1 2D Structure

Potassium Metabisulfite

2 Identification

2.1 Computed Descriptors

2.1.1 InChI

InChI=1S/2K.H2O5S2/c;;1-6(2)7(3,4)5/h;;(H,1,2)(H,3,4,5)/q2*+1;/p-2

2.1.2 InChI Key

RWPGFSMJFRPDDP-UHFFFAOYSA-L

2.1.3 Canonical SMILES

[O-]S(=O)S(=O)(=O)[O-].[K+].[K+]

2.2 Other Identifiers

2.2.1 UNII

65OE787Q7W

2.3 Synonyms

2.3.1 Depositor-Supplied Synonyms

1. 16731-55-8

2. Potassium Disulfite

3. Potassium Pyrosulfite

4. Dipotassium Pyrosulfite

5. Fertisilo

6. Sobisu

7. Potassium Metabisulphite

8. Potassium Pentaoxodisulfate

9. Ins-224

10. Potassium Metabisulfite [nf]

11. Potassium Metabisulfite (e 224)

12. 65oe787q7w

13. Dipotassium Disulfite

14. E-224

15. Potassium Metabisulfite (nf)

16. Dipotassium Disulphite

17. Dipotassium Metabisulfite

18. Ccris 1427

19. Potassium Disulfite (k2s2o5)

20. Hsdb 5062

21. Pyrosulfurous Acid, Dipotassium Salt

22. Einecs 240-795-3

23. Kaliumpyrosulfit

24. Unii-65oe787q7w

25. Potassium Meta-bisulfite

26. Ec 240-795-3

27. Potassium Disulfite, >=98%

28. Potassium Metabisulfite (2:1)

29. Chembl2106901

30. Dtxsid1021293

31. Potassium Disulfite, Ar, >=97%

32. Potassium Disulfite, Lr, >=95%

33. Potassium Metabisulfite [ii]

34. Potassium Metabisulfite [mi]

35. Mfcd00167605

36. Potassium Metabisulfite [fcc]

37. Potassium Metabisulfite [hsdb]

38. Potassium Metabisulfite [inci]

39. Akos015912829

40. Potassium Metabisulfite [mart.]

41. Potassium Metabisulfite [vandf]

42. Potassium Disulfite, Analytical Standard

43. Potassium Metabisulfite [who-dd]

44. Potassium Disulfite, Usp, 51.8-57.6%

45. P2480

46. Potassium Metabisulfite [ep Impurity]

47. Potassium Metabisulfite [ep Monograph]

48. D05581

49. Potassium Disulfite, Bioultra, >=97.0% (rt)

50. Q417881

51. J-010353

52. Potassium Disulfite, Vetec(tm) Reagent Grade, 98%

53. Potassium Disulfite, Puriss. P.a., >=96% (iodometric), Powder

54. Sulfite, Potassium Metabi-dipotassium Oxidosulfanesulfonate Oxide

55. Potassium Disulfite, Puriss., Meets Analytical Specification Of Ph.eur., Bp, Nf, Fcc, E224, 95.0-101.0% (iodometric), Powder, 51.8-57.6% Sulfur Dioxide

2.4 Create Date

2005-08-08

3 Chemical and Physical Properties

Molecular Formula	K₂O₅S₂
Molecular Weight	222.33 g/mol
Hydrogen Bond Donor Count	0
Hydrogen Bond Acceptor Count	6
Rotatable Bond Count	0
Exact Mass	221.8461284 g/mol
Monoisotopic Mass	221.8461284 g/mol
Topological Polar Surface Area	125 Å²
Heavy Atom Count	9
Formal Charge	0
Complexity	136
Isotope Atom Count	0
Defined Atom Stereocenter Count	0
Undefined Atom Stereocenter Count	0
Defined Bond Stereocenter Count	0
Undefined Bond Stereocenter Count	0
Covalently Bonded Unit Count	3

4 Pharmacology and Biochemistry

4.1 Absorption, Distribution and Excretion

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/

IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, p. V54 166 (1992)

4.2 Metabolism/Metabolites

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/

Cosmetic Ingredient Expert Review Panel; Final Report on the Safety Assessment of Sodium Sulfite, Potassium Sulfite, Ammonium Sulfite, Sodium Bisulfite, Ammonium Bisulfite, Sodium Metabisulfite,and Potassium Metabisulfite. International Journal of Toxicology 22 (S2): 63-88 (2003).

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

Cosmetic Ingredient Expert Review Panel; Final Report on the Safety Assessment of Sodium Sulfite, Potassium Sulfite, Ammonium Sulfite, Sodium Bisulfite, Ammonium Bisulfite, Sodium Metabisulfite,and Potassium Metabisulfite. International Journal of Toxicology 22 (S2): 63-88 (2003).

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/

USEPA; National Center for Environmental Assessment-RTP Office of Research and Development: Integrated Science Assessment for Sulfur Oxides-Health Criteria (September, 2008). EPA Docket ID: EPA-HQ-OAR-2010-0162. Available from, as of August 5, 2011: https://www.regulations.gov/#!home

4.3 Mechanism of Action

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/

USEPA; National Center for Environmental Assessment-RTP Office of Research and Development: Integrated Science Assessment for Sulfur Oxides-Health Criteria (September, 2008). EPA Docket ID: EPA-HQ-OAR-2010-0162. Available from, as of August 5, 2011: https://www.regulations.gov/#!home

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/

USEPA; National Center for Environmental Assessment-RTP Office of Research and Development: Integrated Science Assessment for Sulfur Oxides-Health Criteria (September, 2008). EPA Docket ID: EPA-HQ-OAR-2010-0162. Available from, as of August 5, 2011: https://www.regulations.gov/#!home

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/

USEPA; National Center for Environmental Assessment-RTP Office of Research and Development: Integrated Science Assessment for Sulfur Oxides-Health Criteria (September, 2008). EPA Docket ID: EPA-HQ-OAR-2010-0162. Available from, as of August 5, 2011: https://www.regulations.gov/#!home

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/

USEPA; National Center for Environmental Assessment-RTP Office of Research and Development: Integrated Science Assessment for Sulfur Oxides-Health Criteria (September, 2008). EPA Docket ID: EPA-HQ-OAR-2010-0162. Available from, as of August 5, 2011: https://www.regulations.gov/#!home