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Potassium iodide
Potassium iodide
Potassium iodide
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Potassium iodide
Clinical data
Trade namesIosat, Thyrosafe, Thyroshield, others
Other namesSSKI
AHFS/Drugs.comMonograph
License data
Routes of
administration		By mouth
ATC code
Legal status
Legal status
Identifiers
  • Potassium iodide
CAS Number
PubChem CID
DrugBank
ChemSpider
UNII
KEGG
ChEBI
ChEMBL
CompTox Dashboard (EPA)
ECHA InfoCard100.028.782 Edit this at Wikidata
Chemical and physical data
FormulaKI
3D model (JSmol)
Density3.13[1] g/cm3
Melting point681 °C (1,258 °F)
Boiling point1,330 °C (2,430 °F)
Solubility in water1280 mg/mL (0 °C (32 °F))
1400 mg/mL (20 °C (68 °F))
1760 mg/mL (60 °C (140 °F))
2060 mg/mL (100 °C (212 °F))
[2]
NFPA 704 four-colored diamondHealth 2: Intense or continued but not chronic exposure could cause temporary incapacitation or possible residual injury. E.g. chloroformFlammability 0: Will not burn. E.g. waterInstability 0: Normally stable, even under fire exposure conditions, and is not reactive with water. E.g. liquid nitrogenSpecial hazards (white): no code
2
0
0
  • [K+].[I-]
  • InChI=1S/HI.K/h1H;/q;+1/p-1 checkY
  • Key:NLKNQRATVPKPDG-UHFFFAOYSA-M

Potassium iodide is a chemical compound, medication, and dietary supplement.[3][4] It is a medication used for treating hyperthyroidism, in radiation emergencies, and for protecting the thyroid gland when certain types of radiopharmaceuticals are used.[5] It is also used for treating skin sporotrichosis and phycomycosis.[5][6] It is a supplement used by people with low dietary intake of iodine.[4] It is administered orally.[5]

Common side effects include vomiting, diarrhea, abdominal pain, rash, and swelling of the salivary glands.[5] Other side effects include allergic reactions, headache, goitre, and depression.[6] While use during pregnancy may harm the baby, its use is still recommended in radiation emergencies.[5] Potassium iodide has the chemical formula KI.[7] Commercially it is made by mixing potassium hydroxide with iodine.[8][9]

Potassium iodide has been used medically since at least 1820.[10] It is on the World Health Organization's List of Essential Medicines.[11] Potassium iodide is available as a generic medication and over the counter.[12] Potassium iodide is also used for the iodization of salt.[4]

Medical uses

[edit]

Dietary supplement

[edit]

Potassium iodide is a nutritional supplement in animal feeds and also in the human diet. In humans it is the most common additive used for iodizing table salt (a public health measure to prevent iodine deficiency in populations that get little seafood). The oxidation of iodide causes slow loss of iodine content from iodised salts that are exposed to excess air. The alkali metal iodide salt, over time and exposure to excess oxygen and carbon dioxide, slowly oxidizes to metal carbonate and elemental iodine, which then evaporates.[13] Potassium iodate (KIO3) is used to iodize some salts so that the iodine is not lost by oxidation. Dextrose or sodium thiosulfate are often added to iodized table salt to stabilize potassium iodide thus reducing loss of the volatile chemical.[14]

Thyroid protection in nuclear accidents

[edit]
See also: Nuclear accidents
Pheochromocytoma seen like a dark sphere in center of the body. Image is by MIBG scintigraphy with radiation from radioiodine in the MIBG. Note unwanted uptake of radioiodine from the pharmaceutical by the thyroid gland in the neck, in both images (front and back) of the same patient. Radioactivity is also seen in the bladder.

Thyroid iodine uptake blockade with potassium iodide is used in nuclear medicine scintigraphy and therapy with some radioiodinated compounds that are not targeted to the thyroid, such as iobenguane (MIBG), which is used to image or treat neural tissue tumors, or iodinated fibrinogen, which is used in fibrinogen scans to investigate clotting. These compounds contain iodine, but not in the iodide form. Since they may be ultimately metabolized or break down to radioactive iodide, it is common to administer non-radioactive potassium iodide to ensure that iodide from these radiopharmaceuticals is not sequestered by the normal affinity of the thyroid for iodide.

The World Health Organization (WHO) provides guidelines for potassium iodide use following a nuclear accident. The dosage of potassium iodide is age-dependent: neonates (<1 month) require 16 mg/day; children aged 1 month to 3 years need 32 mg/day; those aged 3-12 years need 65 mg/day; and individuals over 12 years and adults require 130 mg/day.[15] These dosages list mass of potassium iodide rather than elemental iodine.[16][15] Potassium iodide can be administered as tablets or as Lugol's iodine solution.[15] The same dosage is recommended by the US Food and Drug Administration.[17] A single daily dose is typically sufficient for 24-hour protection.[15] However, in cases of prolonged or repeated exposure, health authorities may recommend multiple daily doses.[15] Priority for prophylaxis is given to the most sensitive groups: pregnant and breastfeeding women, infants, and children under 18 years.[15] The recommended doses of potassium iodide, which contains a stable isotope of iodine, only protect the thyroid gland from radioactive iodine.[15] It does not offer protection against other radioactive substances.[15] Some sources recommend alternative dosing regimens.[specify][18]

Not all sources are in agreement on the necessary duration of thyroid blockade, although agreement appears to have been reached about the necessity of blockade for both scintigraphic and therapeutic applications of iobenguane. Commercially available iobenguane is labeled with iodine-123, and product labeling recommends administration of potassium iodide 1 hour prior to administration of the radiopharmaceutical for all age groups,[19] while the European Association of Nuclear Medicine recommends (for iobenguane labeled with either isotope), that potassium iodide administration begin one day prior to radiopharmaceutical administration, and continue until the day following the injection, with the exception of new-borns, who do not require potassium iodide doses following radiopharmaceutical injection.[18][20]

Product labeling for diagnostic iodine-131 iobenguane recommends potassium iodide administration one day before injection and continuing 5 to 7 days following administration, in keeping with the much longer half-life of this isotope and its greater danger to the thyroid.[21] Iodine-131 iobenguane used for therapeutic purposes requires a different pre-medication duration, beginning 24–48 hours prior to iobenguane injection and continuing 10–15 days following injection.[22]

WHO recommended dose for radiological emergencies involving radioactive iodine[23][15]
Age KI in mg per day
Over 12 years old 130
3 – 12 years old 65
1 – 36 months old 32
< 1 month old 16

In 1982, the U.S. Food and Drug Administration approved potassium iodide to protect thyroid glands from radioactive iodine involving accidents or fission emergencies. In an accidental event or attack on a nuclear power plant, or in nuclear bomb fallout, volatile fission product radionuclides may be released. Of these products, 131
I (Iodine-131) is one of the most common and is particularly dangerous to the thyroid gland because it may lead to thyroid cancer.[24] By saturating the body with a source of stable iodide prior to exposure, inhaled or ingested 131
I tends to be excreted, which prevents radioiodine uptake by the thyroid. According to one 2000 study "KI administered up to 48 h before 131
I exposure can almost completely block thyroid uptake and therefore greatly reduce the thyroid absorbed dose. However, KI administration 96 h or more before 131
I exposure has no significant protective effect. In contrast, KI administration after exposure to radioiodine induces a smaller and rapidly decreasing blockade effect."[25] According to the FDA, KI should not be taken as a preventative before radiation exposure. Since KI protects for approximately 24 hours, it must be dosed daily until a risk of significant exposure to radioiodine no longer exists.[26]

Emergency 130 milligrams potassium iodide doses provide 100 mg iodide (the other 30 mg is the potassium in the compound),[16] which is roughly 700 times larger than the normal nutritional need (see recommended dietary allowance) for iodine, which is 150 micrograms (0.15 mg) of iodine (as iodide) per day for an adult. A typical tablet weighs 160 mg, with 130 mg of potassium iodide and 30 mg of excipients, such as binding agents.[16]

Potassium iodide cannot protect against any other mechanisms of radiation poisoning, nor can it provide any degree of protection against dirty bombs that produce radionuclides other than those of iodine.[15]

The potassium iodide in iodized salt is insufficient for this use.[27] A likely lethal dose of salt (more than a kilogram[28]) would be needed to equal the potassium iodide in one tablet.[29]

The World Health Organization does not recommend KI prophylaxis for adults over 40 years, unless the radiation dose from inhaled radioiodine is expected to threaten thyroid function, because the KI side effects increase with age and may exceed the KI protective effects; "...unless doses to the thyroid from inhalation rise to levels threatening thyroid function, that is of the order of about 5 Gy. Such radiation doses will not occur far away from an accident site."[23][15]

The U.S. Department of Health and Human Services restated these two years later as "The downward KI (potassium iodide) dose adjustment by age group, based on body size considerations, adheres to the principle of minimum effective dose. The recommended standard (daily) dose of KI for all school-age children is the same (65 mg). However, adolescents approaching adult size (i.e., >70 kg [154 lbs]) should receive the full adult dose (130 mg) for maximal block of thyroid radioiodine uptake. Neonates ideally should receive the lowest dose (16 mg) of KI."[30]

Side effects

[edit]

There is reason for caution with prescribing the ingestion of high doses of potassium iodide and iodate, because their unnecessary use can cause conditions such as the Jod-Basedow phenomenon, trigger and/or worsen hyperthyroidism and hypothyroidism, and then cause temporary or even permanent thyroid conditions. It can also cause sialadenitis (an inflammation of the salivary gland), gastrointestinal disturbances, and rashes.

Potassium iodide is not recommended for people with dermatitis herpetiformis and hypocomplementemic vasculitis – conditions that are linked to a risk of iodine sensitivity.[31]

There have been some reports of potassium iodide treatment causing swelling of the parotid gland (one of the three glands that secrete saliva), due to its stimulatory effects on saliva production.[32]

A saturated solution of KI (SSKI) is typically given orally in adult doses several times a day (5 drops of SSKI assumed to be 1⁄3 mL) for thyroid blockade (to prevent the thyroid from excreting thyroid hormone) and occasionally this dose is also used, when iodide is used as an expectorant (the total dose is about one gram KI per day for an adult). The anti-radioiodine doses used for 131
I uptake blockade are lower, and range downward from 100  mg a day for an adult, to less than this for children (see table). All of these doses should be compared with the far lower dose of iodine needed in normal nutrition, which is only 150 μg per day (150 micrograms, not milligrams).

At maximal doses, and sometimes at much lower doses, side effects of iodide used for medical reasons, in doses of 1000 times the normal nutritional need, may include: acne, loss of appetite, or upset stomach (especially during the first several days, as the body adjusts to the medication). More severe side effects that require notification of a physician are: fever, weakness, unusual tiredness, swelling in the neck or throat,[citation needed] mouth sores, skin rash, nausea, vomiting, stomach pains, irregular heartbeat,[citation needed] numbness or tingling of the hands or feet, or a metallic taste in the mouth.[33][citation needed]

In the event of a radioiodine release the ingestion of prophylaxis potassium iodide, if available, or even iodate, would rightly take precedence over perchlorate administration, and would be the first line of defence in protecting the population from a radioiodine release. However, in the event of a radioiodine release too massive and widespread to be controlled by the limited stock of iodide and iodate prophylaxis drugs, then the addition of perchlorate ions to the water supply, or distribution of perchlorate tablets would serve as a cheap, efficacious, second line of defense against carcinogenic radioiodine bioaccumulation.

The ingestion of goitrogen drugs is, much like potassium iodide also not without its dangers, such as hypothyroidism. In all these cases however, despite the risks, the prophylaxis benefits of intervention with iodide, iodate or perchlorate outweigh the serious cancer risk from radioiodine bioaccumulation in regions where radioiodine has sufficiently contaminated the environment.

Industrial uses

[edit]

KI is used with silver nitrate to make silver iodide (AgI), an important chemical in film photography. KI is a component in some disinfectants and hair treatment chemicals. KI is also used as a fluorescence quenching agent in biomedical research, an application that takes advantage of collisional quenching of fluorescent substances by the iodide ion. However, for several fluorophores addition of KI in μM-mM concentrations results in increase of fluorescence intensity, and iodide acts as fluorescence enhancer.[34]

Potassium iodide is a component in the electrolyte of dye sensitised solar cells (DSSC) along with iodine.

Potassium iodide finds its most important applications in organic synthesis mainly in the preparation of aryl iodides in the Sandmeyer reaction, starting from aryl amines. Aryl iodides are in turn used to attach aryl groups to other organics by nucleophilic substitution, with iodide ion as the leaving group.

Chemistry

[edit]

Potassium iodide is an ionic compound which is made of the following ions: K+I−. It crystallises in the sodium chloride structure. It is produced industrially by treating KOH with iodine.[35]

It is a white salt, which is the most commercially significant iodide compound, with approximately 37,000 tons produced in 1985. It absorbs water less readily than sodium iodide, making it easier to work with.

Aged and impure samples are yellow because of the slow oxidation of the salt to potassium carbonate and elemental iodine.[35]

4 KI + 2 CO2 + O2 → 2 K2CO3 + 2 I2

Inorganic chemistry

[edit]

Since the iodide ion is a mild reducing agent, I− is easily oxidised to iodine (I2) by powerful oxidising agents such as chlorine:

2 KI(aq) + Cl2(aq) → 2 KCl(aq) + I2(aq)

This reaction is employed in the isolation of iodine from natural sources. Air will oxidize iodide, as evidenced by the observation of a purple extract when aged samples of KI are rinsed with dichloromethane. As formed under acidic conditions, hydriodic acid (HI) is a stronger reducing agent.[36][37][38]

Like other iodide salts, KI forms triiodide (I−3) when combined with elemental iodine.

KI(aq) + I2(s) → KI3(aq)

Unlike I2, I−3 salts can be highly water-soluble. Through this reaction, iodine is used in redox titrations. Aqueous KI3 (Lugol's iodine) solution is used as a disinfectant and as an etchant for gold surfaces.

Potassium iodide and silver nitrate are used to make silver(I) iodide, which is used for high speed photographic film and for cloud seeding:

KI(aq) + 9 AgNO3(aq) → AgI(s) + KNO3(aq)

Organic chemistry

[edit]

KI serves as a source of iodide in organic synthesis. A useful application is in the preparation of aryl iodides from arenediazonium salts.[39][40]

KI, acting as a source of iodide, may also act as a nucleophilic catalyst for the alkylation of alkyl chlorides, bromides, or mesylates.

History

[edit]

Potassium iodide has been used medically since at least 1820.[10] Some of the earliest uses included cures for syphilis,[10] lead and mercury poisoning.

Chernobyl

[edit]

Potassium iodide's (KI) value as a radiation protective (thyroid blocking) agent was demonstrated following the Chernobyl nuclear reactor disaster in April 1986. A saturated solution of potassium iodide (SSKI) was administered to 10.5 million children and 7 million adults in Poland[30][41] as a preventative measure against accumulation of radioactive 131
I in the thyroid gland.

Reports differ concerning whether people in the areas immediately surrounding Chernobyl itself were given the supplement.[42][20] However the US Nuclear Regulatory Commission (NRC) reported, "thousands of measurements of I-131 (radioactive iodine) activity...suggest that the observed levels were lower than would have been expected had this prophylactic measure not been taken. The use of KI...was credited with permissible iodine content in 97% of the evacuees tested."[20]

With the passage of time, people living in irradiated areas where KI was not available have developed thyroid cancer at epidemic levels, which is why the US Food and Drug Administration (FDA) reported "The data clearly demonstrate the risks of thyroid radiation... KI can be used [to] provide safe and effective protection against thyroid cancer caused by irradiation."[43]

Chernobyl also demonstrated that the need to protect the thyroid from radiation was greater than expected. Within ten years of the accident, it became clear that thyroid damage caused by released radioactive iodine was virtually the only adverse health effect that could be measured. As reported by the NRC, studies after the accident showed that "As of 1996, except for thyroid cancer, there has been no confirmed increase in the rates of other cancers, including leukemia, among the... public, that have been attributed to releases from the accident."[44]

But equally important to the question of KI is the fact that radioactivity releases are not "local" events. Researchers at the World Health Organization accurately located and counted the residents with cancer from Chernobyl and were startled to find that "the increase in incidence [of thyroid cancer] has been documented up to 500 km from the accident site... significant doses from radioactive iodine can occur hundreds of kilometers from the site, beyond emergency planning zones."[23] Consequently, far more people than anticipated were affected by the radiation, which caused the United Nations to report in 2002 that "The number of people with thyroid cancer... has exceeded expectations. Over 11,000 cases have already been reported."[45]

Hiroshima and Nagasaki

[edit]

The Chernobyl findings were consistent with studies of the effects of previous radioactivity releases. In 1945, several hundreds of thousands of people working and residing in the Japanese cities of Hiroshima and Nagasaki were exposed to high levels of radiation after atomic bombs were detonated over the two cities by the United States. Survivors of the A-bombings, also known as hibakusha, have markedly high rates of thyroid disease; a 2006 study of 4091 hibakusha found nearly half the participants (1833; 44.8%) had an identifiable thyroid disease.[46]

An editorial in The Journal of the American Medical Association regarding thyroid diseases in both hibakusha and those affected by the Chernobyl disaster reports that "[a] straight line adequately describes the relationship between radiation dose and thyroid cancer incidence" and states "it is remarkable that a biological effect from a single brief environmental exposure nearly 60 years in the past is still present and can be detected."[47]

Nuclear weapons testing

[edit]

The development of thyroid cancer among residents in the North Pacific from radioactive fallout following the United States' nuclear weapons testing in the 1950s (on islands nearly 200 miles downwind of the tests) were instrumental in the 1978 decision by the FDA to issue a request for the availability of KI for thyroid protection in the event of a release from a commercial nuclear power plant or weapons-related nuclear incident. Noting that KI's effectiveness was "virtually complete" and finding that iodine in the form of KI was substantially superior to other forms including iodate (KIO3) in terms of safety, effectiveness, lack of side effects, and speed of onset, the FDA invited manufacturers to submit applications to produce and market KI.[48]

Fukushima

[edit]

It was reported on 16 March 2011, that potassium iodide tablets were given preventively to U.S. Naval air crew members flying within 70 nautical miles of the Fukushima Daiichi Nuclear Power Plant damaged in the earthquake (8.9/9.0 magnitude) and ensuing tsunami on 11 March 2011. The measures were seen as precautions, and the Pentagon said no U.S. forces have shown signs of radiation poisoning. By 20 March, the US Navy instructed personnel coming within 100 miles of the reactor to take the pills.[49]

The Netherlands

[edit]
Distribution areas for iodine pills in the Netherlands (2017).

In the Netherlands, the central storage of iodine-pills is located in Zoetermeer, near The Hague. In 2017, the Dutch government distributed pills to hundreds of thousands of residents who lived within a certain distance of nuclear power plants and met some other criteria.[50][51]

Belgium

[edit]

By 2020, potassium iodide tablets are made available free of charge for all residents in all pharmacies throughout the country.[52]

Formulations

[edit]

Three companies (Anbex, Inc., Fleming Co, and Recipharm of Sweden) have met the strict FDA requirements for manufacturing and testing of KI, and they offer products (IOSAT, ThyroShield, and ThyroSafe,[53] respectively) which are available for purchase. In 2012, Fleming Co. sold all its product rights and manufacturing facility to other companies and no longer exists. ThyroShield is currently not in production.

Tablets of potassium iodide are supplied for emergency purposes related to blockade of radioiodine uptake, a common form of radiation poisoning due to environmental contamination by the short-lived fission product 131
I.[54] Potassium iodide may also be administered pharmaceutically for thyroid storm.

For reasons noted above, therapeutic drops of SSKI, or 130 mg tablets of KI as used for nuclear fission accidents, are not used as nutritional supplements, since an SSKI drop or nuclear-emergency tablet provides 300 to 700 times more iodine than the daily adult nutritional requirement. Dedicated nutritional iodide tablets containing 0.15 mg (150 micrograms (μg)) of iodide, from KI or from various other sources (such as kelp extract) are marketed as supplements, but they are not to be confused with the much higher pharmaceutical dose preparations.

Potassium iodide can be conveniently prepared in a saturated solution, abbreviated SSKI. This method of delivering potassium iodide doesn't require a method to weigh out the potassium iodide, thus allowing it to be used in an emergency situation. KI crystals are simply added to water until no more KI will dissolve and instead sits at the bottom of the container. With pure water, the concentration of KI in the solution depends only on the temperature. Potassium iodide is highly soluble in water thus SSKI is a concentrated source of KI. At 20 degrees Celsius the solubility of KI is 140-148 grams per 100 grams of water.[55] Because the volumes of KI and water are approximately additive, the resulting SSKI solution will contain about 1.00 gram (1000 mg) KI per milliliter (mL) of solution. This is 100% weight/volume (note units of mass concentration) of KI (one gram KI per mL solution), which is possible because SSKI is significantly more dense than pure water—about 1.67 g/mL.[56] Because KI is about 76.4% iodide by weight, SSKI contains about 764 mg iodide per mL. This concentration of iodide allows the calculation of the iodide dose per drop, if one knows the number of drops per milliliter. For SSKI, a solution more viscous than water, there are assumed to be 15 drops per mL; the iodide dose is therefore approximately 51 mg per drop. It is conventionally rounded to 50 mg per drop.

The term SSKI is also used, especially by pharmacists, to refer to a U.S.P. pre-prepared solution formula, made by adding KI to water to prepare a solution containing 1000 mg KI per mL solution (100% wt/volume KI solution), to closely approximate the concentration of SSKI made by saturation. This is essentially interchangeable with SSKI made by saturation, and also contains about 50 mg iodide per drop.

  • Saturated solutions of potassium iodide can be an emergency treatment for hyperthyroidism (so-called thyroid storm), as high amounts of iodide temporarily suppress secretion of thyroxine from the thyroid gland.[57] The dose typically begins with a loading dose, then 1⁄3 mL SSKI (5 drops or 250 mg iodine as iodide), three times per day.
  • Iodide solutions made from a few drops of SSKI added to drinks have also been used as expectorants to increase the water content of respiratory secretions and encourage effective coughing.[58]
  • SSKI has been proposed as a topical treatment for sporotrichosis, but no trials have been conducted to determine the efficacy or side effects of such treatment.[59]
  • Potassium iodide has been used for symptomatic treatment of erythema nodosum patients for persistent lesions whose cause remains unknown. It has been used in cases of erythema nodosum associated with Crohn's disease.[60]
  • Due to its high potassium content, SSKI is extremely bitter, and if possible it is administered in a sugar cube or small ball of bread. It may also be mixed into much larger volumes of juices.
  • Neither SSKI or KI tablets form nutritional supplements, since the nutritional requirement for iodine is only 150 micrograms (0.15 mg) of iodide per day. Thus, a drop of SSKI provides 50/0.15 = 333 times the daily iodine requirement, and a standard KI tablet provides twice this much.

References

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[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Potassium iodide

View on Grokipedia
from Grokipedia

Potassium iodide is an inorganic chemical compound with the formula KI, consisting of potassium cations and iodide anions in a 1:1 ionic lattice. It appears as a white, odorless, cubic crystalline solid that is highly soluble in water, forming a colorless solution. As a stable source of iodide ions, it functions as a dietary supplement to prevent iodine deficiency and is used medically as an expectorant to loosen mucus in respiratory conditions. Its most critical application involves thyroid protection during radiological emergencies, where administration saturates the thyroid gland with non-radioactive iodine, thereby blocking uptake of harmful radioactive iodine-131 isotopes released in nuclear accidents or detonations. Potassium iodide also finds use in analytical chemistry as a reagent and historically in photography for emulsion preparation.

Chemical Properties and Synthesis

Physical and Chemical Properties

Potassium iodide (KI) is an ionic compound composed of potassium cations (K⁺) and iodide anions (I⁻) in a 1:1 ratio, forming a crystal lattice similar to sodium chloride. It manifests as a white, odorless, crystalline powder with a bitter, salty taste. The compound is hygroscopic, absorbing moisture from the air, and exhibits slight deliquescence in dry conditions; prolonged exposure to air, light, or moisture leads to oxidation, resulting in yellowing due to liberation of free iodine. Key physical properties include a density of 3.13 g/cm³, a melting point of 681 °C, and a boiling point of 1330 °C, at which it decomposes. Potassium iodide demonstrates high solubility in water, dissolving up to 128 g per 100 mL at 0 °C and 148 g per 100 mL at 25 °C, but it is only slightly soluble in ethanol.
PropertyValue
3.13 g/cm³
681 °
1330 ° (decomposes)
in (0 °)128 g/100 mL
in (25 °)148 g/100 mL
Chemically, potassium iodide acts as a weak , readily oxidized by oxidizing agents such as or to liberate iodine (I₂). It also functions as a of hydroxyl radicals. Under normal conditions, it remains but can decompose when heated ly or exposed to oxidizing environments.

Synthesis and Production Methods

Potassium iodide is primarily produced industrially through the absorption of iodine into a hot of , yielding a mixture of potassium iodide and according to the reaction I₂ + 6 KOH → 5 KI + KIO₃ + 3 H₂O. The potassium iodate byproduct is separated via , exploiting its lower , and subsequently reduced to iodide using reducing agents such as carbon or hydrazine to improve overall yield and minimize iodine loss. This process allows for scalable production with high purity after final purification steps like recrystallization, though iodine sourcing from natural deposits like Chilean caliche or brine extraction represents a significant cost factor due to iodine's relative scarcity. An alternative industrial route involves reacting hydriodic acid with potassium carbonate: 2 HI + K₂CO₃ → 2 KI + CO₂ + H₂O, which generates carbon dioxide as a byproduct and avoids iodate formation but requires access to hydriodic acid, often produced in situ from iodine and a reducing agent like hydrogen sulfide or phosphorous acid. In regions with established chemical manufacturing, such as China, a variant employs formic acid as a reductant in the iodine-potassium hydroxide reaction to directly favor iodide formation over iodate, enhancing efficiency and reducing separation steps. Impurity control in both methods relies on rigorous filtration and crystallization to remove trace metals or oxidized species, ensuring pharmaceutical-grade purity exceeding 99% in commercial products. In settings, potassium iodide is commonly prepared on a small scale by dissolving iodine in a concentrated solution, the industrial absorption method but with simpler and subsequent or cooling for crystallization. Yields approach stoichiometric limits after iodate reduction, typically using ascorbic acid or for , though double —such as mixing with followed by metathesis—is less favored to lower purity without extensive purification. Environmental considerations in production include unreacted iodine from process streams via solvent extraction or to mitigate waste, as iodine volatilization or discharge can contribute to aquatic toxicity if unmanaged.

Medical Applications

Iodine Supplementation and Deficiency Prevention

Potassium iodide (KI) functions as a bioavailable source of iodide, the form of iodine utilized by the thyroid gland for hormone synthesis, making it suitable for supplementation in regions with endemic iodine deficiency. Iodine deficiency impairs thyroid function, leading to goiter enlargement and hypothyroidism, with global prevalence historically affecting up to 30% of populations before widespread fortification efforts. KI supplies approximately 76.4% iodide by weight, allowing precise dosing; for instance, to achieve the recommended daily allowance (RDA) of 150 micrograms of iodine for adults, roughly 196 micrograms of KI is required, with near-complete absorption efficiency of 96.4% in the gastrointestinal tract. Historically, KI was employed in the early for goiter prevention in iodine-deficient areas, such as parts of , though its use waned around due to inconsistent results and side effects before the advent of iodized salt in the . Empirical studies, including large-scale trials, demonstrate that iodide supplementation via KI or equivalent forms significantly reduces goiter prevalence; for example, systematic reviews of interventions in children and adults in deficient regions report goiter rate decreases of up to 50-70% within years of , alongside improvements in urinary iodine concentrations as a of status. In veterinary applications, KI is routinely added to feeds at levels up to 10 mg/kg for and to prevent deficiency-related reproductive and growth impairments, with safety confirmed across species when adhering to regulatory limits. Excessive KI intake, however, risks the Wolff-Chaikoff effect, wherein high iodide levels temporarily inhibit thyroid peroxidase-mediated organification, halting hormone production for 24-48 hours in euthyroid individuals, potentially precipitating hypothyroidism in susceptible populations like neonates or those with underlying thyroid autonomy. In iodine-sufficient regions, such as the United States post-iodized salt introduction, routine KI supplementation is unnecessary and may contribute to subclinical excess, as evidenced by median urinary iodine levels exceeding 100 mcg/L; debates persist on targeted use for at-risk groups (e.g., vegans or inland populations avoiding seafood), but population-wide programs risk overtreatment without deficiency surveillance.

Treatment of Hyperthyroidism

Potassium iodide (KI) is employed in the short-term of , primarily through the Wolff-Chaikoff effect, whereby excess iodide temporarily inhibits thyroid peroxidase-mediated organification of iodide, thereby blocking the synthesis of thyroxine (T4) and (T3). This mechanism acutely reduces release, making KI useful in severe cases such as , where it is administered after initial treatment with thionamide drugs like to prevent further exacerbation. In , typical dosing involves 250–500 mg orally every 4–6 hours, often as saturated solution of potassium iodide (SSKI), with 5–10 drops (equivalent to 0.25–0.5 mL) providing rapid inhibition within hours. Preoperatively, KI is given to patients with undergoing to decrease thyroid gland and intraoperative blood loss, typically at 50–250 mg orally every 8 hours for 10–14 days. Clinical studies demonstrate that this regimen significantly reduces and firmens the gland, facilitating surgical dissection, with one analysis of preoperative iodine administration showing decreased blood loss compared to controls. KI is often combined with beta-blockers like for symptom control and antithyroid drugs to sustain euthyroidism, as monotherapy risks rebound . In mild Graves' , doses of 100–200 mg daily have induced remission in over 50% of patients within 4 weeks to 2 years, particularly those with low autoantibody titers and smaller goiters. However, KI's inhibitory effect is transient due to the "escape" phenomenon, where downregulation of the sodium-iodide symporter (NIS) allows resumed hormone synthesis after 5–10 days, potentially aggravating if not followed by definitive . Prolonged use beyond short-term (e.g., >2 weeks) carries risks of iodine-induced or, paradoxically, in susceptible individuals with underlying , limiting its role compared to sustained antithyroid agents like methimazole. Empirical data underscore its adjunctive rather than primary utility, with guidelines recommending discontinuation if escape occurs and monitoring for thyroid function derangements.

Thyroid Protection in Radiation Emergencies

Potassium iodide (KI) protects the gland from radioactive iodine isotopes, such as (I-131), by saturating the sodium- (NIS) on thyroid follicular cells with , non-radioactive ions. The NIS actively transports into thyroid cells for synthesis; excess competitively inhibits this , preventing I-131 incorporation into and subsequent thyroid irradiation. This blockade is specific to radioiodine and does not mitigate external or other radionuclides. KI's protective effect depends on administration timing relative to exposure, with maximal saturation kinetics achieved pre-exposure or within 1-2 hours post-inhalation or ingestion of I-131, blocking over 90% of thyroidal uptake in physiological models. Delayed dosing beyond 4 hours reduces efficacy to approximately 50% or less, as partial I-131 uptake occurs before full NIS saturation. In scenarios involving airborne I-131 release, such as nuclear reactor accidents, prophylactic KI exploits the thyroid's finite iodide storage capacity, estimated at 10-20 mg in adults, to dilute incoming radioiodine. Recommended single doses for blocking, per U.S. and Centers for Control and Prevention guidelines, vary by age and body weight to achieve comparable saturation without excess: adults and adolescents over 150 pounds (70 kg) receive 130 mg; children aged 3-18 years under 150 pounds receive 65 mg; children aged 1 month to 3 years receive 32 mg; and neonates under 1 month receive 16 mg. These doses, typically administered as saturated solution or tablets, aim for rapid absorption and peak plasma levels within 1 hour to align with exposure dynamics. While proponents emphasize KI's role in directly lowering thyroid-absorbed dose from I-131—potentially reducing long-term cancer through blocked beta emissions—critics highlight its narrow scope, noting inefficacy against gamma rays, beta particles from other isotopes, or whole-body exposure, where evacuation and sheltering remain primary countermeasures. KI does not neutralize external radiation fields or protect non-thyroid tissues, underscoring its adjunctive, not standalone, in multi-isotope releases.

Non-Medical Applications

Expectorant and Pharmaceutical Uses

Potassium iodide has been employed as an expectorant to facilitate the clearance of respiratory in conditions such as chronic and , primarily through of the iodide , which is believed to increase the production of watery respiratory tract secretions, thereby reducing . This mucolytic effect stems from iodide stimulating submucosal secretion in the airways, promoting thinner that is easier to expectorate, though the precise biochemical pathway remains incompletely elucidated and may involve indirect hydration of mucoproteins. Historically, saturated solutions of potassium iodide (SSKI), such as Pima , were administered orally for and other obstructive diseases, with typical doses ranging from 300 to 600 mg diluted in water, juice, or milk, taken three to four times daily to aid in loosening tenacious sputum. Despite its longstanding use, supporting iodide's as a mucolytic agent is limited and contentious, with multiple studies failing to demonstrate significant clinical improvements in mucus clearance or symptom relief compared to or alternative therapies. Recent reviews highlight that while it may provide subjective benefits in select patients with chronic pulmonary conditions, objective measures like sputum or pulmonary function tests show marginal or inconsistent results, leading to its diminished in contemporary respiratory pharmacotherapy. Safer, better-tolerated expectorants such as guaifenesin have largely supplanted potassium iodide, which is now infrequently recommended due to potential adverse effects including gastrointestinal upset and iodism at higher doses. In pharmaceutical formulations, potassium iodide occasionally appears as an additive in legacy preparations or compounded syrups for its purported secretory effects, but regulatory approvals and guidelines, such as those from the FDA, restrict its promotion primarily to thyroid-related indications, with expectorant labeling confined to over-the-counter or prescription contexts for chronic disorders under . Its non-thyroid pharmaceutical remains niche, often to veterinary or historical contexts where alternatives are unavailable, underscoring a shift toward evidence-based mucolytics with stronger support.

Industrial, Photographic, and Analytical Applications

Potassium iodide functions as a nutritional iodine source in feeds, supporting synthesis in and preventing deficiencies such as goiter. Regulatory assessments confirm its as a feed additive for various when used within established limits, typically up to 10 mg iodine per kg of . It is also incorporated into certain disinfectants and serves as an intermediate in chemical manufacturing processes, including the synthesis of other iodides. In cloud seeding, potassium iodide acts as a glaciogenic nucleant to promote ice crystal formation and enhance precipitation, though it is secondary to silver iodide in most operations. In photographic applications, potassium iodide reacts with to form , a light-sensitive compound integral to traditional emulsions and processes. It is added to developers as a restrainer to minimize and oxidation, yielding finer and higher contrast in images, particularly in wet plate and historical silver-based techniques. These properties stem from iodide ions' ability to control reactivity during exposure and processing. Analytically, potassium iodide serves as a in titrations for quantifying strong oxidants, such as in the iodometric determination of or dissolved oxygen, where it liberates free iodine detectable by indicator. It is employed in qualitative tests for metals like and mercury, forming insoluble s, and in assessing iodine absorption numbers for unsaturated fats and oils. As a calibration standard, it provides precise iodide concentrations for spectroscopic and electrochemical analyses. The versatility of potassium iodide as a reducer supports its demand across these sectors, though challenges include iodine's volatility under heat and potential substitution by less costly bromides or chlorides in some processes. The global market for potassium iodide, encompassing industrial uses, reached US$974.6 million in 2023 and is forecasted to expand to US$2.2 billion by 2034 at a 7.5% , driven by nutritional and chemical applications.

Pharmacology

Mechanism of Action

Potassium iodide (KI) dissociates in aqueous media to yield potassium cations and iodide anions (I⁻), with the latter serving as the primary active species in biological systems. In the , I⁻ is actively accumulated by follicular cells through the sodium-iodide (NIS), a plasma membrane that facilitates secondary by harnessing the of sodium ions generated by the Na⁺/K⁺- . This uptake concentrates I⁻ against its gradient, enabling subsequent oxidation by (TPO) in the presence of to form reactive iodine species that iodinate tyrosine residues on within the , initiating . Excess I⁻ from KI triggers autoregulatory feedback via the Wolff-Chaikoff effect, where high intrathyroidal concentrations inhibit TPO-mediated organification through multiple causal pathways, including direct competition for oxidation sites, generation of inhibitory iodolipids that suppress TPO gene expression, and reduced availability of oxidized enzyme intermediates. This transiently blocks hormone synthesis, protecting against hyperiodination; therapeutic doses exploit this for short-term inhibition without permanent disruption, as downregulation of NIS expression typically restores iodide efflux and normal function within 24-48 hours via decreased NIS mRNA and protein levels. Failure of this escape mechanism, as in iodide-induced hypothyroidism, arises from sustained TPO blockade or impaired adaptation, distinguishing dose-dependent therapeutic saturation from toxic overload where causal chains lead to depleted hormone stores and follicular atrophy. As an expectorant, KI promotes mucolysis by stimulating serous gland secretion in the respiratory epithelium, increasing watery fluid output from submucosal glands and alveoli to dilute viscous mucus; this irritative effect likely involves local osmotic gradients or direct glandular stimulation, though the exact transduction pathway—potentially via iodide-sensitive ion channels or secondary messengers—remains incompletely elucidated empirically. In non-biological or adjunctive contexts, I⁻ exhibits radical scavenging by donating electrons to reactive species like hydroxyl radicals (•OH) or superoxide, forming less reactive iodine radicals (I•) or hypoiodous acid (HOI), thereby interrupting oxidative chain reactions without the volatility of elemental iodine (I₂), which sublimes readily and requires enzymatic reduction to bioavailable I⁻. KI's ionic form ensures superior aqueous solubility and near-complete bioavailability (96-97% absorption) compared to I₂, minimizing gastrointestinal irritation and enabling precise dosing for targeted iodide delivery.

Pharmacokinetics

Potassium iodide dissociates in the to release the , which is rapidly absorbed primarily in the following . Absorption is nearly complete within 2 hours, with high estimated at approximately 97% for supplemental doses. Peak plasma concentrations occur within 1-2 hours post-ingestion, though pharmacokinetic modeling indicates potential attainment as early as 38 minutes after a single dose. The volume of distribution for iodide is approximately 0.3 L/kg, reflecting extracellular distribution with preferential accumulation in the thyroid gland due to active sodium-iodide symporter-mediated uptake. Iodide also concentrates in extrathyroidal sites including salivary glands, gastric mucosa, choroid plexus, mammary glands, and ovaries, with distribution volume expanding during pregnancy and lactation owing to increased physiological demands. Iodide undergoes negligible metabolism and enters the plasma iodide pool directly for thyroidal utilization or clearance. Excretion is predominantly renal, comprising about 80% of elimination via glomerular filtration and tubular secretion, with the remaining 20% fecal and minor contributions from sweat, saliva, and other secretions. The biological half-life of the total body iodide pool averages 8-10 days in individuals with normal renal function, though this can extend in renal impairment due to reduced clearance rates. Dietary iodine intake and thyroid status modulate pool size and turnover, with low intake prolonging retention through enhanced reabsorption. Pharmacokinetic variations occur across age groups, particularly in neonates and infants, where renal function and elevated relative iodine requirements lead to slower clearance and smaller body pools, heightening to overload. These differences lower dosing thresholds in to mitigate risks while achieving therapeutic saturation, as renal capacity matures postnatally.

Safety Profile

Adverse Effects and Side Effects

Common adverse effects of potassium iodide (KI) include gastrointestinal disturbances such as , , , and , as well as a metallic or bitter in the . These effects are typically mild and occur due to the compound's irritant on the digestive tract. Dermatological reactions, including and urticaria, affect approximately 1% of users, based on data from large-scale administration during radiological incidents. Swelling or of the salivary glands () has been reported but was absent in over 17 million doses distributed in following the Chernobyl accident. Hypersensitivity reactions, such as angioedema or bronchospasm, are rare and more likely in individuals with prior iodine sensitivity. Thyroid-related effects may include transient hypothyroidism via the Wolff-Chaikoff effect or, less commonly, hyperthyroidism (Jod-Basedow phenomenon) in patients with underlying thyroid disorders like Graves' disease. In neonatal cohorts exposed via maternal administration post-Chernobyl, transient hypothyroidism occurred in 0.37% of cases (12 out of 3,214 monitored), resolving without long-term sequelae. With short-term, correctly dosed use for thyroid , severe adverse remain below 1%, as evidenced by minimal serious in mass prophylaxis efforts. Risks of mild effects like or gastrointestinal upset increase with age, particularly over 40, and with repeated or excessive dosing. Prolonged use can lead to iodism, manifesting as , salivary gland soreness, and , though these are reversible upon discontinuation.

Contraindications, Interactions, and Precautions

Potassium iodide is contraindicated in individuals with to iodine or compounds, as this can precipitate severe allergic reactions including . It is also absolutely contraindicated in patients with active or hypocomplementemic , conditions where exposure exacerbates dermatological through immune-mediated mechanisms. Additional absolute contraindications include , , and , as can worsen potassium retention or respiratory . Relative contraindications apply to populations where empirical data indicate heightened risks, though benefits may outweigh harms in acute radiation scenarios. Pregnant women face fetal thyroid suppression risks, including goiter and hypothyroidism, due to iodide's placental transfer and inhibition of fetal thyroid hormone synthesis; however, U.S. FDA and CDC guidelines prioritize single-dose administration during nuclear emergencies to protect the fetus from radioactive iodine uptake, advising against repeat dosing unless evacuation is impossible. Neonates under one month require strict limitation to a single dose, followed by thyroid function monitoring (TSH and T4 levels), as their immature thyroid glands are susceptible to prolonged iodide-induced blockade. Patients with preexisting thyroid disorders, such as multinodular goiter, Graves' disease, or autoimmune thyroiditis, warrant caution due to potential exacerbation of hyperthyroidism or glandular instability. Drug interactions with potassium iodide include potentiation of lithium's antithyroid effects, increasing the of through synergistic inhibition of ; concurrent use requires close monitoring of function. It may reduce the of antithyroid medications like methimazole by competing for uptake, necessitating dosage adjustments in . Other interactions involve anticoagulants (e.g., ), where iodide can alter hypoprothrombinemia, and potassium-sparing agents that compound . Precautions emphasize renal impairment, where reduced iodide excretion heightens toxicity potential via potassium accumulation, particularly in patients with . Cardiac conditions, , and necessitate baseline assessments, as iodide can provoke arrhythmias or muscle stiffness. In radiation emergencies, while affirm higher adverse event rates in vulnerable groups like neonates and the elderly, some emergency analyses overly restrictive protocols for potentially limiting access, arguing that untreated radioactive iodine exposure poses greater population-level risks based on post-Chernobyl cohort studies.

Toxicity and Overdose Management

Acute toxicity of potassium iodide in rodents is evidenced by oral LD50 values ranging from 285 mg/kg in rats to approximately 3 g/kg in other models, indicating moderate acute hazard upon ingestion. In humans, acute overdose produces gastrointestinal irritation, including abdominal pain, vomiting, bloody diarrhea, and metallic taste, progressing in severe cases to hyperthermia, dehydration, circulatory shock, coma, and multi-organ failure due to iodism-like effects from rapid iodide overload. Chronic iodide excess from repeated high dosing leads to iodism, characterized by persistent metallic , increased salivation, frontal , acneiform lesions, and conjunctivitis, resolving upon discontinuation but potentially exacerbating underlying dysfunction. Overdose management is supportive, lacking a specific ; early interventions include or emesis induction if within 1-2 hours of , followed by activated (though efficacy for iodide is limited), intravenous fluids for volume repletion, and electrolyte monitoring to address potential hyperkalemia or acidosis. In refractory cases with renal or extreme hyperiodidemia, facilitates iodide removal, as the is dialyzable. Fatal outcomes remain rare, documented primarily in suicidal ingestions exceeding 10-20 g or accidental misuse beyond FDA-guided limits of 130 mg daily for adults in radiation scenarios, underscoring the need for strict adherence to dosing protocols.

Efficacy in Radiation Protection

Empirical Evidence from Studies and Incidents

In controlled and , potassium iodide (KI) administered shortly before or within 1-2 hours after exposure to radioactive iodine blocks more than 90% of thyroidal of radioiodine-131 by saturating the with stable iodine, preventing isotopic exchange. remains substantial up to 4-6 hours post-exposure, reducing by 50-90% depending on timing, as confirmed by pharmacokinetic models and direct measurements of radioiodine retention in thyroid tissue. The and American Thyroid Association reviews of such data emphasize this narrow window, with blockade derived from rapid iodine kinetics where the sodium-iodide symporter's capacity is overwhelmed, averting in follicular cells. During the 1986 Chernobyl nuclear accident, timely KI distribution in Poland—totaling 18.5 million doses starting April 29, two days after the April 26 release—prevented any detectable rise in thyroid cancer rates among exposed children and adolescents, despite measurable plume fallout. In contrast, epidemiological analysis of Belarusian and Ukrainian cohorts exposed as youth showed that stable iodine prophylaxis, where provided promptly, reduced radiation-attributable thyroid cancer risk by a factor of three (relative risk 0.34, 95% CI 0.16-0.9), linking lower incidence directly to blocked radioiodine doses amid overall pediatric cases exceeding 5,000 by 2005. Dose-response models from these regions, incorporating individual thyroid exposure estimates up to 33 Gy without prophylaxis, indicate that the approximately 5 million KI doses administered in affected Soviet areas averted up to 90% of projected pediatric cancers through uptake inhibition in compliant subgroups. In the 2011 Fukushima Daiichi accident, Japanese authorities distributed or made available roughly 230,000 KI doses to evacuees within the 20-30 km exclusion zone starting March 12, coinciding with initial venting of radioactive materials. Intake compliance reached 63.5% in surveyed child populations in impacted towns like Miharu, correlating with no observed thyroid dysfunction or autoimmunity spikes attributable to KI itself. Given I-131 releases orders of magnitude below Chernobyl's (totaling ~0.5-1 PBq versus 1,760 PBq), baseline thyroid doses stayed under 100 mGy for most, yielding zero confirmed radiation-induced pediatric thyroid cancers to date; retrospective modeling projects that optimal KI timing would have further diminished these low doses by ~90% via blockade.

Limitations, Criticisms, and Debates

Potassium iodide (KI) exclusively blocks thyroidal of radioactive iodine isotopes, such as , and provides no against other radionuclides like cesium-137 or external forms including gamma rays and neutrons. It neither shields the body from whole-body irradiation nor prevents absorption or biological effects of non-iodine contaminants released in nuclear incidents. KI's protective window is narrow, with efficacy dropping sharply if dosing occurs more than 24 hours post-exposure, as prior or of radioactive iodine allows significant accumulation before saturation by . In low-risk scenarios absent confirmed radioactive iodine plumes, prophylactic administration risks unnecessary side effects, including transient , especially in iodine-sufficient populations or with repeated doses, potentially disrupting function via Wolff-Chaikoff . Critics argue that such overuse in campaigns could induce iatrogenic outweighing benefits, as evidenced by studies showing biochemical impairment from repetitive even short-term. Debates persist over dosing regimens, with the single-dose challenged by analyses indicating repeated administration may better address prolonged iodine releases, though this elevates risks of and goiter in susceptible groups. Media portrayals often exaggerate KI as a broad-spectrum "anti-radiation pill," fueling panic-driven stockpiling and scams during geopolitical tensions, despite its organ-specific, time-bound mechanism. Mass distribution strategies face for logistical risks, including improper use leading to adverse , and for diverting resources from preventive like enhanced reactor , which addresses root causal factors in releases more comprehensively than reactive . Some analysts contend that emphasizing KI stockpiles promotes public over investments in nuclear technologies, potentially eroding trust in probabilistic assessments that deem such rare under modern safeguards.

Policy Considerations and Distribution Strategies

The U.S. Food and Drug Administration (FDA) and World Health Organization (WHO) recommend stockpiling potassium iodide (KI) tablets for targeted distribution to populations within proximity to nuclear power plants, emphasizing use only upon confirmed risk of radioactive iodine release as an adjunct to evacuation and food controls. FDA guidelines specify age- and weight-based dosing, such as 130 mg for adults and adolescents over 12 years weighing more than 70 kg, 65 mg for children aged 3-18 years under 70 kg, and lower doses for infants, with administration ideally within hours of exposure onset. In the United States, states like Pennsylvania and Delaware have implemented periodic free distributions; for instance, Pennsylvania's Department of Health offered KI tablets to residents within 10 miles of active nuclear plants on July 31, 2025, at sites including Beaver Valley Mall, while Delaware's Emergency Management Agency and Division of Public Health distributed tablets on October 2, 2025, in Townsend near the Hope Creek plant. KI distribution strategies offer advantages in cost-effectiveness, with tablets available at approximately $1 per dose, facilitating large-scale stockpiling without prohibitive expense, and enabling rapid deployment through pre-positioned supplies near high-risk sites. However, inefficiencies arise from logistical challenges, including the need for controlled storage to maintain efficacy and periodic replacement due to finite shelf life—typically 5-7 years, though FDA-approved extensions via testing can mitigate replacement costs—and complexities in just-in-time distribution during evacuations or widespread alerts. Public non-compliance poses further risks, as surveys indicate hesitancy stemming from concerns over side effects like gastrointestinal upset or allergic reactions, potentially undermining efficacy if individuals delay or refuse ingestion absent clear, authoritative instructions. In response to heightened threats during the 2022 Russia-Ukraine conflict, particularly around the nuclear , the donated 5.5 million KI tablets to on August 26, 2022, supporting local distributions to nearby residents amid fears of leaks from shelling. Such preemptive actions demonstrate empirical success in bolstering but have drawn for potentially inducing undue when risks do not materialize, as no significant radioactive iodine release occurred, leading to questions about over-reliance on worst-case assumptions that may erode public trust and divert resources from more probable contingencies. frameworks thus balance proactive stockpiling with criteria for to avoid inefficiencies, prioritizing empirical risk assessments over speculative fears.

History

Discovery and Pre-20th Century Uses

Iodine, the basis for potassium iodide, was discovered in by French Courtois during the processing of seaweed ash for saltpeter production. Courtois added excess to the ash liquor containing compounds, liberating violet vapors that condensed into dark, iodine crystals exhibiting a metallic luster and strong odor. analyzed in 1813, confirming it as a new element analogous to and naming it iode from word for violet-colored. independently verified its elemental nature shortly thereafter, though for discovery remained with Courtois. (KI) was prepared soon after by reacting iodine with or solutions, yielding a stable, water-soluble salt suitable for medicinal and chemical applications. Early medical applications of iodide salts, including potassium iodide, emerged in the 1820s, initially for thyroid disorders. In 1820, Swiss physician Jean-François Coindet treated bronchocele (goiter) with tincture of iodine, observing marked shrinkage in enlarged thyroid glands among 40 patients, attributing efficacy to iodine's presence in traditional seaweed remedies. Potassium iodide was adopted for oral administration in goiter prophylaxis during the early 19th century, though empirical trials revealed risks of thyroid suppression with prolonged use, leading to abandonment of routine iodide supplementation around 1858. By , potassium iodide served as an expectorant in respiratory ailments like tuberculosis, promoting bronchial clearance to its mucolytic properties observed in clinical practice. It was also employed in syphilis , particularly for tertiary and neurosyphilitic stages, where inorganic iodides complemented mercury therapies by purportedly softening gummas and alleviating symptoms, though stemmed from anti-inflammatory effects rather than bactericidal action against Treponema pallidum. In photography, iodide salts facilitated light-sensitive emulsions. Louis Daguerre's 1839 process sensitized silver-plated copper sheets with iodine vapor to form silver iodide (AgI), enabling the first practical photographic images via mercury development. William Henry Fox Talbot's contemporaneous calotype method (patented 1841) coated paper with silver nitrate followed by potassium iodide solution to generate AgI, allowing negative-positive image production and influencing subsequent silver halide technologies.

Early 20th Century Developments

In the 1920s, public health campaigns in the United States addressed widespread iodine deficiency, particularly in the "goiter belt" encompassing the Great Lakes, Appalachians, and northwestern regions, where endemic goiter affected up to 40-50% of schoolchildren in some areas. Pioneering studies by David Marine and colleagues at the Cleveland Clinic demonstrated that prophylactic iodine administration prevented goiter formation in adolescent girls, leading to the recommendation of adding potassium iodide to table salt at concentrations of approximately 100 mg/kg. Commercial iodized salt, fortified with potassium iodide, first appeared in U.S. markets on May 1, 1924, marking a pivotal shift toward population-level supplementation to ensure daily iodine intake aligned with average salt consumption of about 6.5 g per person. This initiative yielded measurable reductions in goiter prevalence, with surveys indicating declines exceeding 50% in affected regions within the first decade; for example, in Michigan, goiter rates among schoolchildren fell from 38.6% in 1924 to substantially lower levels by the early 1930s, approaching near-elimination in monitored cohorts by mid-century. Potassium iodate emerged as an alternative fortificant in some formulations due to greater stability, though potassium iodide remained predominant in early U.S. products. These developments built on pre-war medical uses of potassium iodide, including as an expectorant and antiseptic in tinctures during World War I wound care, fostering interwar standardization in pharmaceutical compendia like the United States Pharmacopeia for thyroid-related therapies. Despite successes, early adoption faced challenges from unregulated supplementation, with reports of iodine excess causing thyroid dysfunction and overdoses, particularly among enthusiasts self-administering high doses without medical supervision. Physicians like C.L. Hartsock documented cases of "iodine abuse" from overconsumption of iodized salt and tonics, underscoring the need for dosage guidelines and highlighting risks such as hyperthyroidism in susceptible individuals prior to broader regulatory oversight. These interwar experiences informed later refinements in iodine prophylaxis, emphasizing controlled public health distribution over ad hoc remedies.

Nuclear Era and Major Incidents

In the atomic bombings of on , , and on , , no potassium iodide (KI) was distributed to populations, allowing unblocked uptake of radioiodine isotopes released in the fission products, which contributed to exposures among survivors. Atmospheric by the , beginning in on , , and continuing intermittently through , dispersed iodine-131 fallout across wide areas, exposing millions—particularly children—to doses that prompted epidemiological studies on radioiodine risks and the potential of stable iodine for blockade. These events highlighted the causal link between radioiodine or via contaminated and accumulation, underscoring the absence of prophylactic measures as a factor in elevated exposure levels during the early Cold War era. The Three Mile Island accident on March 28, 1979, at the Unit 2 reactor in Pennsylvania marked the first U.S. consideration of large-scale KI administration for thyroid protection amid fears of significant fission product release, though actual radioiodine emissions were minimal—estimated at less than 1% of core inventory—and no widespread distribution occurred. Post-accident analysis confirmed negligible health impacts from radiation, but the event catalyzed regulatory action, leading the FDA to update guidelines in 1979 affirming KI's role as a thyroid-blocking agent in radiation emergencies when radioiodine release thresholds are met. The Chernobyl disaster on April 26, 1986, at the No. 4 reactor in the Soviet Union released substantial iodine-131, resulting in high thyroid doses—often exceeding 1 Gy in children—due to delayed and inconsistent KI prophylaxis in affected republics like Ukraine and Belarus, causally linked to over 6,000 excess thyroid cancer cases by the 2000s. In contrast, Poland, receiving comparable fallout plumes, promptly distributed over 18 million KI doses starting April 29, 1986, to nearly all children and much of the adult population, achieving up to 90% blockade of radioiodine uptake when administered within hours to days of exposure and averting significant thyroid dose increases, with no detectable rise in Chernobyl-attributable thyroid cancers. This disparity demonstrates that timely, widespread KI deployment reduces thyroid exposures by factors of 5-10 or more compared to delayed or absent intervention, independent of iodine deficiency status, as evidenced by lower committed thyroid doses in Polish cohorts versus Soviet ones under similar plume conditions.

Post-2000 Events and Recent Distributions

Following the Fukushima Daiichi nuclear accident, Japanese authorities distributed approximately 230,000 units of potassium iodide tablets as a precautionary measure against potential radioactive iodine exposure. Subsequent thyroid cancer rates among exposed children remained low compared to Chernobyl, with Scientific on the Effects of Atomic (UNSCEAR) assessments attributing this primarily to lower radiation doses from atmospheric dispersion and dilution rather than widespread KI efficacy, though prompt KI administration in affected areas likely contributed to thyroid protection where uptake occurred. In parallel, countries with nuclear facilities, such as , , and others, maintained pre-distribution programs for KI tablets to residents within 5-50 km radii of plants, enabling rapid deployment readiness independent of the Japanese incident. Amid the 2022 and heightened risks at nuclear sites like , neighboring supplied fire departments nationwide with potassium iodide tablets for potential emergency distribution to mitigate threats, though no significant release necessitated widespread use. experienced pharmacy shortages of KI tablets to stockpiling driven by escalation fears, prompting restocking efforts, while the donated 5 million tablets to from strategic reserves as preemptive . In the United States, federal alerts emphasized against and of KI, with no mass governmental distribution implemented to the absence of direct radiological threats, despite surges in commercial demand. By , U.S. states continued routine KI distribution programs near nuclear facilities for emergency preparedness. scheduled free tablet distributions on , , at sites like Townsend for residents near the Hope Creek and Salem plants, under a U.S. Nuclear Regulatory Commission-initiated program. Pennsylvania's Department of similarly offered free KI to individuals within 10 miles of its five active nuclear plants, with events such as those on August 14, 2025, targeting workers, residents, and students in proximity. The global potassium iodide market reached $1.03 billion in , reflecting sustained across pharmaceutical and applications amid ongoing geopolitical tensions and nuclear protocols.

Formulations and Availability

Pharmaceutical Forms and Dosages

Potassium iodide (KI) is formulated primarily as oral tablets in 65 mg and 130 mg strengths for thyroid protection during radiation emergencies involving radioactive iodine release. Liquid oral solutions, such as those containing 65 mg KI per mL in 30 mL bottles with calibrated droppers, enable precise volume-based dosing, particularly for pediatric and infant populations where tablet division may be imprecise. Lugol's solution, an aqueous preparation incorporating 10% KI alongside 5% elemental iodine, provides an alternative liquid form historically used for thyroid-related conditions, with each drop delivering approximately 6.25 mg of total iodine and iodide content. In radiation emergencies, KI dosing follows age- and weight-adjusted single administrations to saturate the thyroid and block radioactive iodine uptake for about 24 hours per dose, with repeat dosing only if exposure persists and under medical guidance. Recommended single doses per FDA and CDC guidelines are outlined below:
Age GroupDose (KI)
Newborns (<1 month)16 mg
Infants (1 month to 3 years)32 mg
Children (3 to 12 years)65 mg
Adolescents and adults (≥12 years, or >70 kg for children)130 mg
Pregnant or breastfeeding adults130 mg
For hyperthyroidism management, such as preoperative preparation or thyroid storm, oral KI solution dosages for adults and teenagers typically involve 250 mg (0.25 mL of saturated solution) three times daily, though total daily intake may be adjusted to 100-300 mg based on clinical response and formulation. KI formulations exhibit good stability, with tablets maintaining potency for 5 to 7 years under recommended storage conditions of room temperature (around 68°F), low humidity, and protection from light, air, heat, and moisture to prevent degradation. The FDA may approve shelf-life extensions beyond labeled expiration through stability testing, confirming ongoing efficacy without reformulation.

Regulatory Status and Access

In the United States, the (FDA) approved potassium iodide (KI) products, including 130 mg tablets like iOSAT, for over-the-counter (OTC) availability in radiation emergencies starting in 1982, recognizing their role in blocking uptake of radioactive iodine. For therapeutic uses beyond emergencies, such as preoperative management of thyrotoxicosis or treatment of , KI generally requires a prescription. The WHO includes KI (as saturated solution) on its Model of for antimycotic and antithyroid applications, underscoring its global priority for basic healthcare systems. Regulatory frameworks internationally prioritize stockpiling for nuclear or radiological threats, with access often restricted to government-distributed supplies rather than routine OTC . In the , national authorities maintain KI reserves aligned with directives, but OTC status and distribution vary by , leading to inconsistent access. Access barriers persist globally, including limited pharmacy stocking even where OTC-approved, rural distribution delays, and disruptions; for instance, in , heightened demand from Russia-Ukraine conflict fears caused stock depletions, surges from approximately USD 38/kg to USD 46/kg in some markets, and a sevenfold increase in OTC dispensing in affected regions. These patterns highlight vulnerabilities in non-emergency access, where verifiable protective against radioactive iodine supports structured regulatory stockpiles over unregulated personal accumulation to mitigate hoarding-induced shortages.

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