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  Substance Info: (and synonyms)
Acetaldehyde / Ethanal

Background Info:

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Immune Reactions I Non-Immune Reactions I Occupational
Cross-reactions

Colourless, flammable liquid. Has a characteristic odour. Occurs naturally in apples, broccoli, other vegetables and fruit, and cheese and coffee.

Acetaldehyde is an intermediate in the breakdown of ethanol. Acetaldehyde is a powerful muscle poison, roughly 30 times more toxic than ethanol itself. Tobacco smoke, exhaust fumes and foods all contribute to your acetaldehyde load. The bacteria living in your mouth and guts churn it out in bucket loads. Almost every tissue in the body is equipped with the enzymes known as aldehyde dehydrogenases (ALDHs), which convert acetaldehyde to harmless acetic acid. There are 19 different ALDHs in humans but one in particular, ALDH2, does most of the work - especially in the liver. As soon as you start drinking alcohol, your liver converts the ethanol into acetaldehyde using alcohol dehydrogenase. Acetaldehyde is then broken down by ALDH2 and the resulting acetic acid is burned as fuel in the muscles. The liver normally eliminates over 99 per cent of the acetaldehyde. Only minute amounts escape into the bloodstream. But that's where the problems start. The average liver can process about 7 grams of ethanol an hour - though in heavy drinkers that figure can rise to 10 grams - meaning that it takes about 12 hours to eliminate all the ethanol in a bottle of wine. That's 12 hours of continuous exposure to acetaldehyde, possibly longer. However, almost any exposure to acetaldehyde can do serious damage. Acetaldehyde attaches itself to amino groups in proteins to form stable compounds called adducts which cause irreversible damage by messing up protein structure and function. In the wake of a drinking bout, a whole range of adducts are formed in the liver, muscles, heart, brain and gastrointestinal tract. Rats given a single dose of ethanol end up with significant muscle damage as a result of acetaldehyde attacking proteins. The changes persist for more than 24 hours, long after the chemical itself has disappeared from the system (Alcohol and Alcoholism, vol 40, p 485). Among alcoholics, muscle damage is five times more common than cirrhosis of the liver. The immune system sees these adducts as foreign and fires off an inflammatory response. Around 70 per cent of patients with alcoholic liver disease have anti-acetaldehyde antibodies in their bloodstream. The inflammatory response is usually a bad omen as it can result in cell injury and persistent inflammation. Acetaldehyde also attacks DNA. There is growing evidence that acetaldehyde is a human carcinogen too. Roughly 50 per cent of people of Japanese, Chinese, Korean or Taiwanese origin carry at least one faulty copy of the ALDH2 gene and can scarcely break down acetaldehyde at all. The immediate consequences of having the faulty version of the ALDH2 gene are highly visible. Almost as soon these people have an alcoholic drink, their acetaldehyde levels shoot up to between 6 and 20 times that found in people with normal ALDH2. This acetaldehyde "rush" triggers facial flushing, elevated heart rate and dilated blood vessels. Dizziness, headache, nausea and vomiting soon follow. Among the minority of flushers who are also heavy drinkers, the incidence of upper gastrointestinal tract cancer is about 50 times the normal rate. Individuals who are exposed to more acetaldehyde as a result of a genetic defect - the gene for alcohol dehydrogenase - are at greater risk of developing cancers of the upper gastrointestinal tract and liver (International Journal of Cancer, vol 118, p 1998). Up to 5 per cent of all breast cancers attributable to alcohol consumption. There are suggestions of a link between acetaldehyde and Alzheimer's disease. Many alcoholic drinks contain acetaldehyde from the word go. Sherry producers, for instance, encourage acetaldehyde production for its fruity aroma. Calvados is particularly rich in acetaldehyde, and regular calvados drinkers have twice the incidence of oesophageal and oral cancer compared with wine drinkers who consume the same amount of alcohol.

Cigarette smoke results in the acetaldehyde load rising further. Burning tobacco creates acetaldehyde that dissolves in saliva, and acetaldehyde in saliva is a big problem. Among smokers, the risk of oral cancer is 7 to 10 times higher than for people who have never smoked. Of course, there are many carcinogens in tobacco smoke, so acetaldehyde may well not be the only culprit. Combine tobacco and alcohol and the danger multiplies. This could explain the 150-fold rise in oral cancers seen in people who are both alcoholics and smokers, compared with those who abstain from both. Acetaldehyde in saliva also comes from the bugs that colonise the mouth and digestive tract. Many of these produce acetaldehyde as part of their normal biochemistry. Others absorb ethanol from alcoholic drinks and turn it into acetaldehyde. Some people harbour organisms that are particularly good at producing acetaldehyde. The mouth-dwelling Streptococcus salivarius, is particularly good at tossing out acetaldehyde. Another, Neisseria, produces 100 times more acetaldehyde when exposed to ethanol compared with other microorganisms isolated from the mouth. Bacterial fermentation to produce food - everything from pickles and yogurts to bread and cheese, results in formation of acetaldehyde. Acetaldehyde also occurs naturally in ripe fruit and coffee. Dairy products sometimes try to increase the acetaldehyde level to give it a special aromatic taste. Acetaldehyde is spewed out by vehicle engines. Air pollution adds to the toxic load, though nobody is quite sure how much this affects our health. (Melton 2007 ref.20703 7)

 

 

Allergens:

No Allergens characterised


Immune Reactions:

Ingestion can lead to respiratory paralysis. Pulmonary irritant if inhaled. GRAS

Reorganization process. Data in process of being reorganized. Editorial staff 2014

 

A 25-year old patient suffered from urticaria and acute anaphylactoid symptoms after ingestion of alcoholic beverages. The Pricktest for acetic acid (5%) and for acetaldehyde (50 and 100%) was positive. The symptoms could be reproduced in an oral provocation test with pure ethanol (20%). According to the authors, an immunological pathomechanism of this intolerance reaction reported is possible, and the authors state that what is unusual in this case, is that the patient exhibited a positive Pricktest to acetaldehyde and acetic acid additionally. Acetaldehyde was considered as a hapten which may have resulted in the activation of an immunologically mediated alcohol intolerance reaction. (Schwarzenbach-Stöckli 2007 ref.20077 8)

Schwarzenbach-Stöckli S, Bircher AJ. Alkoholintoleranz bei Überempfindlichkeit gegenüber Acetaldehyd und Essigsäure Allergologie 2007

 


Non-Immune Reactions:

Irritating to mucous membranes. CNS depression.

Reorganization process. Data in process of being reorganized. Editorial staff 2014

 

Acetaldehyde, an intermediate in the metabolism of alcohol, appears to be the primary mediator of alcohol-intolerance reactions, with the kinetics of acetaldehyde production in affected individuals following the time-course of symptoms, and individuals with the highest levels of serum acetaldehyde experiencing the most intense intolerance symptoms. Acetaldehyde has also been shown to play an important role in the skin responses of Asians to primary alcohols applied topically. (Vally 2003 ref.20686 0)

Vally H, Thompson PJ. Allergic and asthmatic reactions to alcoholic drinks. Addict Biol 2003

 


Occupational:

No Records


Cross-Reactions:

No Records

Information supplied from an abridged section of:
Allergy Advisor - Zing Solutions
http://allergyadvisor.com/index.html

© zingsolutions.com 2014

Allergy Advisor  - Food Additive and Preservative Allergy and Intolerance Database


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