화학공학소재연구정보센터
Catalysis Today, Vol.111, No.1-2, 44-51, 2006
A density functional study of inhibition of the HDS hydrogenation pathway by pyridine, benzene, and H2S on MoS2-based catalysts
The inhibition of catalytic hydrodesulfurization (HDS) by basic nitrogen compounds is an important problem it) the production of ultra low sulfur transportation fuels and the origin of the inhibition effects is presently elucidated by performing density functional theory (DFT) calculations on the interaction of pyridine with the two types of edges of MoS2 catalyst nanoparticles, Particular attention is given to Studies of the hydrogenation (HYD) pathway in HDS since this is the favored pathway for refractory sulfur compounds and it is the pathway, which is most severely poisoned by basic nitrogen compounds. In order to understand the observed inhibitor trends. DFT studies oil (lie adsorption of benzene which is a weaker poison than pyridine, and H2S, which has no or only a very minor influence on the HYD pathway. have also been made, We find that the adsorption of pyridine is quite strong and especially strong at positions along the so-called Mo edge, Thus, the HYD reaction most likely involves sites at this edge. This suggestion is substantiated by the observation that the adsorption blocks the metallic like so-called brim sites. which were recently shown to be involved in the HYD pathway. Furthermore, H2S is observed not to interact strongly with these sites. The present results have also provided insight into the nitrogen compound inhibition of the direct desulturization DDS pathway. The difference in the poisoning by benzene and pyridine is observed to be related to the ease with which hydrogen from neighboring SH group can he transferred to the pyridine molecule resulting in the creation of more strongly held pyridinium ions. At the so-called S edge, hydrogen is tightly bound and this transfer is not favored. The present results, therefore, also stress the importance of the hydrogen binding properties of HDS catalysts. (c) 2005 Elsevier B.V. All rights reserved.