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Hazardous Organic Waste Amenable to Biological Treatment
Published in Daphne L. Stoner, Biotechnology for the Treatment of Hazardous Waste, 2017
The aerobic degradation of vinyl chloride has been reported for axenic cultures and in groundwater64–67 and degradative pathways determined (Figure 10).68,69 Vinyl chloride is metabolized by resting cell suspensions of Methylosinus trichosporium OB-3b via the epoxide, chloroethylene oxide.68 Further degradation to carbon dioxide and waters occurs by biological and chemical transformations. The dominant biological pathway is the degradation of chloroethylene oxide to ethylene, then sequential degradation to ethylene glycol, hydroxyacetaldehyde, glycolic acid, and carbon dioxide. The dehalogenation of vinyl chloride by the direct hydrolysis of the C-Cl bond by a Pseudomonas sp. results in the formation of acetaldehyde. Further oxidation of the carboxy and methyl groups produces hydroxyacetaldehyde and acetic acid.69 These compounds are oxidized to glycolic acid and metabolized to carbon dioxide.
Hazard Assessment
Published in Leon Golberg, Hazard Assessment of Ethylene Oxide, 2017
Hathway232 attributes the mechanism of carcinogenesis and mutagenesis of vinyl chloride to imidazo-cyclization of deoxyadenosine (dA) and deoxycytidine (dC) in rat liver DNA, forming the relatively persistent product etheno-dC and the less persistent etheno-dA. These adducts induce transversions which are consistent with base-pair-substitution (BPS) mutations induced by metabolically activated vinyl chloride, chloroethylene oxide and chloroacetaldehyde. As noted in , EO induces BPS mutations without activation, especially in Salmonella typhimurium strain TA 1535.
Overview of biological mechanisms of human carcinogens
Published in Journal of Toxicology and Environmental Health, Part B, 2019
Nicholas Birkett, Mustafa Al-Zoughool, Michael Bird, Robert A. Baan, Jan Zielinski, Daniel Krewski
Vinyl chloride is readily absorbed upon inhalation and rapidly metabolized in the liver. The primary metabolites are highly reactive chloroethylene oxide, and its rearrangement product chloroacetaldehyde. Both bind to proteins, DNA and RNA and form ethenoadducts. Chloroethylene oxide is the most reactive with nucleotides. Vinyl chloride is mutagenic, usually in the presence of metabolic activation, in various assays with bacteria, yeast or mammalian cells. This compound is also clastogenic in vivo and in vitro. Vinyl chloride induces unscheduled DNA synthesis, increases the frequency of sister chromatid exchange in rat and human cells, and elevates the frequency of chromosomal aberrations, DNA strand breaks and micronucleus formation in mice, rats, and hamsters in vivo. Polymorphic variations in metabolic genes (e.g. those of the CYP450 family) or DNA repair genes may alter carcinogenicity but do not affect the underlying mechanisms.