Ca- and P-Induced Local Microenvironment Modulation of Redox and Acidic Sites for NOx Catalytic Reduction

The presence of alkali and alkaline earth metals, as well as the increased levels of phosphorus, in biodiesel exhausts poses a great challenge to the durability of emission control catalysts. Thus, a mechanistic understanding of these poisoning effects individually and in combination is crucial for addressing these problems. Herein, we report calcium (Ca)- and phosphorus (P)-induced local microenvironment modulation of the redox and acidic sites on a V2O5-WO3/TiO2 catalyst for NOx reduction. Phosphorus and calcium poison the catalyst and tune the local microenvironments of redox V-O and acidic W-O sites in different ways. Phosphorus poisons the catalyst primarily via impairing the functions of the V-O sites (e.g., redox property and polymerization state) by binding P to the VOx species, forming surface phosphate and crystalline VOx. Calcium, on the other hand, decreases the activity mainly through direct bonding with the acidic W-O sites, which significantly alters the initial W6+-O-V4+ local electronic structure and dramatically decreases its ability to adsorb and activate NH3 due to the diminished active VOx species and weakened redox functionality. In the presence of both Ca and P, the crystalline vanadia species are depolymerized, and the Ca-bonded tungsten species are released, restoring the initial local microenvironment of the acidic WO3 and redox V2O5 sites for SCR catalysis. These findings are supported by our DFT calculations, where Ca-P copoisoning results in a more favorable thermodynamics due to calcium phosphate formation. This work provides new insights about the deactivation mechanism of vanadia-based SCR catalysts in exhausts containing multiple poison components, and these insights would benefit the design of more durable NOx reduction catalysts for biodiesel applications.