Pore mouths reaction with poisoned

For reactor design, it is important to know how the solutions of Eqs. 5.32, 5.34, and 5.35 affect the intrinsic rate of reaction. Wheeler (1955) treated this deactivation-diffusion problem for two limiting cases uniform and pore-mouth (shell-progressive) poisoning. As described in the previous section for noncatalytic gas-solid reactions, the poison will deposit preferentially on the pore-mouth initially and grow progressively inward with time, if the rate of poisoning is rapid relative... 

In order to demonstrate the selective effect of pore-mouth poisoning, it is instructive to consider the two limiting cases of reaction conditions corresponding to large and small values of the Thiele modulus for the poisoned reaction. For the case of active catalysts with small pores, the arguments of all the hyperbolic tangent terms in equation 12.3.124 will become unity and... 

For first order reaction in slab geometry, evaluate the ratio of effectiveness with uniform poisoning, 7)un> and pore mouth poisoning, T)pm, in terms of fractional poisoning and the Thiele modulus. 

For uniform poisoning, the effectiveness is obtained by simply replacing k with kv(l-/3) in the definition of For pore mouth poisoning the equation for if is in P7.06.07. These lesuLts are for first order reaction in slab geometry. 

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... 

Rostrup-Nielsen found that the intrinsic reaction rate, rj, for methane steam reforming is correlated with the sulphur coverage by equation 6 (2). In the adiabatic prereformer, the sulphur acts as a pore mouth poison and as the reactions are restricted by pore diffusion 2,8), the effective activity of the sulphur poisoned catalyst pellet can be described by an empirical relation, equation 7, between the effective pellet reaction rate, rp, and the average sulphur coverage, 0av (7/... 

Pore Mouth (or Shell Progressive) Poisoning This mechanism occurs when the poisoning of a pore surface begins at the mouth of the pore and moves gradmuly inward. This is a moving boundary problem, and the pseudo-steady-state assumption is made that the boundary moves slowly compared with diffusion of poison and reactants and reaction on the active surface. P is the fraction of the pore that is deactivated. The poison diffuses through the dead zone and deposits at the interface between the dead and active zones. The reactants diffuse across the dead zone without reaction, followed by diffusion-reaction in the active zone. 

Consider diffusion with reaction in a pore with pore-mouth poisoning. [8] The governing equation and boundary conditions are ... 

The phosphorus deactivation curve is typical type C, and, according to the Wheeler model, this is associated with selective poisoning of pore mouths. Phosphorus distribution on the poisoned catalyst is near the gas-solid interface, i.e. at pore mouths, which confirms the Wheeler model of pore mouth poisoning for type C deactivation curves. Thus we may propose that in the fast oxidative reactions with which we are dealing, transport processes within pores will control the effectiveness of the catalyst. Active sites at the gas-solid interface will be controlled by relatively fast bulk diffusional processes, whereas active sites within pores of 20-100 A present in the washcoat aluminas on which the platinum is deposited will be controlled by the slower Knudsen diffusion process. Thus phosphorus poisoning of active sites at pore mouths will result in a serious loss in catalyst activity since reactant molecules must diffuse deeper into the pore structure by the slower Knudsen mass transport process to find progressively fewer active sites. 

Figure 7.22 Diagram of pore-mouth poisoning with diffusion and reaction. [After A. Wheeler, Advan. Catal, 3, 249 with permission of Academic Press, New York, NY, (1951).]...

Looking at Fig. 9, we assume that the concentration of reactant at the pore mouth is Co, and we wish to find the rate of reaction in a pore which has its initial length oL poisoned. We assume the transport of reactant through the poisoned portion to be by diffusion. Under steady state conditions this will occur with a linear concentration gradient AC/AL = (Co — Ci)faL where Ci is the (unknown) concentration at the end of the poisoned region. The rate of this diffusion through the poisoned length... 

In summary, the temperature coefficient on catalysts with poisoned pore mouths will behave as follows (a) Over the lowest temperature in which the reaction is measurable the true activation energy will be measured. This is because the reaction will be so slow (k so small) that unpoisoned surface will be completely available to reaction, and diffusion... 

Fig. 10. Effect of poison and pore size on apparent activation energy. Plots of observed reaction rate vs. 1/T for a hypothetical catalyst having 11,000 kcal. intrinsic activation energy (e.g., nickel in ethylene hydrogenation) but prepared with different pore sizes and poisoned to varying extent with poison preferentially adsorbed near the pore mouth. Curve A large pores, no poison. Curve B fairly large pores, 90% poisoned (hioo = 0.1, a = 0.9) Curve C Small pores, no poison. Curve D Moderate size pores, 50 % poisoned (h o 0.5, a — 0.5). Curve E small pores, 50 % poisoned (hno = 2, = 0.5). The horizontal portions of D and E correspond to diffusion controlled reaction.

If, however, tightly absorbed catalyst poisons are present it is easy to show that small pores can completely destroy Type I selectivity. In Section VII, 2, we showed that poisons preferentisdly adsorbed on the pore mouth can reduce the rate of a fast reaction to the rate of diffusion through the poisoned pore mouth. (See eq. 79.) Since diffusion rates of similar molecules are about the same, we could expect the rates of A — B + C and X — Y Z to he reduced to about the same level on catalysts with poisoned pore mouths, regardless of their intrinmc relative rates. Thus the combination of tightly adsorbed poisons and small pores can completely destroy Type I catalyst selectivity, causing reaction rates to be diffusion controlled. 

Nevertheless, sooner or later the alkylation activity of the zeolite will inevitably decline due to the accumulation of carbonaceous deposits on its surface. A thorough understanding of the nature of the carbonaceous deposits formed and the possible deactivation mechanisms is thus crucial for designing zeolite-based alkylation catalysts with enhanced lifetime. In this respect, poisoning of acid sites or pore blockage (or both) caused by the accumulation carbonaceous deposits on the zeolite surface have been proposed as the most likely deactivation mechanisms (143-148). After the initial stable alkylation period, olefins appear in the reaction medium (conversions below 100%) and the rate of olefin addition to an adsorbed carbenium ion to form heavy polyalkylated intermediates increases with respect to that of hydrogen transfer. Such bulky intermediates remain attached to the active site and thus reduce the number of available Bronsted acid sites. Concomitantly, a decrease in the micropore volume does also take place. In the latter stage of the reaction, where deactivation is accelerated, polymers are formed at the outer zeolite surface and may eventually lead to pore mouth... 

Figure 8.4 Selectivity behavior of simple multiple reactions affected by pore-mouth poisoning equal dif-fusivities, = 1, kyiAs = 4, Ca = C . (Sada and Wen 1967. Reprinted with permission from Chemical Engineering Science. Copyright by Pergamon Press, Inc.)...

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