CAS RN: 75-07-0

Toxicity Summary

IDENTIFICATION AND USE: Acetaldehyde is a colorless volatile liquid with a pungent suffocating odor. It is not registered for current pesticide use in the U.S., but approved pesticide uses may change periodically and so federal, state and local authorities must be consulted for currently approved use. Acetaldehyde used as an intermediate in the production of cellulose acetate, vinyl acetate resins, acetate esters, synthetic pyridine derivatives, and terephthalic acid. Other uses include: in the silvering of mirrors; in leather tanning, as a denaturant for alcohol; in fuel mixtures; as a hardener for gelatin fibers; in glue and casein products; as a preservative for fish and fruit; in the paper industry; as a synthetic flavoring agent; and in the manufacture of cosmetics. Acetaldehyde has been identified as being commonly used in hydraulic fracturing fluids. HUMAN EXPOSURE AND TOXICITY: Acetaldehyde is a metabolic intermediate in humans. It has been identified in food, beverages and cigarette smoke. By far, the main source of exposure to acetaldehyde in the general population is through metabolism of ethanol. Workers may be exposed in some manufacturing industries and during alcohol fermentation. Several isoenzymic forms of acetaldehyde dehydrogenase (ALDH) have been identified in the human liver and other tissues. There is polymorphism for mitochondrial ALDH. Subjects that are homozygous or heterozygous for a point mutation in the mitochondrial ADLH corresponding gene have low activity of this enzyme, metabolize acetaldehyde slowly and are intolerant of ethanol alcohol. There is some metabolism of acetaldehyde in human renal tubules; the liver is the most important metabolic site. Limited studies involving human volunteers have shown that acetaldehyde was mildly irritating to the eyes and upper respiratory tract following short term exposures. Intravenous infusion of 5% acetaldehyde at a rate of 20.6- 82.4 mg/min for up to 36 min into normal human subjects caused an increase in heart rate, ventilation and dead space, and a decrease in alveolar carbon dioxide levels. These symptoms are qualitatively and quantitatively similar to those seen after ethanol intake in subjects previously treated with disulfiram (Antabuse), a known inhibitor of ALDH. Large doses may cause death by respiratory paralysis. Symptoms of chronic intoxication resemble those of chronic alcoholism. Acetaldehyde has been implicated as the putatively toxic metabolite in the induction of ethanol alcohol associated liver damage, facial flushing and developmental effects. Human lymphocytes (from known alcoholics) were exposed to acetaldehyde concn of 0.02 mg/mL and 0.04 mg/mL. Results indicate that chromosomal aberrations occurred at both concentrations. Acetaldehyde-DNA adducts have been observed in granulocytes and lymphocytes of human alcohol abusers. ANIMAL STUDIES: In repeated dose studies, both the oral and inhalation routes, toxic effects at relatively low concentrations were limited to the sites of initial contact. In a study where rats were administered acetaldehyde in their drinking water effects were limited to slight focal hyperkeratosis of the forestomach. Respiratory effects were noted in hamsters exposed to acetaldehyde by inhalation, degenerative changes were observed in the trachea. Degenerative changes in respiratory epithelium and larynx were noted at higher concentrations. Following inhalation by rats, acetaldehyde is distributed to the blood, liver, kidney, spleen, heart and other tissues. Low levels were detected in embryos after maternal ip injection of acetaldehyde (mouse) and following maternal exposure to ethanol (mouse and rat). Parenteral exposure of pregnant rats and mice to acetaldehyde induced fetal malformations. Acetaldehyde is genotoxic in vitro, inducing gene mutations, clastogenic effects and sister chromatid exchanges (SCEs) in mammalian cells in the absence of exogenous metabolic activation. Negative results were noted with Salmonella. Following ip injection, acetaldehyde induced SCEs in the bone marrow of Chinese hamsters and mice. This chemical administered ip did not increase the frequency of micronuclei in early mouse spermatids. Increased incidences of tumors have been noted in inhalation studies on rats and hamsters exposed to acetaldehyde. In rats, there were dose related increases in nasal adenocarcinomas and squamous cell carcinomas. In hamsters, increases in nasal and laryngeal carcinomas were non-significant. Distribution of acetaldehyde to brain interstitial fluid, but not to brain cells has been demonstrated following ip injection of ethanol. Acetaldehyde is taken up by red blood cells following consumption in baboons. Following oral administration, virtually no unchanged acetaldehyde is excreted in the urine. The major pathway for the metabolism of acetaldehyde is by oxidation to acetate. ECOTOXICITY STUDIES: Acetaldehyde (0.1% or 1.0% for 2 hr) induced mutations in genes that affect the egg-laying system of Caenorhabditis elegans.
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