Acetaldehyde toxicity

Booze. T.F. Oclinic. F.W. (1986) An investigation of metaldehyde and acetaldehyde toxicities in dogs. Fundam. appl. Toxicol., 6, 440-446... 

Disulfiram (Antabuse). In alcoholics who are well and motivated, an attempt may be made to discourage drinking by inducing immediate unpleasantness. Disulfiram inhibits the enzyme aldehyde dehydrogenase so that acetaldehyde (toxic metabolite of alcohol) accumulates. The objective of administering disulfiram is that patients will find the experience so unpleasant that they will avoid alcohol. It should be administered only under specialist supervision. 

CNS depression 2 metabolic acidosis (ketones) 3 acetaldehyde toxicity ... 

Vinyl ether forms explosive mixtures with air, with LEL and UEL values of 1.7% and 27% by volume of air, respectively. It forms unstable peroxides on long standing or in the presence of oxygen. These peroxides can explode spontaneously or when heated. It decomposes to acetaldehyde (toxic and highly flammable) when exposed to light. 

An interaction has also been reported in association with metabolic acidosis in an intoxicated man 4 hours after he was given intravenous metronidazole as prophylaxis following injury. A fatality occurred in a frail 31-year old woman, which was attributed to cardiac arrhythmia caused by acetaldehyde toxicity resulting from the alcohol/metronidazole interaction, linked to autonomic distress caused by a physical assault. Alcohol is also said to taste unpleasant or to be less pleasurable while taking metronidazole. Some drug abusers apparently exploit the reaction for kicks . ... 

Outside of carbon monoxide for which the toxicity is already well-known, five types of organic chemical compounds capable of being emitted by vehicles will be the focus of our particular attention these are benzene, 1-3 butadiene, formaldehyde, acetaldehyde and polynuclear aromatic hydrocarbons, PNA, taken as a whole. Among the latter, two, like benzo [a] pyrene, are viewed as carcinogens. Benzene is considered here not as a motor fuel component emitted by evaporation, but because of its presence in exhaust gas (see Figure 5.25). 

Interest ia the toxicity of aldehydes has focused primarily on specific compounds, particularly formaldehyde, acetaldehyde, and acroleia (13). Litde evidence exists to suggest that occupational levels of exposure to aldehydes would result ia mutations, although some aldehydes are clearly mutagenic ia some test systems. There are, however, acute effects of aldehydes. 

NOTE - Petrochemical plants also generate significant amounts of solid wastes and sludges, some of which may be considered hazardous because of the presence of toxic organics and heavy metals. Spent caustic and other hazardous wastes may be generated in significant quantities examples are distillation residues associated with units handling acetaldehyde, acetonitrile, benzyl chloride, carbon tetrachloride, cumene, phthallic anhydride, nitrobenzene, methyl ethyl pyridine, toluene diisocyanate, trichloroethane, trichloroethylene, perchloro-ethylene, aniline, chlorobenzenes, dimethyl hydrazine, ethylene dibromide, toluenediamine, epichlorohydrin, ethyl chloride, ethylene dichloride, and vinyl chloride. 

Vapor Density (VD) — the mass per unit volume of a given vapor/gas relative to that of air. Thus, acetaldehyde with a vapor density of 1.5 is heavier than air and will accumulate in low spots, while acetylene with a vapor density of 0.9 is lighter than air and will rise and disperse. Heavy vapors present a particular hazard because of the way they accumulate if toxic they may poison workers if nontoxic they may displace air and cause suffocation by oxygen deficiency if flammable, once presented with an ignition source, they represent a fire or explosion hazard. Gases heavier than air include carbon dioxide, chlorine, hydrogen sulfide, and sulfur dioxide. 

Compounds Causing Cardiovascular Toxicity Alcohols are the most important compounds causing vascular toxicity. Ethanol depresses cardiac muscle and attenuates its contractivity when the concentration of ethanol in the blood exceeds 0.75 mg/100 mL. Ethanol also causes arrhythmias, and a metabolite of ethanol, acetaldehyde, also depresses the heart. Furthermore, high concentrations of acetaldehyde cause cardiac arrhythmias. The cardiovascular toxicity of methanol is about the same as that of ethanol, whereas al cohols with longer chains are more toxic than ethanol. 

Ethanol metabolism occurs mainly in the liver and proceeds by oxidation in two steps, first to acetaldehyde (CHjCHO) and then to acetic add (CH3CO2H)- When continuously present in the body, ethanol and acetaldehyde are toxic, leading to the devastating physical and metabolic deterioration... 

Ethanol is almost entirely metabolized in the liver. The first step, oxidation by alcohol dehydrogenase, yields acetaldehyde, a reactive and toxic compound. Essentially all of the acetaldehyde is converted to acetate by the liver enzyme aldehyde dehydrogenase. Aldehyde dehydrogenase is inhibited by the drag disulfiram. Given alone, disulfiram is a nontoxic substance. However, ethanol consumption in the presence of... 

Alcohol abuse is a major clinical problem in many countries and has been the subject of investigation for many years by those interested in determining the molecular basis of ethanol-induced liver dam e (see Lieber, 1990). These intensive and extended efforts have revealed much about the metabolism of ethanol in the liver and about the toxicity of its primary oxidative product, acetaldehyde. They have not, however, folly elucidated the molecular mechanisms that lead to the typical features of alcoholic liver injury steatosis, necrosis and eventually cirrhosis. 

Disulfiram works by irreversibly blocking the enzyme aldehyde dehydrogenase, a step in the metabolism of alcohol, resulting in increased blood levels of the toxic metabolite acetaldehyde. As levels of acetaldehyde increase, the patient experiences decreased blood pressure, increased heart rate, chest pain, palpitations, dizziness, flushing, sweating, weakness, nausea and vomiting, headache, shortness of breath, blurred vision, and syncope. These effects are commonly referred to as the disulfiram-ethanol reaction. Their severity increases with the amount of alcohol that is consumed, and they may warrant emergency treatment. Disulfiram is contraindicated in patients who have cardiovascular or cerebrovascular disease, because the hypotensive effects of the disulfiram-alcohol reaction could be fatal in such patients or in combination with antihypertensive medications. Disulfiram is relatively contraindicated in patients with diabetes, hypothyroidism, epilepsy, liver disease, and kidney disease as well as impulsively suicidal patients. 

Another specific and important aspect to consider is the possibility that an environmentally heterogeneous photocatalyst can lead to the undesirable formation of reaction intermediates which are more toxic than the starting reagents. For instance, the Ti02-based photodegradation of ethanol, a relatively innocuous air pollutant, occurs through its transformation into the more toxic acetaldehyde. Condensation reactions can also lead to the formation of traces of methyl formate, ethyl formate, or methyl acetate. Catalyst design is therefore important to increase the overall oxidation rate to ensure complete mineralization (formation of C02 and H20). 

Solarization effects on weed population was hypothesized to be due to different mechanisms, such as changes in cell metabolism and ultrastructure (Singla et al. 1997), microbial parasitism on seeds weakened by sublethal temperatures, seed dormancy interruption by raising temperatures, and foliar scorching of weeds under the plastic mulch (Egley 1990 Katan and DeVay 1991). Moreover, imbalance of 02 and C02 or release of acetaldehyde, ethylene, and other volatile toxic compounds were also reported as accounting for weed death (Rubin and Benjamin 1984 Gamliel et al. 2000). 

In this work on compounds containing the C—F link, it was obviously desirable to prepare 2-fluoroethanol, both for toxicity tests on the compound itself, and as a starting material for the production of other fluorine compounds. Swarts1 was unable to obtain 2-fluoroethanol by the action of silver fluoride or mercuric fluoride on either ethylene chlorohydrin or ethylene bromohydrin. He obtained acetaldehyde in each case. He ultimately obtained fluoroethanol in very poor yield by the indirect method of hydrolysing fluoroacetin (from bromoacetin and mercuric fluoride) for 80 hr. with dilute mineral acid. 

PTT has different side reaction products. Instead of the acetaldehyde produced with PET, acrolein and allyl alcohol are the volatile byproducts of PTT production. The generation of acrolein is to be expected since it is one of the starting raw materials for making PDO. Acrolein is toxic and is a very strong lachrymator [22], and requires special handling and treatment. 

As implied above, acetaldehyde is toxic the accumulation of this metabolite leads to many of the deleterious consequences of alcohol intoxication because it is able to alter... 

Acetaldehyde is the product of the Wacker process. At the end of the fifties oxidation of ethene to ethanal replaced the addition of water to acetylene, because the acetylene/coal-based chemistry became obsolete, and the ethene/petrochemistry entered the commercial organic chemicals scene. The acetylene route involved one of the oldest organometallics-mediated catalytic routes started up in the 1920s the catalyst system comprised mercury in sulfuric acid. Coordination of acetylene to mercury(II) activates it toward nucleophilic attack of water, but the reaction is slow and large reactor volumes of this toxic catalyst were needed. An equally slow related catalytic process, the zinc catalysed addition of carboxylic acids to acetylene, is still in use in paint manufacture. 

Disulfiram is the generic name for Antabuse, a drug used in the treatment of chronic alcoholism. Disulfiram potentiates the toxic and carcinogenic effects of 1,2-dibromoethane in experimental animals. Presumably, this occurs by blocking conversion of the aldehyde metabolite as with acetaldehyde from ethanol. There is no evidence that similar effects occur in humans. Based on animal data, however, Ayerst Laboratories, producers of Antabuse (disulfiram), recommended the following in the package insert "Patients taking Antabuse tablets should not be exposed to ethylene dibromide or its vapors" (PDR 1991). 

Appeltnan L.M., Feron, V.J., and der Heijden, C.A. Inhalation toxicity of acetaldehyde in rats. II. Carcinogenicity study interim results after 15 months, Toxicology, 31(2) 123-133, 1984. 

Skog, E. A toxicological investigation of lower aliphatic aldehydes. I. Toxicity of formaldehyde, acetaldehyde, propionaldehyde and butyraldehyde as well as of acrolein and crotonaldehyde. Acta Pharmacol, 6 299-318, 1950. 

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