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Sodium, poisoning

Tomida et al. (73) investigated the temperature-programmed desorption of n-butylamine from silica-alumina and alumina. The desorbed amine products were different in the two cases. n-Butylamine and n-butene were obtained from silica-alumina dibutylamine and n-butene were obtained from alumina. In a subsequent paper by Takahashi et al. (73a), the authors conclude that two types of adsorption sites on silica-alumina account for the desorption behavior of n-butylamine. One type chemisorbs the amine and the other catalyzes the decomposition of the amine to lower olefins at temperatures above 300°C. On the other hand, amine decomposition was not observed when pyridine was desorbed from silica-alumina. The effects of sodium poisoning on desorption behavior of n-butylamine and pyridine were also examined. [Pg.135]

Under these conditions the plasma protein concentration decreases. Sodium is an emetic intake of excess sodium leads to nausea and vomiting. The accidental substitution of table salt for sugar has resulted in sodium poisoning in infants. These infants experienced increased body temperature, muscle twitching, and convulsions in some cases, their kidneys were damaged. Sodium compounds with high pH values in solution (e.g., sodium hydroxide) are extremely corrosive to the skin and mucous membranes. [Pg.2452]

Liang used n.m.r. to characterize amines adsorbed on hydrated silica-alumina they found evidence for protonated species on sites which were not sterically hindered. Further work on the thermal desorption of pyridine and n-butylamine from silica-aluminas (13 and 25 wt % AI2O3) showed that the stronger acid sites, where pyridine was adsorbed, were of varied acid strength, and both number and strength of the sites were affected by alkali poisoning. An i.r. study of pyridine adsorbed on sodium-poisoned silica-alumina also showed both Lewis and Bronsted sites to be affected. [Pg.207]

Keywords Ion exchange. Chemical tempering. Sodium poisoning. Soda-lime-silicate glass... [Pg.153]

FIGURE 7-7 Carry-over of caustic from a mercaptan-extraction unit resulted in sodium poisoning FCCU catalyst. [Pg.87]

Crystallizes from water in large colourless prisms containing 2H2O. It is poisonous, causing paralysis of the nervous system m.p. 101 C (hydrate), 189°C (anhydrous), sublimes 157°C. It occurs as the free acid in beet leaves, and as potassium hydrogen oxalate in wood sorrel and rhubarb. Commercially, oxalic acid is made from sodium methanoate. This is obtained from anhydrous NaOH with CO at 150-200°C and 7-10 atm. At lower pressure sodium oxalate formed from the sodium salt the acid is readily liberated by sulphuric acid. Oxalic acid is also obtained as a by-product in the manufacture of citric acid and by the oxidation of carbohydrates with nitric acid in presence of V2O5. [Pg.291]

Other sources of hazard arise from the handling of such chemicals as concentrated acids, alkalis, metallic sodium and bromine, and in working with such extremely poisonous substances as sodium and potassium cyanides. The special precautions to be observed will be indicated, where necessary, in the experiments in which the substances are employed, and will also be supplied by the demonstrator. The exercise of obvious precautions and cautious handling will in most cases reduce the danger to almost negligible proportions. Thus, if concentrated sulphuric acid should be accidentally spilled, it should be immediately washed with a liberal quantity of water or of a solution of a mild alkali. [Pg.206]

Sodium cyanide is very poisonous and must be handled with great care. The hands should be washed immediately after using it. All the residual solution.s containing alkali cyanides must be emptied into the main drain of the laboratory and washed down with a liberal supply of water they should never be treated with acid. [Pg.409]

Mandelic acid. This preparation is an example of the synthesis of an a-hydroxy acid by the cyanohydrin method. To avoid the use of the very volatile and extremely poisonous hquid hydrogen cyanide, the cyanohydrin (mandelonitrile) is prepared by treatment of the so um bisulphite addition compound of benzaldehj de (not isolated) with sodium cyanide ... [Pg.754]

Both sodium fluoride and sodium bifluoride are poisonous if taken internally. Dust inhalation and skin or eye contact may cause irritation of the skin, eyes, or respiratory tract, and should be avoided by the use of proper protective equipment (1). [Pg.237]

Fluoroacetic acid [144-49-OJ, FCH2COOH, is noted for its high, toxicity to animals, including humans. It is sold in the form of its sodium salt as a rodenticide and general mammalian pest control agent. The acid has mp, 33°C bp, 165°C heat of combustion, —715.8 kJ/mol( —171.08 kcal/mol) (1) enthalpy of vaporization, 83.89 kJ /mol (20.05 kcal/mol) (2). Some thermodynamic and transport properties of its aqueous solutions have been pubHshed (3), as has the molecular stmcture of the acid as deterrnined by microwave spectroscopy (4). Although first prepared in 1896 (5), its unusual toxicity was not pubhshed until 50 years later (6). The acid is the toxic constituent of a South African plant Dichapetalum i mosum better known as gifirlaar (7). At least 24 other poisonous plant species are known to contain it (8). [Pg.307]

Toxicity. Sodium fluoroacetate is one of the most effective all-purpose rodenticides known (18). It is highly toxic to all species of rats tested and can be used either in water solution or in bait preparations. Its absence of objectionable taste and odor and its delayed effects lead to its excellent acceptance by rodents. It is nonvolatile, chemically stable, and not toxic or irritating to the unbroken skin of workers. Rats do not appear to develop any significant tolerance to this compound from nonlethal doses. However, it is extremely dangerous to humans, to common household pets, and to farm animals, and should only be used by experienced personnel. The rodent carcasses should be collected and destroyed since they remain poisonous for a long period of time to any animal that eats them. [Pg.307]


See other pages where Sodium, poisoning is mentioned: [Pg.353]    [Pg.355]    [Pg.132]    [Pg.133]    [Pg.9]    [Pg.12]    [Pg.160]    [Pg.717]    [Pg.382]    [Pg.2]    [Pg.1955]    [Pg.166]    [Pg.425]    [Pg.189]    [Pg.353]    [Pg.355]    [Pg.132]    [Pg.133]    [Pg.9]    [Pg.12]    [Pg.160]    [Pg.717]    [Pg.382]    [Pg.2]    [Pg.1955]    [Pg.166]    [Pg.425]    [Pg.189]    [Pg.95]    [Pg.119]    [Pg.259]    [Pg.334]    [Pg.363]    [Pg.298]    [Pg.182]    [Pg.185]    [Pg.194]    [Pg.206]    [Pg.699]    [Pg.265]    [Pg.279]    [Pg.230]    [Pg.508]    [Pg.524]    [Pg.268]    [Pg.268]    [Pg.268]    [Pg.270]    [Pg.366]    [Pg.47]   
See also in sourсe #XX -- [ Pg.27 , Pg.132 , Pg.133 , Pg.135 ]




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