The effect of SO2 on the structural evolution of a supported Mn2V2O7 catalyst and its DeNOx performance

To investigate the structural evolution of vanadate catalysts in the presence of SO2 and its influence on DeNO(x) behaviors, three typical vanadate catalysts (unsupported Mn2V2O7, Mn2V2O7/TiO2, and sulphated Mn2V2O7/TiO2) were designed for the selective catalytic reduction of NO with NH3. The XRD, Raman, and S 2p XPS spectra and TG results confirmed the SO2-promoted decomposition of supported Mn2V2O7 to form VOx species and MnSO4 on TiO2. The XPS spectra of V 2p and (HR)TEM images further indicated the fusion of the decomposed VOx with TiO2 with increased dispersity for the active V species. The decomposition and sulfation of supported Mn2V2O7 markedly increased the specific surface area with the exposure of more active Mn/V sites, O-alpha species and acid sites as demonstrated by the XPS spectra of O 2p and BET, NH3-TPD and H-2-TPR results. The catalytic test exhibited that the formation of MnSO4 devitalized the Mn-based low-temperature active sites and worsened the low-temperature DeNO(x) performance below 250 degrees C, but the decomposition and sulfation of the supported Mn2V2O7 significantly enhanced the catalytic activity and N-2 selectivity above 250 degrees C owing to the exposure of more active V sites, O-alpha species and acid sites. These research results imply that the vanadate catalysts may be unstable in the presence of SO2 and more suitable for the purification of sulfur-free or pre-desulfurization flue gases in the high temperature range.

Automated summary

The study investigates the structural evolution of vanadate catalysts in the presence of sulfur dioxide and its impact on DeNO(x) behaviors. It was found that sulfur dioxide promoted the decomposition of supported Mn2V2O7, leading to the formation of VOx species and MnSO4 on TiO2, thus increasing the dispersity of active V species and specific surface area. The decomposition and sulfation of supported Mn2V2O7 enhanced catalytic activity and N-2 selectivity due to the exposure of more active V sites, O-alpha species, and acid sites.