Parallel poisoning

Spectroscopic evidence, in particular DEMS [130], strongly suggests that adsorbed CO is not just forming in a parallel poisoning pathway, but that it constitutes a mechanistic intermediate, at least at low to medium electrode potentials of 0.2-... 

The interpretation of these experimental results differed somwhat in approach from that of Petersen and co-workers, since the mechanism of deactivation (parallel poisoning) is well... 

Figure 11, Experimental and computed temperature profiles for a fixed bed reactor parallel poisoning, (a) Hot spot migration, nonisothermal. Profiles at min intervals (1 = 0 min), 4,3% CeHg, ihiopnenelC =- 5.05 X iO. xb,t = fractions, Ba = fraction sites remaining (53) (b) active front migration, adiabatic. Profiles at 30 min intervals. 1.4% CeHe, 0.032% thiophene. Solid lines computed (54).

A typical catalyst bed is very shallow (10 to 50 mm) (76,77). In some plants the catalyst is contained in numerous small parallel reactors in others, catalyst-bed diameters up to 1.7 and 2.0 m (77,80) and capacities of up to 135,000 t/yr per reactor are reported (78). The silver catalyst has a useful life of three to eight months and can be recovered. It is easily poisoned by traces of transition group metals and by sulfur. 

Pt-Re-alumina catalysts were prepared, using alumina containing potassium to eliminate the support acidity, in order to carry out alkane dehydrocyclization studies that paralleled earlier work with nonacidic Pt-alumina catalysts. The potassium containing Pt-Re catalyst was much less active than a similar Pt catalyst. It was speculated that the alkali metal formed salts of rhenic acid to produce a catalyst that was more difficult to reduce. However, the present ESCA results indicate that the poisoning effect of alkali in Pt-Re catalysts is not primarily due to an alteration in the rhenium reduction characteristics. 

Au/C was established to be a good candidate for selective oxidation carried out in liquid phase showing a higher resistance to poisoning with respect to classical Pd-or Pt-based catalysts [40]. The reaction pathway for glycerol oxidation (Scheme 1) is complicated as consecutive or parallel reactions could take place. Moreover, in the presence of a base interconversion between different products through keto-enolic equilibria could be possible. 

Chemical deactivation. In chemical deactivation the active surface area changes by strong chemisorption of impurities in the feed, by blocking of active sites by heavy products formed in parallel or sequential reactions, etc. The most important chemical causes of deactivation are poisoning by impurities in the feed and deposition of carbonaceous material, usually referred to as coke . 

The selectivity in a system of parallel reactions does not depend much on the catalyst size if effective diffusivities of reactants, intermediates, and products are similar. The same applies to consecutive reactions with the product desired being the final product in the series. In contrast with this, for consecutive reactions in which the intermediate is the desired product, the selectivity much depends on the catalyst size. This was proven by Edvinsson and Cybulski (1994, 1995) for. selective hydrogenations and also by Colen et al. (1988) for the hydrogenation of unsaturated fats. Diffusion limitations can also affect catalyst deactivation. Poisoning by deposition of impurities in the feed is usually slower for larger particles. However, if carbonaceous depositions are formed on the catalyst internal surface, ageing might not depend very much on the catalyst size. 

As with parallel reactions, series reactions might not only lead to a loss of materials and useful products, but might also lead to byproducts being deposited on, or poisoning catalysts (see Chapters 6 and 7). 

In summary, the total oxidation of propylene to C02 occurred at a higher rate than partial oxidation to propylene oxide and acetone total and partial oxidations occurred in parallel pathways. The existence of the parallel reaction pathways over Rh/Al203 suggest that the selective poisoning of total oxidation sites could be a promising approach to obtain high selectivity toward PO under high propylene conversion. 

An alternative nomenclature (Type I and Type II) has been proposed for subgroups of pyrethroids based not only on the syndromes of intoxication produced in mammals but also on their chemical structures, their signs of poisoning in insects, and their actions on insect nerve preparations [2, 14, 18]. The Type I/II nomenclature has been used in parallel with the T/CS nomenclature, so that Type I and Type II pyrethroids are generally considered to induce T- or CS syndrome, respectively [4]. However, the relationship between the two syndromes and types are neither necessarily confirmed in all pyrethroids nor absolute from the recent available data. 

On the basis of this concept, one might expect a poison to be relatively uniform in its toxic effect on a series of intact animals because, in the different animals, many different tissues and organs would be involved and the chance exists that the resistance of one tissue might be compensated for by the susceptibility of another. Since from our previous discussions we realize that every individual animal is made up of a coordinated set of organs and tissues, each distinctive (quantitatively) in size, composition, and enzymic make-up, we should expect the greatest interindividual differences to be observed when single tissues from different animals are tested in parallel. This exemplifies the principle which appears to be an important one for our discussions. We expect to find the most striking evidences for biochemical individuality when we look at details, rather than at crude summations. 

In this reaction scheme, the main reaction goes via HCHO and HCOOH to C02- However, the build up of CsHpOq poison occurs on the platinum surface via the parallel reaction and this poison can be removed only by reaction with adsoihed H2O or OH at high potentials. Althou this scheme shows a pathway, details were not given. 

Jellett, J.F., et al.. Detection of paralytic shellfish poisoning (PSP) toxins in shellfish tissue using MIST Alert, a new rapid test, in parallel with the regulatory AOAC mouse bioassay, Toxicon, 40, 10, 1407, 2002. 

Further research will be necessary to demonstrate conclusively that inhibition of histamine metabolism is responsible for the potentiation of histamine toxicity that is apparently observed in scombroid poisoning. In vivo experiments will be necessary to show that hepatic histamine metabolism is also compromised by the ingestion of suspected potentiators. Also, the effectiveness of cadaverine and other possible potentiators must be demonstrated under conditions where the histamine level exceeds the potentiator concentration by a factor of approximately 10. This concentration ratio would parallel that found in spoiled tuna more closely than the levels used in the experiments of Lyons et al. (48). 

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