Pore poisoning model

If a fraction a of the total catalyst surface has been deactivated by poison, the pore-mouth poisoning model assumes that a cylindrical region of length (aL) nearest the pore mouth will have... 

Activity-versus-time curves shown in Fig. 25 for alumina-supported Ni and Ni bimetallic catalysts show two significant facts (1) the exponential decay for each of the curves is characteristic of nonuniform pore-mouth poisoning, and (2) the rate at which activity declines varies considerably with metal loading, surface area, and composition. Because of large differences in metal surface area (i.e., sulfur capacity), catalysts cannot be compared directly unless these differences are taken into account. There are basically two ways to do this (1) for monometallic catalysts normalize time in terms of sulfur coverage or the number of H2S molecules passed over the catalysts per active metal site (161,194), and (2) for mono- or bimetallic catalysts compare values of the deactivation rate constant calculated from a poisoning model (113, 195). 

Some models, such as those proposed by Wheeler (1955) and others (Weisz and Goodwin, 1963) concentrate on the loss of catalyst activity due to pore mouth poisoning. Generally such models blame decay on the increase in diffusion limitations as pore mouths are blocked by the accumulation of solid poisons. Wheeler s theory relates catalyst deactivation to the pore poisoning phenomenon but fails to produce an expression relating the degree of poisoning to time on stream or to... 

Two other compounds have been examined for therapeutic action in animal (rat) models of chlordecone poisoning. Sporopollenin, a carotenoid polymer derived from the cell walls of the alga Chlorella prothecoides, was reported to bind to chlordecone (Pore 1984). In animal studies using rats, sporopollenin decreased the half life of chlordecone from 40 days to 19 days. The excretion rate in control animals fed a-cellulose, in the same bulk amount as sporopollenin, did not change. Prevention of enterohepatic recirculation of chlordecone was also evaluated with liquid paraffin. 

This review will only focus on the modeling efforts in pore diffusion and reaction in single-catalyst pellets which have incorporated pore plugging as a deactivation mechanism. A broad literature exists on the deactivation of catalysts by active site poisoning, and it has been reviewed by Froment and Bischoff (1979). The behavior of catalytic beds undergoing deactivation is... 

The model formulated by Ahn and Smith (1984) considered partial surface poisoning for HDS and pore mouth plugging for HDM reactions. The conservation equations with first-order reactions for metal-bearing and sulfur-bearing species were based on spherical pellet geometry rather than on single pores. Hence, a restricted effective diffusivity was employed... 

Haynes apd Leung (1983) formulated a similar configurational diffusion model combining the effects of active site poisoning as well as pore plugging on the HDM reaction. In this case the reaction form in the conservation equation is multiplied by a deactivation function which accounts for the loss of intrinsic activity, (1 - ) is frequently chosen, where x is the fractional coverage of the sites. Other forms of the site deactivation function have been discussed by Froment and Bischoff (1979). The deactivation was found to depend on a dimensionless parameter given by... 

Due to the fact that protein adsorption in fluidized beds is accomplished by binding of macromolecules to the internal surface of porous particles, the primary mass transport limitations found in packed beds of porous matrices remain valid. Protein transport takes place from the bulk fluid to the outer adsorbent surface commonly described by a film diffusion model, and within the pores to the internal surface known as pore diffusion. The diffusion coefficient D of proteins may be estimated by the semi-empirical correlation of Poison [65] from the absolute temperature T, the solution viscosity rj, and the molecular weight of the protein MA as denoted in Eq. (16). 

Various mechanisms of coke poisoning active site coverage, pore filling as well as pore blockage have been observed in FCC [18, 19, 43] and Percolation theory concepts have been proposed for the modelling here of [45, 46, 47, 48]. This approach provides a framework for describing diffusion and accessibility properties of randomly disordered structures. 

Pommersheim and Dixit (7 ) have developed models for poisoning occurring in the pores of flat plate and spherical catalyst pellets. 

They considered deactivation to occur by either pore-mouth (shell-progressive) or uniform (homogeneous) poisoning and examined the effect these types of deactivation had on overall activity and production rates for a single catalyst pellet. Analytical solutions were obtained for the production per pore by considering the time dependence of activity. Their results will be used here as the basis for the development of models for deactivation in fixed bed reactors. 

When gum formation proceeds, the minimum temperature in the catalyst bed decreases with time. This could be explained by a shift in the reaction mechanism so more endothermic reaction steps are prevailing. The decrease in the bed temperature speeds up the deactivation by gum formation. This aspect of gum formation is also seen on the temperature profiles in Figure 9. Calculations with a heterogenous reactor model have shown that the decreasing minimum catalyst bed temperature could also be explained by a change of the effectiveness factors for the reactions. The radial poisoning profiles in the catalyst pellets influence the complex interaction between pore diffusion and reaction rates and this results in a shift in the overall balance between endothermic and exothermic reactions. 

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