Correlation between in Situ Diagnostics of the Hydrogen Plasma and the Interface Passivation Quality of Hydrogen Plasma Post-Treated a-Si:H in Silicon Heterojunction Solar Cells.

Passivation of the interface defect states is crucial to mitigate the recombination losses in silicon solar cells. In this work, we have investigated the role of hydrogen plasma treatment (HPT) to passivate the interfacial defects between crystalline (c-Si) and hydrogenated amorphous silicon (a-Si:H) in silicon heterojunction (SHJ) solar cells. For the first time, we have found a correlation between the dynamic properties of hydrogen plasma and passivation quality of the films by using in situ optical emission spectroscopy and quasi-steady state photoconductance measurement. The optimum condition for saturation of the dangling bonds by HPT has been studied in detail by tuning the excited hydrogen (H) species and ion bombardment energies by controlling physical parameters like plasma current and chamber pressure. We have investigated the role of annealing after HPT to redistribute the H in the post-treated a-Si:H film and have obtained an i V of 755 mV, minority carrier lifetime (τ) of 4.6 ms, and SRV of 1.5 cm/s on test structures having only an 10 nm intrinsic a-Si:H layer on textured silicon wafers. The H bond configuration at the interface of a-Si:H and c-Si has been investigated by Fourier transform infrared spectroscopy, which demonstrates improved monohydride bonding in the films after HPT derived from the analysis of microstructure parameter and H concentration values. Raman spectroscopy shows the absence of the nanocrystalline fraction after HPT and verifies reduced coordination defects due to annealing after HPT. The proof of concept has been validated by fabricated SHJ solar cells having a V of 729 mV and efficiency of 18.7% after HPT, with the best cell efficiency reaching 20.2% after doped layer optimization. The decrease in reverse saturation current and ideality factor after HPT verifies that the improvement in performance is from reduced recombination losses at the interface due to passivation of defects in midgap states.