4 years ago

Steam and alkali resistant Cu-SSZ-13 catalyst for the selective catalytic reduction of NOx in diesel exhaust

Steam and alkali resistant Cu-SSZ-13 catalyst for the selective catalytic reduction of NOx in diesel exhaust
The resistances of Cu-SSZ-13 to hydrothermal aging and alkali metal poisoning for selective catalytic reduction of NOx with NH3 (NH3-SCR) were studied and comprehensive investigations were performed to better understand the poisoning mechanisms of the Cu-SSZ-13 catalyst. The NH3-SCR performance was well maintained after 700 °C hydrothermal aging for 12 h. With the aging temperature increasing to 750 °C, small decrease in the catalytic activity over the low temperature (<250 °C) and high temperature (>475 °C) range was observed due to the loss of some isolated Cu2+ ions and surface acidity in the hydrothermal-treated catalyst, whilst the NO conversion could still maintain over 90% in a wide temperature range (250–475 °C). Alkali metal (K, Ca, Na and Mg) was impregnated on Cu-SSZ-13 by an incipient wetness impregnation method, respectively. The Cu-SSZ-13 catalyst clearly exhibited a high resistance to alkali metal poisoning in a certain amount (0.50 mmol/gcatal), with the surface area, isolated Cu2+ ions and zeolite acidity largely maintaining after the alkali metal impregnation. The NH3-SCR activity was greatly reduced with a high content of alkali metal (1.50 mmol/gcatal) introduction, the zeolite structures were seriously deteriorated and the transformation of isolated Cu2+ ions to CuO was observed for all poisoned catalysts. The poisoning effect of studied alkali metal on the NH3-SCR performance was shown as follows: Mg > Ca > Na > K. The impregnation with Mg and Ca may cause more severe damage to zeolite structures and have more influence on the distribution of Cu2+/Cu+ than K and Na in the same metal loading. Furthermore, Mg2+ with the smallest diameter could replace with more isolated Cu2+ ions in the exchange sites and lead to the formation of abundant extra-framework CuO cluster.

Publisher URL: www.sciencedirect.com/science

DOI: S1385894717316881

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