15N Labeling Studies of the Reduction of Nitric Oxide by Ammonia over Amorphous and Crystalline Chromia in the Presence and Absence of Oxygen

Abstract

Isotopic labeling studies of the reaction between 15NO and 14NH3 have been performed, under selective catalytic reduction (SCR) conditions, for amorphous and crystalline chromia catalysts over a wide range of temperatures (140-350°C) and oxygen concentrations (0-1.8% O2). At low temperatures, and with 1.8% O2, nitrogen is formed largely by the selective reduction of NO and NH3 over both catalysts. However, crystalline chromia has a much higher activity for ammonia oxidation. Thus, at ≍ 200°C, the major form of nitrogen produced by amorphous chromia is 14N15N, whereas, for crystalline α-Cr2O3, nitrogen is mainly 14N2 and is therefore produced largely from ammonia oxidation. The dominant form of nitrous oxide produced in the presence of O2 over both morphologies of chromia is always 14N15NO. Thus, formation of N2O, an undesirable product, involves the reaction of one molecule of NO and one molecule of NH3. It has been shown that Fourier transform infrared (FTIR) spectroscopy can be used to distinguish between 14N15N and 15N14N. In the presence of excess O2, NO decomposition is unimportant for both catalysts. In the absence of O2, very similar product distributions are observed for the two morphologies of chromia. The dominant form of nitrogen is 14N15N, but the nitrous oxide is largely 15N2O15N, and therefore formed by NO decomposition. Evidence is presented for some conversion of N2O to N2 in the absence of oxygen by a reaction conforming to 3N2O + 2NH3 → 4N2 + 3H2O. This reaction increases in importance with temperature. Concentrations of O2 comparable to the NO and NH3 concentrations (i.e., approximate to 1000 ppm) are sufficient to prevent the NO decomposition reactions, implying that O2 effectively competes with NO for the available adsorption sites. Product distributions obtained in the presence of small amounts of O2 are very similar to those achieved with excess O2.