Alkali Poisoning Research Articles

Deterioration Mechanism of Direct Internal Reforming Catalyst.

The deterioration mechanism of reforming catalysts used for internal reforming molten carbonate fuel cells is studied through post-test analyses of the used catalysts. The catalysts studied are Ni/MgO-Al2O3. Deactivation of the catalysts is caused both by a decrease in Ni surface area of the catalyst and by loss of specific activity of the Ni surface (alkali poisoning). The decrease in Ni surface area is characterized firstly by accelerated sintering of Ni particles due to the existence of alkali metals (attached electrolyte). Secondly, sulfur poisoning also plays an important role, especially for sintered catalysts with small Ni surface areas. As for the effect of alkali poisoning, the specific activity of the Ni surface decreases to 15–60% of the original one. Blockage of pore structure by the electrolyte does not seem to be important for the loss of Ni surface area.

Internal steam reforming in fuel cells and alkali poisoning

Thermodynamics predict high electrical efficiency, when converting methane directly in a fuel cell. This is possible in high temperature fuel cells, such as the molten carbonate (MCFC) and the solid oxide fuel cells (SOFC), utilizing the heat from the electrochemical reaction for the steam reforming of methane. The heat balance is not a limiting factor. Internal reforming in a molten carbonate fuel cell involves the risk of alkali poisoning of the catalyst. The mechanism of alkali-poisoning is discussed. Laboratory tests on alkali containing catalysts are described and data from internal reforming in a MCFC-plant are presented. On basis of a simple model, an assessment is made of the required catalyst activity. Only a few percents of the original activity is needed for 95% conversion.

The nature of adsorbed sites on catalysts: II. Behavior of basic compounds on silica-alumina catalyst at elevated temperatures

The behavior of n-butylamine and pyridine adsorbed on the silica-alumina catalysts at elevated temperatures was investigated by a thermal desorption method. The results showed that there are two kinds of adsorption sites on the surface except for a physical adsorption; one is an adsorption site for amine and the other is an acidic site on which the amine decomposes to lower olefins at temperatures above 300 °C. The amount of the former is about five times larger than the latter. The decomposed products of the amine were a mixture of n-butene and propylene. Total lower olefins were equivalent to about 0.1 mmole/g of the precursor. On the other hand, desorption of pyridine from the catalyst surface showed that only one peak was observed in the desorption curve, and the minute amount of pyridine was desorbed without decomposition even at temperatures above 400 °C. From this fact, it follows that the stronger acid sites on the silica-alumina are distributed in the different acid strengths. The acid sites were inhibited rather nonselectively by the alkali poisoning in comparison with such a basic compound as n-butylamine or pyridine. The formation of n-butene from n-butylamine on the stronger acid sites was more suppressed than that of propylene by the alkali poisoning.

Jejunal stricture due to ingestion of ammonia; report of a case complicated by severe potassium deficiency.

Ingestion of a caustic substance, such as lye or ammonium hydroxide, frequently results in ulcerative esophagitis and esophageal stricture. Although cases occasionally have been reported of pyloric stricture due to alkali poison, in general, gastric lesions more frequently follow ingestion of strong acids than of alkalies. 1 Lesions of the small bowel following ingestion of either acid or alkali are rare. Review of the literature disclosed only two cases of jejunal lesions due to alkali poisoning 2 ; both were fatal. No report of a nonfatal case could be found. The case described in the present communication appears to be unique in that a corrosive esophagitis and jejunitis coexisted, with no gross lesion of the stomach or duodenum. Successful resection of a jejunal stricture was accomplished 67 days after ingestion of the poison. In addition, this case is of interest because of the development of a severe, almost fatal potassium deficiency

A HIGH FLUID INTAKE IN THE MANAGEMENT OF EDEMA, ESPECIALLY CARDIAC EDEMA. II. CLINICAL OBSERVATIONS AND DATA

Excerpt It is only in the last 50 years that the limitation of fluids in the presence of edema has been taught and practiced so universally. Earlier clinicians noted that the theoretical fear of wa...

ALKALI POISONING IN GASTRIC ULCER

Medical Journal of AustraliaVolume 1, Issue 17 p. 521-521 Current Comment ALKALI POISONING IN GASTRIC ULCER First published: 01 April 1941 https://doi.org/10.5694/j.1326-5377.1941.tb95337.xAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Volume1, Issue17April 1941Pages 521-521 RelatedInformation

Caustic soda poisoning

The authors cite Balazs'ao data of 754 alkali poisonings during 3 years, of which 163 cases, or 21.6% ended in death. In England in 1930-32 there were 92 deaths from alkali poisoning, of which 78 were for suicide and the rest were accidents.