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Acrylonitrile is a polar molecule that exists in a vapor state due to its vapor pressure of 109 mm HG. This is even though Acrylonitrile has a boiling point of 77.3 ºC. As a monomer, acrylonitrile is used in the manufacture of acrylonitrile-butadiene-styrene, modacrylic, and acrylic fibers. It also acts as a chemical intermediate. The production and handling of acrylonitrile take place in closed systems but occasionally, occupational exposure to the chemical can occur through dermal absorption or inhalation during transport or transfer.
The metabolism of acrylonitrile is via multiple pathways but the main one involves the pairing of acrylonitrile with glutathione-S-transferase as a catalyst. Thereafter, the conjugate is converted enzymatically to cyanoethylated mercapturic acid, and cyanide is produced as a metabolite. Another pathway involves the enzymatic oxidation of acrylonitrile to 2-cyanoethylene oxide with an additional metabolism of the conjugate resulting in the release of cyanide and water-soluble organic acids. Acrylonitrile and its oxide metabolite (2-cyanoethylene oxide) bind covalently to DNA, protein, and other macromolecules. In the process, they are effectively eliminated from the cyanide-forming pathways.
Some foods such as almonds, lima beans, spinach, and cassava roots contain low concentrations of cyanide chemicals and in case they are consumed by humans, the body is in a position to handle these low cyanide concentrations. At a high level of exposure to acrylonitrile, acute toxicity can occur and it presents with similar symptoms to those manifested by acute cyanide toxicity. The extent to which the aforementioned pathways can be followed is determined by the amount of cyanide produced.
A study was carried out to determine factors affecting human response to acrylonitrile exposure. The study consisted of 59 workers who had been exposed to low acrylonitrile levels. Part of the group had also been overexposed to this chemical as well. The study failed to identify a relationship between, on the one hand, N-2-cyanoethylvaline adduct levels and on the other hand, glutathione-S-transferase GSTM3 and GSTP1 genotype. On the other hand, when one amino acid on GSTP1 was substituted, there was a resultant increase in the adduct levels of N-2-cyanoethylvaline. This led the authors to conclude that the individual toxicity levels of acrylonitrile can be affected by glutathione-S-transferase poly-morphisms.
Another study failed to locate any apparent relationship between N-2-cyanoethylvaline adduct level and glutathione-S-transferase genotype, and this could be an indication of the lack of effect of multiple genetic variations on individual acrylonitrile metabolism. Some of the most prominent symptoms manifested by subjects who have been over-exposed to acrylonitrile at the industrial level include nausea, fatigue, and headache. At the same time, we need to note that the ability of a conjugator to synthesize and get rid of acrylonitrile is higher in comparison with that of the nonconjugated. Also, if an occupational overexposure has occurred, deficiency of GSTT1 and GSTM1 genes may result in a dramatic effect.
Overexposure to acrylonitrile also leads to increased levels of cyanide in subjects. To overcome this risk, subjects should not be overexposed to the chemical. There is a growing need among toxicological, environmental, and pharmaceutical experts to better understand how genetic variations influence exposure to toxic chemicals. The study talks of the need to better understand the relationship between the susceptibility of humans to diseases and environmental exposure. In addition, we need to locate valuable biomarkers of disease as well as exposure to various toxic substances.
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