Poisoning, active sites

Poisons ndInhibitors. Catalyst poisons and inhibitors can come from the fuel, the lube oil, from engine wear and corrosion products, and from air ingestion. There are two types of catalyst poisons one poisons active sites, the other is a masking agent. 

D - Other poisons - Active site poisoning by e.g. Sodium - Sodium Catcher/Resistance... 

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. 

Cce being the concentration of poisoned active sites. When no pore blockage occurs in general... 

Roles of Coke and Metals on Catalyst Deactivation. The model compound activity test (Figure 4) and the diffusivity test (Figure 6) clearly show that both coke and metal sulfides have a responsibility for decreasing intrinsic reaction rate and effective diffusivity. However, the former test suggests that coke and metal sulfides do not independently affect the active sites. As shown in Figure 4, in the third bed, coke rapidly covered more than 70% of the original active sites at the start of the run. However, after the run, the ratio of the coke-covered active sites to the original ones dropped drastically to less than 10%, while that of the metal-poisoned active sites became around 70%. This indicates that the metal sulfides deposit on part of the active sites which coke initially covers and permanently poison them. 

C = initial concentration of active sites, moles of sites/g C = poisoned active sites, moles of sites/g F = molar flow rate, moles/hr... 

The cause of catalyst deactivation has been addressed by Iglesia et al. These authors observe by electron microscopy that after catalytic operation the Pt particles that are located outside the L zeolite are covered with a carbonaceous layer, whereas intrachannel Pt particles are apparently free of coke. For these particles the active catalytic life is limited by their agglomeration with concomitant loss of Pt surface area. Sulfur not only poisons active sites on the Pt particles, but also accelerates the rate of agglomeration (334). 

Carbonaceous deposits are the principle cause of zeolite deactivation in processes involving hydrocarbon conversions. Firstly they can poison active sites or block their access. Secondly, their removal, which is carried out through oxidative treatment at high temjjeratures, has detrimental effects i.e., dealumination and degradation of the zeolite and sintering of supported metals. 

In situ tracer experiments with n-octane aromatization on Cr203/La203/Zr02 catalysts allowed conclusions on the deactivation mechanism. Coke as the main source of deactivation acts by poisoning active sites rather than by lowering mass transport rates. 

Both nickel and vanadium poison active sites on zeolite, but this effect is more... 

Contamination effects of impurities on a PEMFC may be classified into three categories (1) kinetic effects, caused by adsorbing onto the catalyst surface and poisoning active sites on both the anode and cathode catalyst layers (2) mass transfer effects, due to changes in the structure, pore size, pore size distribution, and hydrophobicity/hydrophilicity of the catalyst layers or gas... 

Anotlier important modification metliod is tire passivation of tire external crystallite surface, which may improve perfonnance in shape selective catalysis (see C2.12.7). Treatment of zeolites witli alkoxysilanes, SiCl or silane, and subsequent hydrolysis or poisoning witli bulky bases, organophosphoms compounds and arylsilanes have been used for tliis purjDose [39]. In some cases, tire improved perfonnance was, however, not related to tire masking of unselective active sites on tire outer surface but ratlier to a narrowing of tire pore diameters due to silica deposits. 

Elucidating Mechanisms for the Inhibition of Enzyme Catalysis An inhibitor interacts with an enzyme in a manner that decreases the enzyme s catalytic efficiency. Examples of inhibitors include some drugs and poisons. Irreversible inhibitors covalently bind to the enzyme s active site, producing a permanent loss in catalytic efficiency even when the inhibitor s concentration is decreased. Reversible inhibitors form noncovalent complexes with the enzyme, thereby causing a temporary de-... 

Catalytic Properties. In zeoHtes, catalysis takes place preferentially within the intracrystaUine voids. Catalytic reactions are affected by aperture size and type of channel system, through which reactants and products must diffuse. Modification techniques include ion exchange, variation of Si/A1 ratio, hydrothermal dealumination or stabilization, which produces Lewis acidity, introduction of acidic groups such as bridging Si(OH)Al, which impart Briimsted acidity, and introducing dispersed metal phases such as noble metals. In addition, the zeoHte framework stmcture determines shape-selective effects. Several types have been demonstrated including reactant selectivity, product selectivity, and restricted transition-state selectivity (28). Nonshape-selective surface activity is observed on very small crystals, and it may be desirable to poison these sites selectively, eg, with bulky heterocycHc compounds unable to penetrate the channel apertures, or by surface sdation. 

Catalytic Oxidation. Catalytic oxidation is used only for gaseous streams because combustion reactions take place on the surface of the catalyst which otherwise would be covered by soHd material. Common catalysts are palladium [7440-05-3] and platinum [7440-06-4]. Because of the catalytic boost, operating temperatures and residence times are much lower which reduce operating costs. Catalysts in any treatment system are susceptible to poisoning (masking of or interference with the active sites). Catalysts can be poisoned or deactivated by sulfur, bismuth [7440-69-9] phosphoms [7723-14-0] arsenic, antimony, mercury, lead, zinc, tin [7440-31-5] or halogens (notably chlorine) platinum catalysts can tolerate sulfur compounds, but can be poisoned by chlorine. 

The typical industrial catalyst has both microscopic and macroscopic regions with different compositions and stmctures the surfaces of industrial catalysts are much more complex than those of the single crystals of metal investigated in ultrahigh vacuum experiments. Because surfaces of industrial catalysts are very difficult to characterize precisely and catalytic properties are sensitive to small stmctural details, it is usually not possible to identify the specific combinations of atoms on a surface, called catalytic sites or active sites, that are responsible for catalysis. Experiments with catalyst poisons, substances that bond strongly with catalyst surfaces and deactivate them, have shown that the catalytic sites are usually a small fraction of the catalyst surface. Most models of catalytic sites rest on rather shaky foundations. 

In service, supported catalysts frequentiy undergo loss of activity over a period of time. In many cases, such catalyst deactivation is accompanied by the loss of accessible surface area of the active phase by sintering, by the accumulation of poisons, or by conversion of active sites to inactive species. 

Catalyst contamination from sources such as turbine lubricant and boiler feed water additives is usuaUy much more severe than deactivation by sulfur compounds in the turbine exhaust. Catalyst formulation can be adjusted to improve poison tolerance, but no catalyst is immune to a contaminant that coats its surface and prevents access of CO to the active sites. Between 1986 and 1990 over 25 commercial CO oxidation catalyst systems operated on gas turbine cogeneration systems, meeting both CO conversion (40 to 90%) and pressure drop requirements. 

There is a complication in choosing a catalyst for selective reductions of bifunctional molecules, For a function to be reduced, it must undergo an activated adsorption on a catalytic site, and to be reduced selectively it must occupy preferentially most of the active catalyst sites. The rate at which a function is reduced is a product of the rate constant and the fraction of active sites occupied by the adsorbed function. Regardless of how easily a function can be reduced, no reduction of that function will occur if all of the sites are occupied by something else (a poison, solvent, or other function). 

As discussed in Chapter 2, nickel, vanadium, and sodium are the metal compounds usually present in the FCC feedstock. These metals deposit on the catalyst, thus poisoning the catalyst active sites. Some of the options available to refiners for reducing the effect of metals on catalyst activity are as follows ... 

This paper surveys the field of methanation from fundamentals through commercial application. Thermodynamic data are used to predict the effects of temperature, pressure, number of equilibrium reaction stages, and feed composition on methane yield. Mechanisms and proposed kinetic equations are reviewed. These equations cannot prove any one mechanism however, they give insight on relative catalyst activity and rate-controlling steps. Derivation of kinetic equations from the temperature profile in an adiabatic flow system is illustrated. Various catalysts and their preparation are discussed. Nickel seems best nickel catalysts apparently have active sites with AF 3 kcal which accounts for observed poisoning by sulfur and steam. Carbon laydown is thermodynamically possible in a methanator, but it can be avoided kinetically by proper catalyst selection. Proposed commercial methanation systems are reviewed. 

FIGURE 13.42 (a) An enzyme poison (represented by the blue sphere) can act by attaching so strongly to the active site that it blocks the site, thereby taking the enzyme out of action, (b) Alternatively, the poison molecule may attach elsewhere, so distorting the enzyme molecule and its active site that the substrate no longer fits. 

One form of biological poisoning mirrors the effect of lead on a catalytic converter. The activity of an enzyme is destroyed if an alien substrate attaches too strongly to the enzyme s active site, because then the site is blocked and made unavailable to the true substrate (Fig. 13.42). As a result, the chain of biochemical reactions in the cell stops, and the cell dies. The action of nerve gases is believed to stem from their ability to block the enzyme-controlled reactions that allow impulses to travel through nerves. Arsenic, that favorite of fictional poisoners, acts in a similar way. After ingestion as As(V) in the form of arsenate ions (As043 ), it is reduced to As(III), which binds to enzymes and inhibits their action. 

CBs, like OPs, act as inhibitors of ChE. They are treated as substrates by the enzyme and carbamylate the serine of the active site (Figure 10.8). Speaking generally, car-bamylated AChE reactivates more rapidly than phosphorylated AChE. After aging has occurred, phosphorylation of the enzyme is effectively irreversible (see Section 10.2.4). Carbamylated AChE reactivates when preparations are diluted with water, a process that is accelerated in the presence of acetylcholine, which competes as a substrate. Thus, the measurement of AChE inhibition is complicated by the fact that reactivation occurs during the course of the assay. Carbamylated AChE is not reactivated by PAM and related compounds that are used as antidotes to OP poisoning (see Box 10.1). 

Citrate is isomerized to isocitrate by the enzyme aconitase (aconitate hydratase) the reaction occurs in two steps dehydration to r-aconitate, some of which remains bound to the enzyme and rehydration to isocitrate. Although citrate is a symmetric molecule, aconitase reacts with citrate asymmetrically, so that the two carbon atoms that are lost in subsequent reactions of the cycle are not those that were added from acetyl-CoA. This asymmetric behavior is due to channeling— transfer of the product of citrate synthase directly onto the active site of aconitase without entering free solution. This provides integration of citric acid cycle activity and the provision of citrate in the cytosol as a source of acetyl-CoA for fatty acid synthesis. The poison fluo-roacetate is toxic because fluoroacetyl-CoA condenses with oxaloacetate to form fluorocitrate, which inhibits aconitase, causing citrate to accumulate. 

Hydrodenitrogenation (HDN) is an important process in petroleum refining. It removes nitrogen from oil distillates, so that less NOx pollutes the air when oil is burned and poisoning of the subsequent refining catalysts is reduced when the oil is processed further. Although HDN has been studied intensively and different reaction mechanisms, catalytic active sites, and functions of the catalytic components have been proposed, there are stiU many questions to be answered in order to better mderstand the reaction and the catalyst (1-4). 

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