Re: Detoxifying acetaldahyde

Acetaldehyde will react with atmospheric oxygen (autoxidation) to form the peroxide peracetic acid:



Peracetic acid is a strong oxidant with a reduction potential similar to that of the bleaching agent chlorine dioxide. It is used in applications requiring chlorine-free bleaching sequences [1] and for dental sterilization [2] where it can inhibit the growth of Candida Albicans. Its potency is underscored by its usage in conjunction with hydrogen peroxide for anthrax spore decontamination [3].

The product peracetic acid can further react with additional acetaldehyde to form the highly shock sensitive and explosive diacetyl peroxide [4] which can degrade into acetic acid and the flammable and irritating acetic anhydride [5]:



Hydrogen peroxide also has the oxygen to oxygen bond that characterizes oxidizing agents used as disinfectants:



Peracetic acid (CH3COOOH) can be formed in an acidic environment by the reaction of acetic acid (CH3COOH) with hydrogen peroxide (H2O2):

CH3COOH + H2O2 (Hydrogen-Peroxid) <--> CH3COOOH + H2O

When peracetic acid formed by the atmospheric oxidation of acetaldehyde degrades it can split via the above reversible reaction into acetic acid and hydrogen peroxide. This means that yeast-released acetaldehyde has the potential for spawning trace amounts of diacetyl peroxide, acetic anhydride, and hydrogen peroxide in the body in addition to the peracetic acid from autoxidation.

Peroxides in general are unstable since the oxygen-oxygen chemical bond can easily cleave forming reactive radical species. Not only are they irritating and inflammatory, they are toxic to living cells resulting from the oxidation of proteins, membrane lipids and DNA. Organic compounds can even ignite on contact with concentrated peroxides. [If levels are elevated in just the "right" amounts and locales, could this be the ignition source [6] for rare but inexplicable cases of spontaneous human combustion?]

Occupational exposure to exogenous sources of these chemicals confirms their toxicity, as in the case of occupational asthma induced by pulmonary mucous membrane irritation by a peracetic-hydrogen peroxide sanitizing mixture [7]. Aerosolized acetaldehyde, even in the absence of its peroxide derivatives, is capable of inducing histamine-mediated bronchostriction in asthmatics [8]. When acetaldehyde dehydrogenase-2 genotype differences create an abnormality in the handling of acetaldehyde as an intermediate of alcohol metabolism, incidence of alcohol-induced asthma increases [9]. Smooth muscle contraction, regulated by G-Protein-Coupled-Receptors (GPCRs):

See "Acetaldehyde + GPCRs" //www.curezone.org/forums/fm.asp?i=1955511

is often aberrant in pulmonary diseases [10].

Lung disorders such as asthma, adult respiratory distress synrome (ARDS) and chronic obstructive pulmonary disease (COPD) are all characterized by increased levels of hydrogen peroxide in expired breath condensates [11]. Although the increased presence of H2O2 (Hydrogen-Peroxid) has a strong correlation to the severity of these disease, it has been attributed to the byproducts of the inflammatory process; in other words, a consequence rather than a cause of the distress.

Although phagocytic immune system cells do utilize hydrogen peroxide and free radical species in their destruction of pathogens including yeast cells [12], the production of these dangerous substances is restricted to lysosomes that normally prevent exposure of the extracellular environment to peroxides. The autoxidation route from yeast-released extracellular acetaldehyde to peracetic acid to hydrogen peroxide is not limited by any such constraints. It produces a host of toxic derivatives along the way that have the same effect as spraying disinfectant into the lungs on a daily basis, something that would increase the sensitivity of the epithelial tissues to any airborne allergens or irritants.

Consider again the initial reaction of this post, acetaldehyde plus inhaled oxygen yielding peracetic acid. If either of the concentrations of the reactants on the left side of the reaction increases, this can be expected to increase the output of the product, peracetic acid. The level of acetaldehyde depends upon the level of yeast colonization and the intake of dietary simple carbohydrates. Any increase of inhaled oxygen in the presence of acetaldehyde should also raise the output of peracetic acid.

Exercise-induced asthma [13] is triggered after at least several minutes of vigorous, "aerobic" activity with normal nasal breathing supplemented by mouth-breathing. But such activity can be expected to increase the exposure of yeast-released acetaldehyde in the mouth and esophageal region to inhaled oxygen with the dispersion of the peroxide byproducts into the airways -- pulmonary peroxidosis. The resulting caustic cocktail then triggers the inflammatory response in the irritated tissues.

But if everyone has yeast, and yeast releases acetaldehyde, why doesn't everyone develop pulmonary complications? The potential may be there in everyone, but genetics again plays a role. Genetic variants of GSDMB/ORMDL3 [14], proteins involved in the apoptosis of epithelial cells and the unfolded protein response, respectively, are associated with the susceptibility to the hyper-responsiveness of asthma. Whether pulmonary symptoms manifest before other types of symptoms is a function of the amount of acetaldehyde being released, of where it ends up, and the genetic vulnerability (innate scavenging potential and tolerance threshold) of each individual .

Although the reactivity of acetaldehyde means that little of it is left in its native form, when you start to look really hard for its traces in relation to disease, a veritable stampede of footprints emerge where it has trampled all over the body's biochemistry. Why has it taken so long to realize this...especially when medical doctors like Truss and Crook started to sound the alarm more than 30 years ago?


[1] Brasileiro LB et al., " The use of peracids in delignification and cellulose pulp bleaching.", Quím. Nova [online]. 2001, vol.24, n.6, pp. 819-829. ISSN 0100-4042. 
http://dx.doi.org/10.1590/S0100-40422001000600020

[2] Stopiglia CDO et al., "Microbiological evaluation of peracetic acid for disinfection of acrylic resins.", Rev. Odonto Ciencia (Online) vol.26 no.3 Porto Alegre 2011
http://dx.doi.org/10.1590/S1980-65232011000300008

[3] US EPA, "Anthrax spore decontamination using hydrogen peroxide and peroxyacetic acid", 2007
http://www.epa.gov/opp00001/factsheets/chemicals/hydrogenperoxide_peroxyaceti...

[4] Chemical Book, "Acetyl Peroxide"
http://www.chemicalbook.com/ChemicalProductProperty_EN_CB6256911.htm

[5] Bawn et al., "The oxidation of acetaldehyde in solution. Part I.—The chemistry of the intermediate stages", Trans. Faraday Soc. 1951,47, 721-734
http://pubs.rsc.org/en/content/articlelanding/1951/tf/tf9514700721

[6] Doruntz et al., "Low temperature ignition of acetaldehyde/oxygen mixtures initiated by organic peroxides adsorbed on the surface of a reaction vessel", Combustion and Flame, Volume 69, Issue 3, September 1987, Pages 251–255
http://www.sciencedirect.com/science/article/pii/0010218087901180

[7] Cristofari-Marquand E et al., "Asthma caused by peracetic acid-hydrogen peroxide mixture.", J Occup Health. 2007 Mar;49(2):155-8.
http://www.ncbi.nlm.nih.gov/pubmed/17429174

[8] Myou S et al., "Aerosolized acetaldehyde induces histamine-mediated bronchoconstriction in asthmatics.", Am Rev Respir Dis. 1993 Oct;148(4 Pt 1):940-3.
http://www.ncbi.nlm.nih.gov/pubmed/7692778

[9] Takao A et al., "Correlation between alcohol-induced asthma and acetaldehyde dehydrogenase-2 genotype.", J Allergy Clin Immunol. 1998 May;101(5):576-80.
http://www.ncbi.nlm.nih.gov/pubmed/9600491

[10] Deshpande DA et al., "Targeting G protein-coupled receptor signaling in asthma.", Cell Signal. 2006 Dec;18(12):2105-20.
http://www.ncbi.nlm.nih.gov/pubmed/16828259

[11] Loukides S et al., "Elevated levels of expired breath hydrogen peroxide in bronchiectasis.", Am J Respir Crit Care Med. 1998 Sep;158(3):991-4.
http://www.ncbi.nlm.nih.gov/pubmed/9731036

[12] Lehrer RI, "Antifungal effects of peroxidase systems.", J Bacteriol. 1969 Aug;99(2):361-5.
http://www.ncbi.nlm.nih.gov/pubmed/5817553

[14] Kang MJ et al., "GSDMB/ORMDL3 variants contribute to asthma susceptibility and eosinophil-mediated bronchial hyperresponsiveness.", Hum Immunol. 2012 Sep;73(9):954-9. http://www.ncbi.nlm.nih.gov/pubmed/22732088