Alcohol - Toxicity

Toxicity

Ethanol in alcoholic beverages has been consumed by humans since prehistoric times for a variety of hygienic, dietary, medicinal, religious, and recreational reasons. The consumption of large doses of ethanol causes drunkenness (intoxication), which may lead to a hangover as its effects wear off. Depending upon the dose and the regularity of its consumption, ethanol can cause acute respiratory failure or death. Because ethanol impairs judgment in humans, it can be a catalyst for reckless or irresponsible behavior. The LD50 of ethanol in rats is 10.3 g/kg.

Ethanol's toxicity is largely caused by its primary metabolite; acetaldehyde and secondary metabolite; acetic acid. All primary alcohols are broken down into aldehydes then to carboxylic acids, and whose toxicities are similar to acetaldehyde and acetic acid. Metabolite toxicity is reduced in rats fed N-acetylcysteine and thiamine.

Some secondary and tertiary alcohols are less poisonous than ethanol because the liver is unable to metabolise them into these toxic by-products. This makes them more suitable for recreational and medicinal use as the chronic harms are lower. Ethchlorvynol is a good example of a tertiary alcohol which saw both medicinal and recreational use.

Other alcohols are substantially more poisonous than ethanol, partly because they take much longer to be metabolized and partly because their metabolism produces substances that are even more toxic. Methanol (wood alcohol), for instance, is oxidized to formaldehyde and then to the poisonous formic acid in the liver by alcohol dehydrogenase and formaldehyde dehydrogenase enzymes, respectively; accumulation of formic acid can lead to blindness or death. Likewise, poisoning due to other alcohols such as ethylene glycol or diethylene glycol are due to their metabolites, which are also produced by alcohol dehydrogenase. An effective treatment to prevent toxicity after methanol or ethylene glycol ingestion is to administer ethanol. Alcohol dehydrogenase has a higher affinity for ethanol, thus preventing methanol from binding and acting as a substrate. Any remaining methanol will then have time to be excreted through the kidneys.

Methanol itself, while poisonous, has a much weaker sedative effect than ethanol. Some longer-chain alcohols such as n-propanol, isopropanol, n-butanol and t-butanol do, however, have stronger sedative effects, but also have higher toxicity than ethanol. These longer chain alcohols are found as contaminants in some alcoholic beverages and are known as fusel alcohols, and are reputed to cause severe hangovers although it is unclear if the fusel alcohols are actually responsible. Many longer chain alcohols are used in industry as solvents and are occasionally abused by alcoholics, leading to a range of adverse health effects.

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