Literature DB >> 8599034

Fate and effects of acrolein.

D P Ghilarducci1, R S Tjeerdema.   

Abstract

Acrolein is a highly toxic, reactive, and irritating aldehyde that occurs as a product of organic pyrolysis, as a metabolite of a number of compounds, and as a residue in water when used for the control of aquatic organisms. It is an intermediate in the production of acrylic acid, DL-methionine, and numerous other agents. Its major direct use is as a biocide for the control of aquatic flora and fauna. It is introduced to the environment from a variety of sources, including organic combustion such as automobile exhaust, cigarette smoke, and manufacturing and cooking emissions, as well as direct biocidal applications. Organic combustion from both fixed and mobile sources is the significant source of acrolein in the atmosphere; it represents up to 8% of the total aldehydes generated from vehicles and residential fireplaces and 13% of total atmospheric aldehydes. This reactive aldehyde also occurs in organisms as a metabolite of allyl alcohol, allylamine, spermine, spermidine, and the anticancer drug cyclophosphamide, and as a product of UV radiation of the skin lipid triolein. Furthermore, small amounts are found in foods; when animal or vegetable fats are overheated, however, large amounts are produced. Most human contact occurs during exposure to smoke from cigarettes, automobiles, industrial processes, and structural and vegetation fires. Besides cigarette smoke, occupational exposures are a common mode of human contact, particularly in industries that involve combustion of organic compounds. Firefighters, in particular, are exposed to extremely high levels during the extinguishment and overhaul phases of their work. Water may contain significant levels of the herbicide. It has been found in paper mill and municipal effluents at 20-200 micrograms/L, and at 30 micrograms/L as far as 64 km downstream from the point of application. The USEPA-recommended water quality criteria for freshwater are only 1.2 micrograms/L (24-hr avg) and 2.7 micrograms/L (maximum ceiling). Acrolein is highly reactive, and intercompartmental transport is limited. However, it is eliminated from aqueous environments by volatilization and hydration to beta-hydroxypropanal, after which biotransformation occurs, with a half-life of 7-10 d. The Koc for acrolein is 24, and it is not likely to be retained in soil; activated carbon adsorbs only 30% from solution. Thus, the aldehyde is either leached extensively in moist soil or volatilizes quickly from dry soil. It is eliminated from air by reaction with .OH (half-life, 0.5-1.2 d), NOx (half-life, 16 d), and O3 (half-life, 59 d), as well as by photolysis and wet deposition. As expected from its high water solubility, bioaccumulation is low. Acrolein is highly toxic by all routes of exposure. The respiratory system is the most common target: exposure causes localized irritation, respiratory distress, pulmonary edema, cellular necrosis, and increased susceptibility to microbial diseases. Additionally, acute inhalation studies verify that it is a severe respiratory irritant that affects respiratory rates. Respiratory rate depression may have a protective effect by minimizing vapor inhalation, thereby explaining the subadditive effect of acrolein when combined with the other toxic combustion by-products CO and HCHO. Liquid contact with the skin and eyes causes severe irritation, opaque or cloudy corneas, and localized epidermal necrosis, but no allergic contact dermatitis. The cardiovascular system is affected, resulting in increased blood pressure, platelet aggregation, and quick cessation of beating in perfused rat hearts. It may also inhibit mitochondrial oxidative phosphorylation in the myocardium. Acute LD50s and LC50s are low. Levels are 7-46 mg/kg and 18-750 mg/m3, respectively, in rats; aquatic organisms are affected above 11.4 micrograms/L.(ABSTRACT TRUNCATED)

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Year:  1995        PMID: 8599034     DOI: 10.1007/978-1-4612-2550-8_2

Source DB:  PubMed          Journal:  Rev Environ Contam Toxicol        ISSN: 0179-5953            Impact factor:   7.563


  68 in total

Review 1.  Molecular mechanisms of acrolein-mediated myelin destruction in CNS trauma and disease.

Authors:  R Shi; J C Page; M Tully
Journal:  Free Radic Res       Date:  2015-04-16

2.  Effect of carcinogenic acrolein on DNA repair and mutagenic susceptibility.

Authors:  Hsiang-Tsui Wang; Yu Hu; Dan Tong; Jian Huang; Liya Gu; Xue-Ru Wu; Fung-Lung Chung; Guo-Min Li; Moon-shong Tang
Journal:  J Biol Chem       Date:  2012-01-24       Impact factor: 5.157

3.  Acrolein-induced dyslipidemia and acute-phase response are independent of HMG-CoA reductase.

Authors:  Daniel J Conklin; Russell A Prough; Peter Juvan; Tadeja Rezen; Damjana Rozman; Petra Haberzettl; Sanjay Srivastava; Aruni Bhatnagar
Journal:  Mol Nutr Food Res       Date:  2011-08-03       Impact factor: 5.914

4.  Neuroprotective role of hydralazine in rat spinal cord injury-attenuation of acrolein-mediated damage.

Authors:  Jonghyuck Park; Lingxing Zheng; Andrew Marquis; Michael Walls; Brad Duerstock; Amber Pond; Sasha Vega-Alvarez; He Wang; Zheng Ouyang; Riyi Shi
Journal:  J Neurochem       Date:  2013-12-15       Impact factor: 5.372

5.  Mechanisms Underlying Acrolein-Mediated Inhibition of Chromatin Assembly.

Authors:  Lei Fang; Danqi Chen; Clinton Yu; Hongjie Li; Jason Brocato; Lan Huang; Chunyuan Jin
Journal:  Mol Cell Biol       Date:  2016-11-14       Impact factor: 4.272

6.  Role of endoplasmic reticulum stress in acrolein-induced endothelial activation.

Authors:  Petra Haberzettl; Elena Vladykovskaya; Sanjay Srivastava; Aruni Bhatnagar
Journal:  Toxicol Appl Pharmacol       Date:  2008-10-07       Impact factor: 4.219

7.  A comparative 90-day toxicity study of allyl acetate, allyl alcohol and acrolein.

Authors:  Scott S Auerbach; Joel Mahler; Gregory S Travlos; Richard D Irwin
Journal:  Toxicology       Date:  2008-09-04       Impact factor: 4.221

8.  Mutagenicity and sequence specificity of acrolein-DNA adducts.

Authors:  Hsiang-Tsui Wang; Siyi Zhang; Yu Hu; Moon-Shong Tang
Journal:  Chem Res Toxicol       Date:  2009-03-16       Impact factor: 3.739

9.  Effects of Phenelzine Administration on Mitochondrial Function, Calcium Handling, and Cytoskeletal Degradation after Experimental Traumatic Brain Injury.

Authors:  Rachel L Hill; Indrapal N Singh; Juan A Wang; Edward D Hall
Journal:  J Neurotrauma       Date:  2018-12-12       Impact factor: 5.269

Review 10.  Cardiovascular injury induced by tobacco products: assessment of risk factors and biomarkers of harm. A Tobacco Centers of Regulatory Science compilation.

Authors:  Daniel J Conklin; Suzaynn Schick; Michael J Blaha; Alex Carll; Andrew DeFilippis; Peter Ganz; Michael E Hall; Naomi Hamburg; Tim O'Toole; Lindsay Reynolds; Sanjay Srivastava; Aruni Bhatnagar
Journal:  Am J Physiol Heart Circ Physiol       Date:  2019-02-01       Impact factor: 4.733

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