This article provides environmental information on acrolein including environmental fate, potential for human exposure, analytical methods, and a listing of regulations and advisories. Acrolein may be released to the environment in emissions and effluents from its manufacturing and use facilities, in emissions from combustion processes (including cigarette smoking and combustion of petrochemical fuels), from direct application to water and waste water as a slimicide and aquatic herbicide, as a photooxidation product of various hydrocarbon pollutants found in air (including propylene and 1,3-butadiene), and from land disposal of some organic waste materials. Acrolein is a reactive compound and is unstable in the environment. The general population may be exposed to acrolein through inhalation of contaminated air and through ingestion of certain foods. Important sources of acrolein exposure are via inhalation of tobacco smoke and environmental tobacco smoke and via the overheating of fats contained in all living matter. There is potential for exposure to acrolein in many occupational settings as the result of its varied uses and its formation during the combustion and pyrolysis of materials such as wood, petrochemical fuels, and plastics.

Acrolein is a chemical used as an intermediate reactive aldehyde in chemical industry. It is used for synthesis of many organic substances, methionine production, and methyl chloride refrigerant. The general population is exposed to acrolein via smoking, second-hand smoke, exposure to wood and plastic smoke. Firefighters and population living or working in areas with heavy automotive traffic may expose to higher level of acrolein via inhalation of smoke or automotive exhaust. Degradation of acrolein in all environmental media occurs rapidly, therefore, environmental accumulation is not expected. Acrolein degrade in 6A days when applied to surface water, and it has not been found as a contaminant in municipal drinking water. Acrolein vapor may cause eye, nasal and respiratory tract irritations in low level exposure. A decrease in breathing rate was reported by volunteers acutely exposed to 0.3A ppm of acrolein. At similar level, mild nasal epithelial dysplasia, necrosis, and focal basal cell metaplasia have been observed in rats. The acrolein effects on gastrointestinal mucosa in the animals include epithelial hyperplasia, ulceration, and hemorrhage. The severity of the effects is dose dependent. Acrolein induces the respiratory, ocular, and gastrointestinal irritations by inducing the release of peptides in nerve terminals innervating these systems. Levels of acrolein between 22 and 249 ppm for 10 min induced a dose-related decrease in substance P (a short-chain polypeptide that functions as a neurotransmitter or neuromodulator).

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