Nitrite methemoglobinemia

Carbon monoxide Carboxyhemoglobinemia Cyanide Cytochrome oxidase inactivation Paraquat Pulmonary fibrosis Sodium nitrite Methemoglobinemia... 

NOr/NOj 50,000 (nitrate) 500 (nitrite) Methemoglobinemia, shortness of breath, hepatotoxicity nitrite may also be the origin of certain cancers through the formation of nitrosamide and nitrosamine compounds Fertilizers, explosives, ink, tanning manufacture, petroleum refiner, meat preservatives, vegetable juice, industrial salts 0.005-0.01 mg/1 (nitrite) and 0.01-1 mg/1 (nitrate) by spec-trometric techniques 0.022 mg/ 1 (nitrate) and 0.035 mg/1 (nitrite) by ion chromatography 0.1 mg/1 (nitrate) and 0.05 mg/1 (nitrite) by LC... 

Nitrate and Nitrite. Nitrate is usually present in trace quantities in surface waters but occasionally occurs in high concentrations in some groundwaters. If present in excessive amounts, it can contribute to the illness infant methemoglobinemia. Nitrate is an essential nutrient for many photosynthetic autotrophs. Nitrite is an intermediate in the reduction of nitrate as well as in the oxidation of ammonia it is also used as a corrosion inhibitor in some industrial processes. 

Combined intoxications of carbon monoxide and cyanide should not be treated with the nitrites found in cyanide antidote kits. These nitrites are used to create methemoglobinemia, which will exacerbate carbon monoxide poisoning by further reducing the ability of the blood to deliver oxygen to body tissue. 

As noted under Mechanisms of Toxicity (Section 4.2), nitrate and nitrite esters are vasodilators with resulting hypotension (Nickerson 1975). Therapeutic doses of nitroglycerin for relief of angina are associated with headaches of vascular origin. Both PGDN and the structurally related ethylene glycol dinitrate produce headaches in humans and methemoglobinemia and hypotension in rats (Andersen and Mehl 1979). 

Donovan JW. 1990. Nitrates, nitrites, and other sources of methemoglobinemia. In LM Haddad and... 

Ellenhorn MJ, Barceloux DG. 1988. Nitrates, nitrites, and methemoglobinemia. In Medical toxicology Diagnosis and treatment of human poisoning. New York, NY Elsevier, 844-851. 

Since nitrite ions oxidize the iron atoms of hemoglobin and convert it to methemoglobin, there may be a loss in oxygen delivery to tissues. While methemoglobinemia does not follow therapeutic doses of organic nitrates, it can be observed after overdosage or accidental poisoning. 

Some amines react very rapidly with nitrite in aqueous solution, which limits the interpretation which can be placed on the results of testing the combination in drinking water such compounds are better tested in food. Other amines are too insoluble in water to ensure administration of an adequate dose to the animals, The doses that can be administered are somewhat restricted, since no more than 0.2% of nitrite in food or water can be given to rats without risking induction of often fatal methemoglobinemia. The dose of amine given simultaneously is such that there is a ratio of amine to nitrite between 1 to 2 and 1 to 4, which favors formation of N-nitroso derivatives and ensures effective utilization of nitrite. 

Nitrous oxide can react with vitamin B12, preventing its use in red blood cell development and resulting in anemia. Use of nitrites can rapidly result in fatal methemoglobinemia, a condition that reduces the ability of the blood to transport oxygen. In 1944,11 men were admitted to a New York hospital with bluish discoloration of the skin due to methemoglobinemia. The city toxicologist and the health department eventually determined that salt shakers in a food establishment visited by all of the men contained sodium nitrite instead of table salt, sodium chloride. 

Fan, A.M. Steinberg, VE. (1996) Health implications of nitrate and nitrite in drinking water an npdate on methemoglobinemia occnrrence and reprodnctive and developmental toxicity. Regul. Toxicol. Pharmacol, 23, 35-43... 

Treatment Conventional antidote kit consists of nitrites to induce methemoglobinemia (which binds cyanide) and thiosulfate (which hastens conversion of cyanide to less toxic thiocyanate) a newer antidote kit (Cyanokit) consists of concentrated hydroxocobalamin, which directly converts cyanide into cyanocobalamin... 

Treatment of cyanide poisoning includes rapid administration of activated charcoal (although charcoal binds cyanide poorly, it can reduce absorption) and general supportive care. The conventional antidote kit available in the USA includes two forms of nitrite (amyl nitrite and sodium nitrite) and sodium thiosulfate. The nitrites induce methemoglobinemia, which binds to free CI T creating the less toxic cyanomethemoglobin thiosulfate is a cofactor in the enzymatic conversion of CN to the much less toxic thiocyanate (SCINT). Recently, the FDA approved a concentrated form of hydroxocobalamin, which is now available as the Cyanokit (EMD Pharmaceuticals, Durham, North Carolina). Hydroxocobalamin (one form of vitamin B12) combines rapidly with CN to form cyanocobalamin (another form of vitamin B12). 

The gut bacteria may also reduce nitrates to nitrites, which can cause methemoglobinemia or may react with secondary amines in the acidic environment of the gut, giving rise to carcinogenic nitrosamines. 

Numerous substances detected in drinking waters are known to induce toxicity but usually at dose levels much higher than those found in water. Nitrates or nitrites can cause infant methemoglobinemia, lead can affect the hematopoetic or nervous system, cadmium can cause renal damage, and some organohalogens may cause liver toxicity (12). 

After intravenous injection of a fatal dose of NG in rabbits, immediate respiratory stimulation was observed, closely followed by slowing of the heartbeat, muscular twitchings and convulsions. Between convulsions, the heart rate was accelerated and the respiratory rate decreased the animals died of respiratory paralysis. The toxicological picture of NG poisoning is similar to that of asphyxiation, due either to the fall in blood pressure or methemoglobinemia. Despite similarities to Na nitrite poisoning, the toxic effects of NG cannot be explained solely on the basis of its nitrite action... 

Nitrate accumulation may occur in plants growing on soil fertilized with nitrate under moisture-deficient conditions. In the stomachs of ruminant animals, nitrate (NOj) ingested with plant material is reduced to nitrite (N02). The nitrite product enters the bloodstream and oxidizes the iron(II) in hemoglobin to iron(III). The condition that results is methemoglobinemia, which was discussed in Section 15.3 in connection with aniline poisoning. 

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