Potassium Metabisulfite

Cosmetic ingredients (Potassium Metabisulfite) -> CIR (Cosmetic Ingredient Review)

Preservative

Sulfur dioxide odor

Pungent, sharp odor

2.3 g/cu cm

Relative density (water = 1): 2.34

2.3 @25 °C

White crystals or crystalline powder

White powder

Freely soluble in water; insoluble in alcohol

Reacts with acid solutions; insoluble in ethanol

49.5 g/100 g water at 25 °C

Solubility in water, g/100ml at 25 °C: 49.5 (good)

Potassium metabisulfite decomposes at temperatures above 150 °C. In the air, it oxidizes to the sulfate, more readily in the presents of moisture.

When heated to decomposition it emits toxic fumes of /sulfur oxides/ and /potassium sulfate/.

150 °C

Potassium metabisulfite appears as a white granular or powdery solid with a sharp odor of sulfur dioxide. Decomposes at 150 to 190 °C. Density 2.3 g / cm3. Contact severely irritates skin, eyes, and mucous membranes. Low toxicity. Used as a food preservative and an antioxidant.

Dry Powder; Large Crystals

Colourless crystals or white crystalline powder

A white granular or powdery solid with a sharp odor of sulfur dioxide; [CAMEO]

WHITE CRYSTALLINE POWDER WITH PUNGENT ODOUR.

Liberates SO2 with acids; oxidizes in air to sulfate, more readily in presence of moisture

It may catch fire if too much heat develops in powdering it.

This chemical does not meet GHS hazard criteria for 2.8% (43 of 1552) of reports.

Danger

H315 (90%): Causes skin irritation [Warning Skin corrosion/irritation]

P261, P264, P264+P265, P271, P280, P302+P352, P304+P340, P305+P354+P338, P317, P319, P321, P332+P317, P362+P364, P403+P233, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 1552 reports by companies from 15 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Danger

Chemical: Disulfurous acid, dipotassium salt

Regulation (EC) No 1935/2004 (amended)

Disulfurous acid, potassium salt (1:2) is listed on the EPA's Chemical Data Reporting (CDR) system. Manufacturers and importers of Disulfurous acid, potassium salt (1:2) are required to report information about their production and use of this chemical to the EPA under the Toxic Substances Control Act (TSCA). (40 eCFR Part 711)

Status: Active Update: 16-12-2022 https://echa.europa.eu/registration-dossier/-/registered-dossier/5221

Potassium disulfite: Does not have an individual approval but may be used under an appropriate group standard

Excerpt from ERG Guide 154 [Substances - Toxic and/or Corrosive (Non-Combustible)]:

Not combustible. Gives off irritating or toxic fumes (or gases) in a fire.

A case of occupational asthma, confirmed by specific inhalation challenge, was reported in a worker whose job was to sprinkle dry metabisulfite on potatoes. [Malo JL, Cartier A, Desjardins A. Occupational asthma caused by dry metabisulphite. Thorax 1995 May;50(5); 585-6.] Similar cases have been reported in the wine, laundry, and lobster fishing industries. [Madsen J, Sherson D, Kjoller H, Hansen I, Rasmussen K. Occupational asthma caused by sodium disulphite in Norwegian lobster fishing. Occup Environ Med 2004;61:873-874] In the presence of water and acid, metabisulfite can generate toxic amounts of SO2. [ATSDR Med. Manag. Guidelines] See SULFITES. May cause skin sensitization and asthma after prolonged contact; [ICSC] Reactions to both sodium and potassium metabisulfite are expected. [Kanerva, p. 1828]

Potassium metabisulfite is generally recognized as safe when used as a chemical preservative in accordance with good manufacturing practice, except that it is not used in meats; in food recognized as a source of vitamin B1; on fruits and vegetables intended to be served raw to consumers or sold raw to consumers, or to be presented to consumers as fresh.

Potassium metabisulfite used as a chemical preservative in animal drugs, feeds, and related products is generally recognized as safe when used in accordance with good manufacturing or feeding practice, except that it is not used in meats or in food recognized as source of vitamin B1.

POTASSIUM METABISULFITE reacts with oxidizing agents to generate heat and products that may be flammable, combustible, or otherwise reactive. Can react explosively with strong oxidizing agents. Generates gaseous sulfur dioxide in contact with acids. Aqueous solutions are acidic and corrosive.

Excerpt from ERG Guide 154 [Substances - Toxic and/or Corrosive (Non-Combustible)]:

In case of fire in the surroundings, use appropriate extinguishing media.

Fresh air, rest. Artificial respiration may be needed. Refer for medical attention.

Remove contaminated clothes. Rinse skin with plenty of water or shower.

Rinse with plenty of water for several minutes (remove contact lenses if easily possible). Refer immediately for medical attention.

Rinse mouth. Refer for medical attention .

If material on fire or involved in fire: Extinguish fire using agent suitable for type of surrounding fire. (Material itself does not burn or burns with difficulty.) Use "alcohol" foam, dry chemical or carbon dioxide. Keep run-off water out of sewers and water sources.

Potassium metabisulfite should be stored in a cool, dark place.

Keep dry and well closed.

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity or environmental contamination. Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in soil or water; effects on animal and plant life; and conformance with environmental and public health regulations.

Personal protection: particulate filter respirator adapted to the airborne concentration of the substance. Sweep spilled substance into covered containers. If appropriate, moisten first to prevent dusting. Wash away remainder with plenty of water. Then store and dispose of according to local regulations.

Personnel protection: Keep upwind. Avoid breathing dusts, and fumes from burning material. Avoid bodily contact with the material.

If material not on fire and not involved in fire: Keep material out of water sources and sewers.

Sulfites, including potassium metabisulfite, can react with various pharmaceutical compounds including sympathomimetics such as epinephrine (adrenaline), chloramphenicol, cisplatin, and amino acids which can result in their pharmacological inactivation. Sulfites are also reported to react with phenylmercuric nitrate, and may adsorb onto rubber closures.

/GENOTOXICITY/ Potassium metabisulfite at a concentration of 3.75 mM inactivated the mutagenic activity of coffee preparations at doses of 2-20 mg/plate when tested with Salmonella typhimurium strain TA100 without S9 mix.

Cough. Shortness of breath. Wheezing.

Redness.

Redness. Pain. Burns.

Abdominal pain. Nausea. Vomiting.

/HUMAN EXPOSURE STUDIES/ /Investigators/ reported the results of patch testing 2894 eczematous patients over a 2-year period. Positive reactions to Sodium Metabisulfite in 1% pet. (following a 2-day occlusive exposure) were noted in 50 patients (1.7% incidence). All 50 patients also reacted to Potassium Metabisulfite in 1% pet., and to Sodium Bisulfite 1% and 5% pet. Only two reacted to Sodium Sulfite 1% pet.

/HUMAN EXPOSURE STUDIES/ The prevalence of sulfite sensitivity was determined in a group of 51 children with chronic asthma, who were recruited from an allergy clinic. They ranged in age from five to 16 years, with a mean age of 10.3 years. Nearly 90% of the children were atopic, and 18% were steroid-dependent. Potassium metabisulfite was administered in lemonade in an open challenge, in graduated doses of 0.5-100 mg. Eighteen of the 51 reacted with a decrease > or = 20% in FEV1 after drinking the metabisulfite solution. Placebo challenges given to 14 of the 18 subjects resulted in one positive reaction. There was no difference in the prevalence of sulfite sensitivity between steroid-dependent and non-steroid-dependent subjects. All of the patients who reacted to metabisulfite solution but only two-thirds of those who did not react were reported to be sensitive to smog.

/HUMAN EXPOSURE STUDIES/ Bronchoconstrictive airway responses were evaluated in a group of 35 boys and 21 girls aged 6-14 years with chronic asthma, by open challenge after ingestion of incremental doses of potassium metabisulfite solution or capsules. All but two of the children had a history of allergy to various agents, but none showed allergy to metabisulfite in a skin-prick test. When the challenge was given with capsules, positive responses (reduction in pulmonary function) were noted in four of the children, only at the maximum challenge of 200 mg. Two children who had not reacted to the challenge with encapsulated metabisulfite responded positively to metabisulfite solution. None had systemic symptoms (flushing, tingling, and/or faintness) or hypotensive symptoms after metabisulfite challenge. All the patients who reacted positively to either challenge had severe to moderate bronchial reactivity to methacholine, while those who did not react had only mild reactivity to methacholine.

/HUMAN EXPOSURE STUDIES/ A group of patients with chronic asthma and histories suggestive of sulfite sensitivity was studied in order to determine whether the ingestion of aqueous potassium metabisulfite was associated with degranulation of mast cells, as measured by the release of the neutrophil chemotactic factor of anaphylaxis. Single-blind, oral aqueous challenges of up to a maximum of 200 mg potassium metabisulfite were given to 13 patients. Serum samples were obtained from all the patients before the challenge and for 180 min afterwards. The samples were tested for the presence of neutrophil chemotactic factor by both a (51)Cr microchamber chemotaxis assay and a leukocyte polarization technique. Six of the patients gave positive responses, as indicated by a fall in FEV1 > or = 20% of prechallenge values. No significant increase in the amount of neutrophil chemotactic factor was detected in post-challenge serum samples from any patient. Skin testing with potassium metabisulfite in 10 of the patients yielded uniformly negative reactions. The authors concluded that sensitivity to aqueous metabisulfite is not associated with mast-cell degranulation in patients in whom the result of a skin test is negative.

For more Human Toxicity Excerpts (Complete) data for POTASSIUM METABISULFITE (12 total), please visit the HSDB record page.

/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ In a two-stage stomach carcinogenesis experiment, male outbred Wistar rats were given MNNG in the drinking water and sodium chloride in the feed for 8 weeks. They then received drinking water containing 1% Potassium Metabisulfite (or other test substances) for 32 weeks. Animals were killed for necropsy and tissue was collected. Potassium Metabisulfite significantly (p < 0.05) increased the incidence of adenocarcinoma of the pylorus of the glandular stomach after initiation with MNNG and sodium chloride compared to controls (initiated rats that had not received treated water). No carcinomas developed in rats given Potassium Metabisulfite without MNNG or sodium chloride. Potassium Metabisulfite was considered to exert tumor-promoting activity in the rat glandular stomach.

/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ Groups of 100 ICR/JCL mice (50 each sex) received 1% or 2% Potassium Metabisulfite in the drinking water for 24 months. A control group received distilled water. The 2% dose was the maximum tolerated dose determined by subacute toxicity testing. Mice were necropsied at death or at the termination of the study. Ninety-nine of the mice of the control group survived beyond 180 days; 96 mice of the 1% group survived, and 94 mice of the 2% group survived. No significant difference in tumor incidence was observed between treated and control mice. Total tumor incidence was 14.1% for the control group, 14.6% for the 1% dose group, and 17.0% for the 2% dose group.

/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ Male rats were initially given a single dose of diethylnitosamine (200 mg/kg ip) and, starting 2 weeks later, were treated in feed with potassium metabisulfite (500 mg/kg equivalent to 10,000 ppm) for 6 weeks and then killed. All rats were subjected to a two-thirds partial hepatectomy at week 3. Carcinogenic potential was scored by comparing the numbers and areas of induced glutathione S-transferase placental form positive foci in the liver of treated rats and with those of control groups given diethylnitosamine alone. Positive was a scored for a significant increase in quantitative values of glutathione S-transferase placental positive foci; for a negative score no change or a decrease. /Potassium metabisulfite/ was negative.

/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Potassium Metabisulfite was not teratogenic to mice at 125 mg/kg or rats at 155 mg/kg.

For more Non-Human Toxicity Excerpts (Complete) data for POTASSIUM METABISULFITE (9 total), please visit the HSDB record page.

Ingestion of sulfites has been postulated to be a cause of rapid, acute allergic reactions, including fatal anaphylactic-like responses. A sulfite-sensitive subpopulation of asthmatics has been postulated to exist who have a relative deficiency of sulfite oxidase. The possibility that sulfur dioxide may be generated from sulfite in the low pH of the stomach has been considered as a mechanism of sulfite sensitivity. /Sulfites/

Some asthmatics are said to be dangerously sensitive to minute amounts of sulfites in foods. /Sulfites/

Evaluation: There is inadequate evidence for the carcinogenicity in humans of sulfur dioxide, sulfites, bisulfites and metabisulfites. There is limited evidence for the carcinogenicity in experimental animals of sulfur dioxide. There is inadequate evidence for the carcinogenicity in experimental animals of sulfites, bisulfites and metabisulfites. Overall evaluation: Sulfur dioxide, sulfites, bisulfites and metabisulfites are not classifiable as to their carcinogenicity to humans (Group 3).

According to the 2006 TSCA Inventory Update Reporting data, the number of persons reasonably likely to be exposed in the industrial manufacturing, processing, and use of potassium metabisulfite is 100 to 999; the data may be greatly underestimated(1).

/SRP:/ Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on the left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Poisons A and B/

/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/

/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/

Potassium metabisulfite is generally recognized as safe when used as a chemical preservative in accordance with good manufacturing practice, except that it is not used in meats; in food recognized as a source of vitamin B1; on fruits and vegetables intended to be served raw to consumers or sold raw to consumers, or to be presented to consumers as fresh.

Potassium metabisulfite used as a chemical preservative in animal drugs, feeds, and related products is generally recognized as safe when used in accordance with good manufacturing or feeding practice, except that it is not used in meats or in food recognized as source of vitamin B1.

Bisulfite participates in three important types of reactions with biomolecules: sulfonation (sulfitolysis), autooxidation with generation of free radicals, and addition to cytosine. Products of sulfonation reactions have been shown to be long-lived in vivo and may be highly reactive. Products of autooxidation may be responsible for the initiation of lipid peroxidation, which, among other effects, could damage plasma membranes. In addition, bisulfite can react with nucleic acids to convert cytosine to uracil, thus resulting in mutational events. /Sulfites/

It is now widely appreciated that bronchoconstriction following SO2 exposure is mediated by chemosensitive receptors in the tracheobronchial tree. Rapidly activating receptors (RARs) and sensory C-fiber receptors found at all levels of the respiratory tract are sensitive to irritant gases such as SO2. Activation of these vagal afferents stimulates central nervous system reflexes resulting in bronchoconstriction, mucus secretion, mucosal vasodilation, cough, apnea followed by rapid shallow breathing, and effects on the cardiovascular system such as bradycardia and hypotension or hypertension. /Sulfur Oxide/

Early experiments demonstrated that SO2-induced reflexes were mediated by cholinergic parasympathetic pathways involving the vagus nerve and inhibited by atropine. Bronchoconstriction was found to involve smooth muscle contraction since beta-adrenergic agonists such as isoproterenol reversed the effects. Histamine was also thought to be involved in SO2-induced bronchoconstriction. ... Experiments in animal models ... have demonstrated that both cholinergic and noncholinergic mechanisms may be involved in SO2-induced effects. In two studies utilizing bilateral vagotomy, vagal afferents were found to mediate the immediate ventilatory responses to SO2, but not the prolonged bronchoconstrictor response. Other studies showed that atropine failed to block SO2-induced bronchoconstriction, and that a local axon reflex resulting in C-fiber secretion of neuropeptides (i.e., neurogenic inflammation) was responsible for the effect. Neurogenic inflammation has been shown to play a key role in animal models of airway inflammatory disease. /Sulfur Oxide/

In humans, the mechanisms responsible for SO2-induced bronchoconstriction are not fully understood. In non-asthmatics, near complete attenuation of bronchoconstriction has been demonstrated using the anticholinergic agents atropine and ipratropium bromide. However, in asthmatics, these same anticholinergic agents, as well as short- and long-acting beta2-adrenergic agonists, theophylline, cromolyn sodium, nedocromil sodium and leukotriene receptor antagonists only partially blocked SO2-induced bronchoconstriction. That none of these therapies have been shown to completely attenuate the effects of SO2 implies the involvement of both parasympathetic pathways and inflammatory mediators in asthmatics. Strong evidence of this was borne out in /a subsequent study/, in which asthmatic adults were exposed to SO2 following pretreatment with cromolyn sodium (a mast cell stabilizer), atropine (a muscarinic receptor antagonist), and the two medications together. While both treatments individually provided some protection against the bronchoconstrictive effects of SO2, there was a much stronger and statistically significant effect following concurrent administration of the two medications. /Sufur Oxide/

Sulfites are generated in the human body by processing of the sulfur-containing amino acids, cysteine and methionine. Endogenous sulfite is maintained at a low, steady-state concentration by a mitochondrial enzyme, sulfite oxidase, that promotes the oxidation of sulfite to sulfate that is excreted in the urine. Sulfites can also be metabolized to thiosulfates (enzymatic reaction of sulfite with 3-mercaptopyruvate) or S-sulfonate compounds (nonenzymatic reaction with disulfide bonds). Thiosulfate and S-sulfonate were detected at very low concentrations in the urine of normal humans or rats, but were excreted in large amounts by those deficient in sulfite oxidase. /Sulfites/

Sulfite that enters the body via ingestion, inhalation, or injection is metabolized by sulfite oxidase to sulfate. Oral dose studies using dogs and rats and intravenous (IV) dose studies using rabbits, rats, and rhesus monkeys, demonstrated rapid metabolic clearance. In all species </= 10% of the administered dose was excreted unchanged in the urine. One difference in the metabolism kinetics of exogenous sulfite versus endogenous sulfite is that hepatic oxidation of exogenous sulfite (at least in rats) is diffusion limited. The liver metabolizes a constant fraction of sulfite it receives, but a finite amount will pass through the organ and enter the systemic circulation. /Sulfites/

A principal mechanism of detoxification of SO2 (and sulfite/bisulfite) occurs through the enzymatic activity of sulfite oxidase, resulting in the production of sulfate. /Sulfites/

Ingested radiolabelled sulfite was reported to be excreted almost entirely in the urine of monkeys within 24 hr, but no free sulfite was detected in rat urine. Seven days after dosing, mice retained < 1% and rats, 2% of the radiolabel. In rabbits, sulfite was cleared predominantly by metabolism to sulfate. /Sulfite/

CIR ingredient: Potassium Metabisulfite

Sodium and potassium metabisulfite are used as antioxidants in photographic film development. [Kanerva, p. 1637]

Photographic Processing [Category: Other]

As antifermentative in breweries and wineries; bleaching straw; preservative for fruits and vegetables.

Antiseptic reagent, source of sulfurous acid, brewing (cleaning casks and vats), winemaking (to kill undesirable yeast and bacteria), food preservative, developing agent, process engraving, dyeing, antioxidant and bleaching agent.

Antimicrobial preservative; antioxidant.

(1977) AT LEAST 6.36X10+8 G

(1982) No Data

2023: 829,274 lb

Production volumes for non-confidential chemicals reported under the Inventory Update Rule. [Table#5111]

Production volume for non-confidential chemicals reported under the 2006 Inventory Update Rule. Chemical: Disulfurous acid, potassium salt. Aggregated National Production Volume: 1 to < 50 million lbs.

Article of commerce contains approx 95% K2S2O5.

Grades: Technical; reagent; FCC.

Food additives

Food Additives -> ANTIOXIDANT; PRESERVATIVE -> JECFA Functional Classes

Cosmetics -> Preservative

Food, beverage, and tobacco product manufacturing

Disulfurous acid, potassium salt (1:2): ACTIVE

Potassium metabisulfite is plant-growth regulator.

Five cmpd were evaluated against B theobromae in vitro and in vivo. Aureofungin exhibited the greatest inhibitory activity, followed by potassium metabisulfite, Sodium benzoate, thiourea, and boric acid.

Of the antioxidants and chelating agents tested, potassium bisulfite, sodium hypophosphite, EDTA, and cysteine were the most effective.