Editing Acetaldehyde (section)

==Safety==
===Exposure limits===
The [[threshold limit value]] is 25ppm (STEL/ceiling value) and the MAK (Maximum Workplace Concentration) is 50 ppm. At 50 ppm acetaldehyde, no irritation or local tissue damage in the [[Nasal cavity|nasal]] [[Mucous membrane|mucosa]] is observed. When taken up by the organism, acetaldehyde is metabolized rapidly in the liver to acetic acid. Only a small proportion is exhaled unchanged. After [[Intravenous therapy|intravenous]] injection, the half-life in the blood is approximately 90 seconds.<ref name=Ull/>

===Dangers===
====Toxicity====
Many serious cases of acute intoxication have been recorded.<ref name=Ull/> Acetaldehyde naturally breaks down in the human body.<ref name=chem/><ref>{{Cite journal
| pmid = 2719768
| year = 1989
| last1 = Tsukamoto
| first1 = S
| title = Determinations of ethanol, acetaldehyde and acetate in blood and urine during alcohol oxidation in man
| journal = Alcohol and Alcoholism
| volume = 24
| issue = 2
| pages = 101–8
| last2 = Muto
| first2 = T
| last3 = Nagoya
| first3 = T
| last4 = Shimamura
| first4 = M
| last5 = Saito
| first5 = M
| last6 = Tainaka
| first6 = H
| doi=10.1093/oxfordjournals.alcalc.a044872
}}</ref>

====Irritation====
Acetaldehyde is an irritant of the skin, eyes, mucous membranes, throat, and respiratory tract. This occurs at concentrations as low as 1000 ppm. Symptoms of exposure to this compound include [[nausea]], [[vomiting]], and [[headache]]. These symptoms may not happen immediately. The [[perception]] threshold for acetaldehyde in air is in the range between 0.07 and 0.25 ppm.<ref name=Ull/> At such concentrations, the [[fruit]]y [[odor]] of acetaldehyde is apparent. [[Conjunctiva]]l irritations have been observed after a 15-minute exposure to concentrations of 25 and 50 ppm, but transient conjunctivitis and irritation of the [[Respiratory system|respiratory]] tract have been reported after exposure to 200 ppm acetaldehyde for 15 minutes.

====Carcinogenicity====
Acetaldehyde is [[carcinogenic]] in humans.<ref name="Chemical Summary For Acetaldehyde">[http://www.epa.gov/chemfact/s_acetal.txt Chemical Summary For Acetaldehyde], US Environmental Protection Agency</ref><ref>{{cite web |url= http://ec.europa.eu/health/ph_risk/committees/sccp/documents/out275_en.pdf |archive-url=https://ghostarchive.org/archive/20221009/http://ec.europa.eu/health/ph_risk/committees/sccp/documents/out275_en.pdf |archive-date=2022-10-09 |url-status=live|title= Opinion of the Scientific Committee on Cosmetic Products and Non-Food Products Intended for Consumers Concerning Acetaldehyde  |author= Scientific Committee on Cosmetic Products and Non-Food Products|date=2004-05-25 |page=11|access-date=2011-09-28}}</ref> In 1988 the [[International Agency for Research on Cancer]] stated, "There is ''sufficient'' evidence for the carcinogenicity of acetaldehyde (the major metabolite of ethanol) in [[experimental animal]]s."<ref name="International1988">{{Cite book |title=Alcohol drinking |publisher=[[World Health Organization]], [[International Agency for Research on Cancer]] |location=Lyon |year=1988 |isbn=978-92-832-1244-7 |url=https://archive.org/details/alcoholdrinking0044iarc |author=International Agency for Rescarch on Cancer, World Health Organization. |url-access=registration }} p3</ref> In October 2009 the [[International Agency for Research on Cancer]] updated the classification of acetaldehyde stating that acetaldehyde included in and generated [[endogenous]]ly from [[alcoholic beverage]]s is a Group I human carcinogen.<ref>{{cite journal |vauthors=Secretan B, Straif K, Baan R, Grosse Y, El Ghissassi F, Bouvard V, Benbrahim-Tallaa L, Guha N, Freeman C, Galichet L, Cogliano V |title=A review of human carcinogens—Part E: tobacco, areca nut, alcohol, coal smoke, and salted fish |journal=Lancet Oncol |volume=10 |issue=11 |pages=1033–4 |date=November 2009 |pmid=19891056 |doi=10.1016/s1470-2045(09)70326-2 }}</ref> In addition, acetaldehyde is damaging to [[DNA]]<ref>{{Cite journal
| pmid = 3389666
| year = 1988
| last1 = Lambert
| first1 = B
| title = DNA and chromosome damage induced by acetaldehyde in human lymphocytes in vitro
| journal = Annals of the New York Academy of Sciences
| volume = 534
| issue = 1
| pages = 369–76
| last2 = He
| first2 = S. M.
| bibcode = 1988NYASA.534..369L |doi = 10.1111/j.1749-6632.1988.tb30124.x | s2cid = 22732731
}}</ref> and causes abnormal muscle development as it binds to proteins.<ref name="Nicholas2004">{{Cite journal | doi = 10.1093/alcalc/agh085| pmid = 15304379| title = Acetaldehyde-Induced Cardiac Contractile Dysfunction May Be Alleviated by Vitamin B1 but Not by Vitamins B6 or B12| journal = Alcohol and Alcoholism| volume = 39| issue = 5| pages = 450–4| year = 2004| last1 = Aberle | first1 = N. S.| last2 = Burd| first2 = L| last3 = Zhao| first3 = B. H.| last4 = Ren| first4 = J| doi-access = free}}</ref>

====DNA crosslinks====
Acetaldehyde induces DNA interstrand crosslinks, a form of DNA damage. These can be repaired by either of two replication-coupled DNA repair pathways.<ref name="Hodskinson2020">{{cite journal |vauthors=Hodskinson MR, Bolner A, Sato K, Kamimae-Lanning AN, Rooijers K, Witte M, Mahesh M, Silhan J, Petek M, Williams DM, Kind J, Chin JW, Patel KJ, Knipscheer P |title=Alcohol-derived DNA crosslinks are repaired by two distinct mechanisms |journal=Nature |volume=579 |issue=7800 |pages=603–8 |date=March 2020 |pmid=32132710 |pmc=7116288 |doi=10.1038/s41586-020-2059-5 }}</ref>  The first is referred to as the FA pathway, because it employs gene products defective in [[Fanconi's anemia]] patients.  This repair pathway results in increased mutation frequency and altered mutational spectrum.<ref name = Hodskinson2020/>  The second repair pathway requires replication fork convergence, breakage of the acetaldehyde crosslink, translesion synthesis by a Y-family DNA polymerase and homologous recombination.<ref name = Hodskinson2020/>

===Aggravating factors===
====Alzheimer's disease====
People with a genetic deficiency for the enzyme responsible for the conversion of acetaldehyde into [[acetic acid]] may have a greater risk of [[Alzheimer's disease]]. "These results indicate that the [[ALDH2]] deficiency is a risk factor for LOAD [late-onset Alzheimer's disease] ..."<ref name=ohta>{{Cite journal|last= Ohta |first=S |author2=Ohsawa I|author3=Kamino K|author4=Ando F|author5= Shimokata H. |date=April 2004 |title=Mitochondrial ALDH2 Deficiency as an Oxidative Stress |journal=Annals of the New York Academy of Sciences |volume=1011 |issue=1 |pages=36–44 |doi= 10.1196/annals.1293.004 |pmid= 15126281|bibcode=2004NYASA1011...36O |s2cid=28571902 }}</ref>

====Genetic conditions====
A study of 818 heavy drinkers found that those exposed to more acetaldehyde than normal through a genetic variant of the gene encoding for [[ADH1C]], ADH1C*1, are at greater risk of developing cancers of the [[upper gastrointestinal tract]] and liver.<ref>{{Cite journal | last1 = Homann | first1 = N. | last2 = Stickel | first2 = F. | last3 = König | first3 = I. R. | last4 = Jacobs | first4 = A. | last5 = Junghanns | first5 = K. | last6 = Benesova | first6 = M. | last7 = Schuppan | first7 = D. | last8 = Himsel | first8 = S. | last9 = Zuber-Jerger | first9 = I. | last10 = Hellerbrand | first10 = C. | last11 = Ludwig | first11 = D. | last12 = Caselmann | first12 = W. H. | last13 = Seitz | first13 = H. K. | title = Alcohol dehydrogenase 1C*1 allele is a genetic marker for alcohol-associated cancer in heavy drinkers | doi = 10.1002/ijc.21583 | journal = International Journal of Cancer | volume = 118 | issue = 8 | pages = 1998–2002 | year = 2006 | pmid = 16287084| s2cid = 11716548 | doi-access = free }}</ref>

====Disulfiram====
The drug [[disulfiram]] (Antabuse) inhibits acetaldehyde dehydrogenase, an enzyme that oxidizes the compound into acetic acid. Metabolism of ethanol forms acetaldehyde before acetaldehyde dehydrogenase forms acetic acid, but with the enzyme inhibited, acetaldehyde accumulates. If one consumes ethanol while taking disulfiram, the hangover effect of ethanol is felt more rapidly and intensely ([[disulfiram-alcohol reaction]]). As such, disulfiram is sometimes used as a deterrent for alcoholics wishing to stay sober.<ref name=disul-new>{{cite journal |last1=Omran |first1=Z |title=Development of new disulfiram analogues as ALDH1a1-selective inhibitors. |journal=Bioorganic & Medicinal Chemistry Letters |date=15 May 2021 |volume=40 |pages=127958 |doi=10.1016/j.bmcl.2021.127958 |pmid=33744437|s2cid=232311209 }}</ref>

===Sources of exposure===
====Indoor air====
Acetaldehyde is a potential contaminant in workplace, indoors, and ambient environments. Moreover, the majority of humans spend more than 90% of their time in indoor environments, increasing any exposure and the risk to human health.<ref>{{Cite book |author=Spengler, John D. |author2=McCarthy, John F. |author3=Samet, Jonathan M. | date = 2000 | title = Indoor Air Quality Handbook |url=https://archive.org/details/indoorairquality00spen |url-access=limited | publisher =  McGraw-Hill | isbn = 978-0-07-445549-4 |oclc=50566621 | page = [https://archive.org/details/indoorairquality00spen/page/n11 761]}}</ref>

In a study in [[France]], the mean indoor concentration of acetaldehydes measured in 16 homes was approximately seven times higher than the outside acetaldehyde concentration. The [[living room]] had a mean of 18.1±17.5 μg m<sup>−3</sup> and the [[bedroom]] was 18.2±16.9 μg m<sup>−3</sup>, whereas the outdoor air had a mean concentration of 2.3±2.6 μg m<sup>−3</sup>.{{citation needed|date=June 2018}}

It has been concluded that [[Volatile organic compound|volatile organic compounds (VOC)]] such as benzene, formaldehyde, acetaldehyde, toluene, and [[xylene]]s have to be considered priority [[pollutant]]s with respect to their health effects. It has been pointed that in renovated or completely new buildings, the VOCs concentration levels are often several orders of magnitude higher. The main sources of acetaldehydes in homes include building materials, laminate, PVC flooring, varnished wood flooring, and varnished cork/pine flooring (found in the varnish, not the wood). It is also found in plastics, oil-based and water-based paints, in composite wood ceilings, particle-board, plywood, treated pine wood, and laminated chipboard furniture.<ref name = dafni>{{cite journal | author1 = Dafni A. Missia | author2 = E. Demetriou | author3 = N. Michael | author4= E.I. Tolis | author5 = J.G. Bartzis | title = Indoor exposure from building materials: A field study | journal = Atmospheric Environment | year = 2010 |  volume = 44 | pages = 4388–95 | doi = 10.1016/j.atmosenv.2010.07.049 | issue = 35| bibcode = 2010AtmEn..44.4388M }}</ref>

====Outdoor air====
The use of acetaldehyde is widespread in different industries, and it may be released into waste water or the air during production, use, transportation and storage. Sources of acetaldehyde include fuel combustion emissions from stationary internal combustion engines and power plants that burn fossil fuels, wood, or trash, oil and gas extraction, refineries, cement kilns, lumber and wood mills and paper mills.<ref>{{Cite journal|last1=Shrestha|first1=Krishna Prasad|last2=Giri|first2=Binod Raj|last3=Adil|first3=Mohammad|last4=Seidel|first4=Lars|last5=Zeuch|first5=Thomas|last6=Farooq|first6=Aamir|last7=Mauss|first7=Fabian|date=2021-09-16|title=Detailed Chemical Kinetic Study of Acetaldehyde Oxidation and Its Interaction with NOx|url=https://doi.org/10.1021/acs.energyfuels.1c01948|journal=Energy & Fuels|volume=35|issue=18|pages=14963–83|doi=10.1021/acs.energyfuels.1c01948|s2cid=239683740|issn=0887-0624|hdl=10754/670859|hdl-access=free}}</ref> Acetaldehyde is also present in automobile and [[diesel exhaust]].<ref>{{Cite journal | last1 = Clements | first1 = A. L. | last2 = Jia | first2 = Y. | last3 = Denbleyker | first3 = A. | last4 = McDonald-Buller | first4 = E. | last5 = Fraser | first5 = M. P. | last6 = Allen | first6 = D. T. | last7 = Collins | first7 = D. R. | last8 = Michel | first8 = E. | last9 = Pudota | first9 = J. | last10 = Sullivan | first10 = D. | last11 = Zhu | first11 = Y. | doi = 10.1016/j.atmosenv.2009.06.044 | title = Air pollutant concentrations near three Texas roadways, part II: Chemical characterization and transformation of pollutants | journal = Atmospheric Environment | volume = 43 | issue = 30 | pages = 4523–34 | year = 2009 |bibcode = 2009AtmEn..43.4523C }}</ref> As a result, acetaldehyde is "one of the most frequently found air toxics with cancer risk greater than one in a million".<ref name=":0" />

====Tobacco smoke====
Natural tobacco [[polysaccharides]], including [[cellulose]], have been shown to be the primary precursors making acetaldehyde a significant constituent of [[tobacco smoke]].<ref>{{cite journal | last1 = Talhout | first1 = R | last2 = Opperhuizen | first2 = A | last3 = van Amsterdam | first3 = JG | date = Oct 2007 | title = Role of acetaldehyde in tobacco smoke addiction | journal = Eur Neuropsychopharmacol | volume = 17 | issue = 10| pages = 627–36 | pmid = 17382522 | doi = 10.1016/j.euroneuro.2007.02.013 | s2cid = 25866206 }}</ref><ref name="TalhoutSchulz2011">{{cite journal|last1=Talhout|first1=Reinskje|last2=Schulz|first2=Thomas|last3=Florek|first3=Ewa|last4=Van Benthem|first4=Jan|last5=Wester|first5=Piet|last6=Opperhuizen|first6=Antoon|title=Hazardous Compounds in Tobacco Smoke|journal=International Journal of Environmental Research and Public Health|volume=8|issue=12|year=2011|pages=613–628|issn=1660-4601|doi=10.3390/ijerph8020613|pmid=21556207|pmc=3084482|doi-access=free}}</ref> It has been demonstrated to have a [[Synergy|synergistic]] effect with [[nicotine]] in [[animal testing on rodents|rodent studies]] of [[addiction]].<ref>[http://drugabuse.gov/NIDA_notes/NNvol20N3/Study.html "NIDA — Publications — NIDA Notes — Vol. 20, No. 3"] {{Webarchive|url=https://web.archive.org/web/20090825223924/http://drugabuse.gov/NIDA_notes/NNvol20N3/Study.html |date=25 August 2009 }}. drugabuse.gov.</ref><ref>[https://web.archive.org/web/20110209232332/http://www.universityofcalifornia.edu/news/article/6726 Nicotine's addictive hold increases when combined with other tobacco smoke chemicals, UCI study finds]. University of California. 2004-10-28</ref> Acetaldehyde is also the most abundant carcinogen in tobacco smoke; it is dissolved into the [[saliva]] while smoking.

====Cannabis smoke====
Acetaldehyde has been found in [[Cannabis smoking|cannabis smoke]]. This finding emerged through the use of new chemical techniques that demonstrated the acetaldehyde present was causing DNA damage in laboratory settings.<ref>{{cite journal | last1 = Singh | first1 = R | year = 2009 | title = Evaluation of the DNA Damaging Potential of Cannabis Cigarette Smoke by the Determination of Acetaldehyde Derived N2-Ethyl-2'-deoxyguanosine Adducts | journal = Chem. Res. Toxicol. | volume = 22 | issue = 6| pages = 1181–8 | doi = 10.1021/tx900106y | pmid = 19449825 }}</ref>

====Alcohol consumption====
Many [[microbes]] produce acetaldehyde from ethanol, but they have a lower capacity to eliminate the acetaldehyde, which can lead to the accumulation of acetaldehyde in saliva, stomach acid, and intestinal contents. [[Fermentation|Fermented]] food and many alcoholic beverages can also contain significant amounts of acetaldehyde. Acetaldehyde, derived from mucosal or microbial oxidation of ethanol, tobacco smoke, and diet, appears to act as a cumulative carcinogen in the upper digestive tract of humans.<ref name="SALASPURO M 2011">{{cite journal | author = Salaspuro, M. | title = Acetaldehyde as a common denominator and cumulative carcinogen in digestive tract cancers | year = 2009 | volume = 44 | issue = 8 | pages = 912–925 | doi = 10.1080/00365520902912563 | journal = Scandinavian Journal of Gastroenterology | pmid = 19396661| s2cid = 23291758 }}</ref> According to European Commission's Scientific Committee on Consumer Safety's (SCCS) "Opinion on Acetaldehyde" (2012) the [[Cosmetics|cosmetic]] products special risk limit is 5&nbsp;mg/L and acetaldehyde should not be used in [[Mouthwash|mouth-washing]] products.<ref>[http://ec.europa.eu/health/scientific_committees/consumer_safety/docs/sccs_o_104.pdf Scientific Committee on Consumer Safety SCCS OPINION ON Acetaldehyde]. European Commission. 18 September 2012</ref>

====Plastics====
Acetaldehyde can be produced by the [[Photo-oxidation of polymers|photo-oxidation]] of [[polyethylene terephthalate]] (PET), via a [[Norrish reaction|Type II Norrish reaction]].<ref name="Wiles&DayIII">{{cite journal |last1=Day |first1=M. |last2=Wiles |first2=D. M. |title=Photochemical degradation of poly(ethylene terephthalate). III. Determination of decomposition products and reaction mechanism |journal=Journal of Applied Polymer Science |date=January 1972 |volume=16 |issue=1 |pages=203–215 |doi=10.1002/app.1972.070160118}}</ref>

[[File:Poly(ethylene terephthalate) - Type II Norrish to acetaldehyde.png|600px|center]]

Although the levels produced by this process are minute acetaldehyde has an exceedingly low taste/[[odor threshold]] of around 20–40 ppb and can cause an off-taste in bottled water.<ref>{{cite journal |last1=Nawrocki |first1=J |last2=Dąbrowska |first2=A |last3=Borcz |first3=A |title=Investigation of carbonyl compounds in bottled waters from Poland |journal=Water Research |date=November 2002 |volume=36 |issue=19 |pages=4893–4901 |doi=10.1016/S0043-1354(02)00201-4|pmid=12448533 |bibcode=2002WatRe..36.4893N }}</ref> The level at which an average consumer could detect acetaldehyde is still considerably lower than any toxicity.<ref>{{cite web|title=Do Acetaldehyde and Formaldehyde from Pet Bottles Result in Unacceptable Flavor or Aroma in Bottled Water?|url=http://www.petresin.org/pdf/PETRAACETALDEHYDE_AND_FORMALDEHYDE_FROM_PET_BOTTLES_August_2006.pdf |archive-url=https://ghostarchive.org/archive/20221009/http://www.petresin.org/pdf/PETRAACETALDEHYDE_AND_FORMALDEHYDE_FROM_PET_BOTTLES_August_2006.pdf |archive-date=2022-10-09 |url-status=live|publisher=PET Resin Association|access-date=26 February 2015}}</ref>

====Candida overgrowth====
[[Candida albicans]] in patients with potentially carcinogenic oral diseases has been shown to produce acetaldehyde in quantities sufficient to cause problems.<ref>{{cite journal|last1=Gainza-Cirauqui|first1=M.L.|last2=Nieminen|first2=M.T.|last3=Novak Frazer|first3=L.|last4=Aguirre-Urizar|first4=J.M.|last5=Moragues|first5=M.D.|last6=Rautemaa|first6=R.|title=Production of carcinogenic acetaldehyde by ''Candida albicans'' from patients with potentially malignant oral mucosal disorders|journal=Journal of Oral Pathology and Medicine|date=March 2013|volume=42|issue=3|pages=243–9|doi=10.1111/j.1600-0714.2012.01203.x|pmid=22909057|url=https://www.um.edu.mt/library/oar//handle/123456789/16302 }}</ref>