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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
| Molecular Weight | 222.33 g/mol |
|---|---|
| Molecular Formula | K2O5S2 |
| 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 Ų |
| 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 |
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)
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
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
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