Following inhalation exposure, acrolein can be deposited in the nasal cavity and respiratory tract, where it is largely irreversibly retained due to its high tissue reactivity. Eventually, some trace elements are absorbed into the blood and distributed throughout the body. Absorption of acrolein in the nasal cavity is influenced by its solubility and inspiratory flow rate. Glutathione conjugation is the main detoxification pathway for acrolein. Further metabolism occurs in the liver, yielding glycidylaldehyde and a number of metabolites that can be excreted in the urine as well as some unchanged acrolein. Most of the free acrolein is excreted with exhaled air.
Acrolein is highly toxic to aquatic organisms. There have been some studies on the toxic effects in the aquatic environment due to the use of acrolein as a herbicide in irrigation canals (Table 6). Most algae and weeds showed high sensitivity to acrolein. Most terrestrial crop plants can tolerate 25 mg of acrolein per liter of irrigation water without damage. Toxicity data relevant to terrestrial wildlife are limited. The data indicated that terrestrial organisms were less sensitive to a single exposure to acrolein than aquatic organisms (Table 7). Acrolein is a highly reactive compound that can be polymerized into dimethylaniline through a violent reaction (possibly explosive) in the presence of strong acid or strong base. Care should be taken to prevent miscibility with amines, sulfur dioxide, metal salts, and oxidants. Acrolein is sensitive to heat, light and air. Direct exposure to high concentrations of unsaturated aldehydes is cardiotoxic, and acrolein is as toxic as or greater than any other α,β-unsaturated (e.g., 4-hydroxy-trans-2-nonanal) (HNE), crotonaldehyde ) or saturated (eg, formaldehyde, benzaldehyde) aldehydes were tested in cultured myocytes, smooth muscle cells, and endothelial cells (Conklin et al., 1998).
