generally observed immobile B peak during TED of ion-implanted B. Injected interstitials undergo retarded diffusion in the MBE-grown Si with an effective migration energy of ϳ3.5 eV, which arises from trapping at substitutional C. The concept of trap-limited diffusion provides a stepping stone for understanding the enormous disparity among published values for the interstitial diffusivity in Si. The population of excess interstitials is strongly reduced by incorporating substitutional C in Si to levels of ϳ10 19 /cm 3 prior to ion implantation. This provides a promising method for suppressing TED, thus enabling shallow junction formation in future Si devices through dopant implantation. The present insights have been implemented into a process simulator, allowing for a significant improvement of the predictive modeling of TED.
A comprehensive model for B implantation, diffusion and clustering is presented. The model, implemented in a Monte Carlo atomistic simulator, successfully explains and predicts the behavior of B under a wide variety of implantation and annealing conditions by invoking the formation of immobile precursors of B clusters, prior to the onset of transient enhanced diffusion. The model also includes the usual mechanisms of Si self-interstitial diffusion and B kick-out. The immobile B cluster precursors, such as BI2 (a B atom with two Si self-interstitials) form during implantation or in the very early stages of the annealing, when the Si interstitial supersaturation is very high. They then act as nucleation centers for the formation of B-rich clusters during annealing. The B-rich clusters constitute the electrically inactive B component, so that the clustering process greatly affects both junction depth and doping level in high-dose implants.
A comprehensive model of the nucleation, growth, and dissolution of B clusters in Si is presented. We analyze the activation of B in implanted Si on the basis of detailed interactions between B and defects in Si. In the model, the nucleation of B clusters requires a high interstitial supersaturation, which occurs in the damaged region during implantation and at the early stages of the postimplant anneal. B clusters grow by adding interstitial B to preexisting B clusters, resulting in B complexes with a high interstitial content. As the annealing proceeds and the Si interstitial supersaturation decreases, the B clusters emit Si interstitials, leaving small stable B complexes with low interstitial content. The total dissolution of B clusters involves thermally generated Si interstitials, and it is only achieved at very high temperatures or long anneal times.
A new atomistic approach to Si device process simulation is presented. It is based on a Monte Carlo diffusion code coupled to a binary collision program. Besides diffusion, the simulation includes recombination of vacancies and interstitials, clustering and re-emission from the clusters, and trapping of interstitials. We discuss the simulation of a typical room-temperature implant at 40 keV, 5×1013 cm−2 Si into (001)Si, followed by a high temperature (815 °C) anneal. The damage evolves into an excess of interstitials in the form of extended defects and with a total number close to the implanted dose. This result explains the success of the ‘‘+1’’ model, used to simulate transient diffusion of dopants after ion implantation. It is also in agreement with recent transmission electron microscopy observations of the number of interstitials stored in (311) defects.
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