摘要
This paper presents the application of lifetime spectroscopy to the study of carrier-induced degradation ascribed to the boron-oxygen （BO） defect. Specifically, a large data set of p-type silicon samples is used to investigate two important aspects of carrier lifetime analysis： ① the methods used to extract the recombination lifetime associated with the defect and ② the underlying assumption that cartier injection does not affect lifetime components unrelated to the defect. The results demonstrate that the capture cross section ratio associated with the donor level of the BO defect （kl） vary widely depending on the specific method used to extract the defect-specific recombination lifetime. For the data set studied here, it was also found that illumination used to form the defect caused minor, but statistically significant changes in the surface passivation used. This violation of the fundamental assumption could be accounted for by applying appropriate curve fitting methods, resulting in an improved estimate of k1 （11.90±0.45） for the fully formed BO defect when modeled using the donor level alone. Illumination also appeared to cause a minor, apparently injectionindependent change in lifetime that could not be attributed to the donor level of the BO defect alone and is likely related to the acceptor level of the BO defect. While specific to the BO defect, this study has implications for the use of lifetime spectroscopy to study other carrier induced defects. Finally, we demonstrate the use of a unit-less regression goodness-of-fit metric for lifetime data that is easy to interpret and accounts for repeatability error.
This paper presents the application of lifetime spectroscopy to the study of carrier-induced degradation ascribed to the boron-oxygen （BO） defect. Specifically, a large data set of p-type silicon samples is used to investigate two important aspects of carrier lifetime analysis： ① the methods used to extract the recombination lifetime associated with the defect and ② the underlying assumption that cartier injection does not affect lifetime components unrelated to the defect. The results demonstrate that the capture cross section ratio associated with the donor level of the BO defect （kl） vary widely depending on the specific method used to extract the defect-specific recombination lifetime. For the data set studied here, it was also found that illumination used to form the defect caused minor, but statistically significant changes in the surface passivation used. This violation of the fundamental assumption could be accounted for by applying appropriate curve fitting methods, resulting in an improved estimate of k1 （11.90±0.45） for the fully formed BO defect when modeled using the donor level alone. Illumination also appeared to cause a minor, apparently injectionindependent change in lifetime that could not be attributed to the donor level of the BO defect alone and is likely related to the acceptor level of the BO defect. While specific to the BO defect, this study has implications for the use of lifetime spectroscopy to study other carrier induced defects. Finally, we demonstrate the use of a unit-less regression goodness-of-fit metric for lifetime data that is easy to interpret and accounts for repeatability error.
