Vanadium poisoning

There are several theories about the chemistry of vanadium poisoning. The most prominent involves conversion of VjOj to vanadic acid (H-iVO ) under regenerator conditions. Vanadic acid, through hydrolysis, extracts the tetrahedral alumina in the zeolite crystal structure, causing it to collapse. 

The severity of vanadium poisoning depends on the following factors ... 

The alumina content, the amount of rare-earth, and the type and amount of zeolite affect catalyst tolerance to vanadium poisoning. 

Under FCCU operating conditions, almost 100% of the metal contaminants in the feed (such as nickel, vanadium, iron and copper porphyrins) are decomposed and deposited on the catalyst (2). The most harmful of these contaminants are vanadium and nickel. The deleterious effect of the deposited vanadium on catalyst performance and the manner in which vanadium is deposited on the cracking catalyst differ from those of nickel. The effect of vanadium on the catalyst performance is primarily a decrease in catalyst activity while the major effect of nickel is a selectivity change reflected in increased coke and gas yields (3). Recent laboratory studies (3-6) show that nickel distributes homogeneously over the catalyst surface while vanadium preferentially deposits on and reacts destructively with the zeolite. A mechanism for vanadium poisoning involving volatile vanadic acid as the... 

Faced with the need of obtaining more transportation fuels from a barrel of crude, Ashland developed the Reduced Crude Conversion Process (RCC ). To support this development, a residuum or reduced crude cracking catalyst was developed and over 1,000 tons were produced and employed in commercial operation. The catalyst possessed a large pore volume, dual pore structure, an Ultrastable Y zeolite with an acidic matrix equal in acidity to the acidity of the zeolite, and was partially treated with rare earth to enhance cracking activity and to resist vanadium poisoning. 

Catalyst replacement costs and yield loss costs can rise rapidly if poisoning occurs. Obviously, a high metals level must be dealt with appropriately. We accelerated our effort to discover a way to deal with vanadium poisoning. 

Unlabeled Uses Antimony poisoning, bismuth poisoning, selenium poisoning, silver poisoning, vanadium poisoning... 

Physiological Action.—Vanadium compounds are poisonous when taken internally.1 The usual symptoms are paralysis, convulsions, lowering of the body temperature, and feeble pulse. The fatal dose in the case of a rabbit is between 0-00918 and 0-01466 gram. Workmen exposed to fumes of vanadium compounds, especially those engaged on ore-reduction plants, are said to be susceptible to vanadium poisoning, but this has been denied.2 Vanadium compounds have been shown... 

According to Yoo [9] some of the vanadium poisoning is regenerate. While the poisoning effect of Vanadium on the FCC catalyst can at least be partially reversed, this type of regeneration does not take place in conventional FCC operations. 

R. F. Uormsbecber, A. V. Peters, J. M. Maselli, Vanadium poisoning of cracking catalysts mechanism of poisoning and design of vanadium tolerant catalyst system, J. Catal, 100, (1986), pp. 130-137,... 

Enhanced excretion of vanadium was achieved with chelation therapy provided by deferoxamine mesylate (DFOA) (Gomez et al. 1988). Humans or animals with vanadium poisoning have not been helped by the chelating agent dimercaprol (BAL), which is often effective in lessening the toxicity of other metals (Lusky et al. 1949). Intraperitoneal injections of ascorbic acid and of ethylene diamine tetraacetate (EDTA) reduced vanadium-induced morbidity in mice and rats (Jones and Basinger 1983 Mitchell and Floyd 1954). 

Macintosh OC, Steeves B. 1976. Vanadium poisoning from fuel oil ash. Nova Scotia Medical Bulletin 55 85-86. 

Mitchell WG, Floyd EP. 1954. Ascorbic acid and ethylene diamine tetraacetate as antidotes in experimental vanadium poisoning. Proc Soc Exp Biol Med 85 206-208. 

Thomas DL, G., Stiebris K. 1956. Vanadium poisoning in industry. The Medical Journal of Australia 1 607-609. 

Some evidence supports an association of vanadium with mania or bipolar disorder. Vanadium poisoning alters levels of neurotransmitters in rat brains, and two studies correlated elevated vanadium with mania. One study placed manic, depressed, and individuals without such symptoms on a low-vanadium diet. Most of the manic and depressed patients improved (Naylor and Smith 1981). Another study failed to find an association of vanadium with mania (Kumar et al. 1989). 

Stevens H, Forster FM Effect of carbon tetrachloride on the nervous system. AMA Archives of Neurology and Psychiatry 70 635-649,1953 Thomas DLG, Stiebris K Vanadium poisoning in industry. Med J Aust 1 607-609, 1956... 

Frank A, Madej A, Galgan V and Petersson LR (1996) Vanadium poisoning of cattle with basic slag. Concentrations in tissues from poisoned animals and from a reference, slaughterhouse material. Sd Total Environ 181 73-92. 

The D-USY catalyst presented high cracking activity. The results indicate that both nickel and vanadium poison zeolite activity sites. But vanadium poisons preferentially zeolite activities sites for the cracking reaction. Selectivity Sc2-c5 is 49.8 for D-USY, decreased to 42,6 for 1-Ni catalyst and with vanadium adding (from 8Ni-lV to INi-lV catalysts) Sc2-c5 decreases. For the 1-V catalyst selectivity Sc2-c5 is 27,9, 40% lower than D-USY catalyst. This result also confirms a nickel vanadium interaction. The isomerization reaction also increases on 1-V catalyst. This behavior can be related to vanadium acid species formation [8]. 

The poisoning effect of metals on zeolite sites is also observed when in catalyst test is used low temperature. D-USY only presents mcp formation, while nickel poisons around 50% activity. Vanadium poisoning is drastically higher and only 6% of activity remains. The decrease in the activity is lower for the 3NMV, compared to 1 V, also suggesting a nickel vanadium interaction. 

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

Metals passivation in the resid FCC unit may also be accomplished through the addition of metal traps. Tin, barium titanate, strontium titanate, magnesium oxide, manganese oxide, and specialized zeolite types and contents have all been used for vanadium trapping. In addition, zeolites coated with alumina and catalyst particles coated with rare earth have also been applied to resist vanadium poisoning. Antimony, bismuth, and specialized active high crystalline aluminas have all been used successfully to counteract the negative effect of nickel in the FCC unit. 

The first reports of vanadium poisoning in humans described rather widespread systemic effects consisting of polycythemia, followed by red blood cell destruction and anemia, loss of appetite, pallor and emaciation, albumin and blood in the urine, gastrointestinal disorders, nervous complaints and cough, sometimes severe enough to cause hemoptysis. More recent reports describe symptoms that are restricted to the conjunctivae and respiratory system. No evidence is found for disturbances of the gastrointestinal tract, kidneys, blood, or central nervous system. 

The easiest procedures to compensate for vanadium poisoning are to increase the zeolite content of the cat yst or to replace a larger proportion of the catalyst inventoiy every day. Those options are expensive and when equilibrium catalyst contains more than about 5000 ppm of vanadium it is more cost effective to use a vanadium trap. The role of the trap is to stop the migration of vanadium and therefore to prevent deactivation of the zeohte. The trap must not interfere with the cracking reaction and must maintain the vanadium at a lower oxidation state with a high melting point. 

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