Potassium nitrite is a solid yellowish white crystal. It has a chemical formula of KNO2. In this compound the potassium forms an ionic bond with the nitrite.
In general, nitrites occur naturally in soil, water, animal and vegetable tissue, and fertilisers.
Potassium nitrite was first obtained by the Swedish chemist Carl Wilhelm Scheele when he worked in a pharmacy laboratory in Köping. He heated potassium nitrate until it was red for half an hour until the new salt, potassium nitrite, was produced.
The two salts, nitrate and nitrite, were written about by the French chemist Eugène-Melchior Péligot, who worked out the reaction as:
This process is still used today to produce KNO2. The reduction of potassium nitrate forms potassium nitrite. Nitrites are produced through the absorption of nitrous oxides in potassium hydroxide or potassium carbonate solutions.
However, it is not produced on a large scale due to the high cost of the bases, as well as the fact that the high solubility level of potassium nitrite in water means it is difficult to retrieve.
Chemical and physical properties
Potassium nitrite is a solid crystal at room temperature, with a whiteish-yellow colour. Its molecular mass is 85.1 /mol and its density is 1.915 g/mol. It has a melting point of 441°C and begins to disintegrate at 350°C. Its boiling point is 537°C, at which it explodes.
Potassium nitrite is highly soluble in water. It is possible to dissolve 281g in 100ml of water at 0°C, 413g in 100ml of water at 100°C. Its room-temperature solubility is 312g in 100ml of water. It is also soluble in ammonia and hot alcohol.
Reactivity and risks
Potassium nitrite is a strong oxidiser that can accelerate the combustion of other materials. It may react explosively when in contact with phosphorous, tin (II) chloride, and other strong reducing agents.
If it comes into contact with ammonium compounds, spontaneous decomposition may occur. The resulting heat may cause nearby combustible material to catch fire.
Potassium nitrite reacts with acids to form toxic nitrogen dioxide gas. When mixed with liquid ammonia it forms dipotassium nitrite, which is extremely reactive and very explosive. If mixed with ammonium salts violent reactions will occur.
Explosions may occur if potassium nitrite is mixed with potassium cyanide. When small quantities of ammonium sulphate are added to molten potassium nitrite, there is a vigorous reaction accompanied by a flame (potassium nitrite, 2016).
Dangers to skin
Potassium nitrite is extremely dangerous to skin and eyes. It should not be ingested or inhaled. The severity of the damage will depend on the duration of contact. Contact with skin may cause irritation, inflammation, and abrasion (Material Safety Data Sheet, Potassium nitrite, 2013).
Potassium nitrite may affect breathing: inhaling it in powder form may irritate the throat, nose, and lungs, and may cause a phlegmy cough. Long-term exposure can cause pulmonary oedema, which will eventually lead to death (Pohanish, 212).
High levels of potassium nitrate may affect the circulatory system and interfere with the ability of the blood to transport oxygen (methaemoglobinaemia), causing head pain; weakness; dizziness; blue skin and mucous (known as cyanosis). Even higher levels can cause breathing problems, collapse, and death (Food Additives in Europe 2000, 2002).
Prolonged exposure can cause chapped skin, dryness, and dermatitis. It may cause lung irritation, resulting in bronchitis. There is also evidence to suggest that potassium nitrite can damage foetal development.
Potassium nitrite is toxic at a level of 235mg per kg of body weight (Royal Society of Chemistry, 2015) and studies of rats have demonstrated that there are no effects in doses lower than 10mg per kg of body weight, per day (H. P. Til, 1988).
Handling and storage
Potassium nitrite is stored with other oxidisers, separate from combustible or flammable substances, reducing agents, acids, cyanides, ammonium compounds, amides, and other nitrogen salts, in dry, well-ventilated, room-temperature places.
It should not be ingested or inhaled. In the case of insufficient ventilation, appropriate breathing equipment should be used, for example, a gas mask. It is important to avoid contact with skin and eyes.
If it is ingested seek immediate medical help. It may be helpful to show the container or sticker to your doctor. When handling this product you should always wear a lab coat, safety goggles, and latex gloves, to avoid accidents (Material Safety Data Sheet, Potassium Nitrate, 2013).
Medical interest in inorganic nitrites rose when their effectiveness in treating chest angina was noticed. Previously, treatment for this condition was done by venesection. This was based on the incorrect theory that the pain was caused by elevated blood pressure, leading medics to cut veins and bleed the patient. This treatment had many downsides.
In the 1860s, the medic Thomas Lauder Brunton decided to test patients with chest angina, making them inhale amyl nitrite (a compound which had been recently produced by one of his colleagues and had been shown to decrease blood pressure in animals).
His results were positive. The pain associated with chest angina diminished rapidly, and lasted for several minutes, giving the patient enough time to rest and recuperate.
For many years amyl nitrite was the treatment of choice for chest angina, but due to its volatility it was replaced by potassium nitrite salts, which had the same effect (Butler & Feelisch, 2008).
In healthy volunteers the effect of potassium nitrite on the nervous system, spinal cord, brain, pulse, blood pressure, and respiration, was measured.
The most important observation was that in small oral doses of approximately 30mg it causes a rise in blood pressure. However, this was followed by a drop in blood pressure. With higher doses significant hypotension was noticed.
It was also observed that potassium nitrite had a noticeable effect on the blood’s ability to transport oxygen, no matter how it was administered. The biological action of potassium nitrite was compared to that of amyl nitrite and ethyl nitrite, and it was concluded that the similarities depended on the conversion of organic nitrites to nitric acid.
In conditions of hypoxia, nitrite gives off nitric oxide, which causes vasodilation. Various methods for the conversion of nitrite to NO have been tested, including the enzymatic reduction by xanthine oxidoreductase, nitrate reductase, and NO synthase (NOS), as well as non-enzymatic dismutation reactions. (Albert L. Lehnigner, 2005).
Patients with hypertension are usually given potassium salts instead of sodium salts.
Potassium nitrate, like sodium nitrate, is also used for food preservation, especially in cured meats such as cured bacon and chorizo. Sodium nitrite and potassium nitrite are used as anti-microbial preservatives, which prevent the deterioration of these foods.
These compounds inhibit bacterial growth through inhibiting specific enzymes.
Sodium nitrite is used to cure meat, not only because it prevents the growth of bacteria, but also because it is an oxidiser. In a reaction with myoglobin, it gives the product a desirable pinkish-red colour.
This use of the nitrite dates back to the Middle Ages, and in the US it has been officially used since 1925. Despite the relatively high toxicity level of nitrite, the nitrite concentration in meat products is 200 ppm, the maximum concentration allowed.
Between 80-90% of nitrite in the average American diet does not come from cured meat, but rather from the natural production of nitrite from the ingestion of vegetable-borne nitrites.
Under certain conditions (especially during cooking), nitrites in meat can react with products produced by the break down of amino acids, forming nitrosamines, which are known carcinogenics.
However, the role of nitrites (and to a certain point nitrates) in the prevention of botulism through the prevention of the emergence of the C. botulinum spore, has prevented the complete elimination of nitrites from cured meats in the US.
Meat cannot technically be cured without the addition of nitrites. There is no substitute for these in the prevention of botulinum poisoning from the consumption of dried sausage, such as pepperoni or chorizo, preventing the germination of the spore. In mice, nitrite-rich foods together with unsaturated fat, can prevent hypertension. This seems to explain the benefits of a Mediterranean diet (Nathan S. Bryan, 2011).
Other uses of potassium nitrite include the production of molten salts; corrosion prevention; anti-fouling agents; as a reagent for redox reactions; as an additive in paint; and for water treatment.
Nitrates and nitrites given orally are absorbed into the blood in the upper part of the gastrointestinal tract. Foods containing pectin may delay absorption in the intestine, with a bigger risk of microbial transformation from nitrate to nitrite.
Nitrate and nitrites are absorbed quickly into the blood, no matter how they are administered. The nitrite gradually oxidises to the nitrate, which is easily distributed in most bodily liquids (urine, saliva, gastric juices, sweat). Nitrate does not accumulate in the body.
The main threat of nitrites is their oxidisation of the ferrous iron (Fe2+) in deoxygenated haemoglobin to Fe3+, producing methemoglobin. Methemoglobin cannot join with oxygen and therefore cannot transport it.
Depending on the percentage of oxidised methemoglobin, the symptoms will usually be those of oxygen shortage with cyanosis, cardiac arrhythmia, circulatory failure, and progressive effects of the central nervous system (CNS). Effect on the CNS can vary, from mild dizziness and lethargy, to a coma and seizures.
The main concern of long-term exposure to nitrites and nitrates is associated with the formation of nitrous compounds, many of which are carcinogenic. This can take place anywhere where nitrite and nitrosatable compounds are present, but especially in acidic conditions or in the presence of certain bacteria.
The gastrointestinal tract, and in particular the stomach, are considered as the main formation sites, but nitrosation reactions can also occur in bladders with urinary tract infections.
Urinal and fecal excretion of nitrite is very low, as most of what enters bloodstream or passes through the gastrointestinal tract is converted into nitrate, mixed with the contents of the gastrointestinal tract, or reduced by enteric bacteria.
The rapid eradication of nitrite in the blood is attributed to the reactivity of nitrite with haemoglobin and other endogenous compounds, a hypothesis which is supported by the increase in the nitrate concentration after intravenous intervention of nitrites in rats.
- Albert L. Lehninger, D. L. (2005 ). Lehninger Principles of Biochemistry. W. H. Freeman.
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- Food Additives in Europe 2000. (2002). copenaghen: tema nord.
- H.P. Til, H. F. (1988). Evaluation of the oral toxicity of potassium nitrite in a 13-week drinking-water study in rats. Food and Chemical Toxicology Volume 26, Issue 10, 851–859. sciencedirect.com.
- material safety data sheet potassium nitrate. (2013, mayo 21). Retrieved from science lab:sciencelab.com.
- Nathan S. Bryan, J. L. (2011). Nitrite and Nitrate in Human Health and Disease. humana press.
- Pohanish, R. P. (2012). Sittig’s Handbook of Toxic and Hazardous Chemicals and Carcinogens, Volumen 1 sixth edition. elsevier.
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- royal society of chemistry. (2015). potassium nitrite. Retrieved from chem spider: chemspider.com.