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In an aquifer-acquitard system in the subsoil of the city of Ferrara (Emilia-Romagna region, northern Italy) highly contaminated with chlorinated aliphatic toxic organics such as trichloroethylene (TCE) and tetrachloroethylene (PCE), a strong microbial-dependent dechlorination activity takes place during migration of contaminants through shallow organic-rich layers with peat intercalations. The in situ microbial degradation of chlorinated ethenes, formerly inferred by the utilization of contaminant concentration profiles and Compound-Specific Isotope Analysis (CSIA), was here assessed using Illumina sequencing of V4 hypervariable region of 16S rRNA gene and by clone library analysis of dehalogenase metabolic genes. Taxon-specific investigation of the microbial communities catalyzing the chlorination process revealed the presence of not only dehalogenating genera such as Dehalococcoides and Dehalobacter but also of numerous other groups of non-dehalogenating bacteria and archaea thriving on diverse metabolisms such as hydrolysis and fermentation of complex organic matter, acidogenesis, acetogenesis, and methanogenesis, which can indirectly support the reductive dechlorination process. Besides, the diversity of genes encoding some reductive dehalogenases was also analyzed. Geochemical and 16S rRNA and RDH gene analyses, as a whole, provided insights into the microbial community complexity and the distribution of potential dechlorinators. Based on the data obtained, a possible network of metabolic interactions has been hypothesized to obtain an effective reductive dechlorination process. [ABSTRACT FROM AUTHOR]

In Japan, chloroethylene is a regulated substance under the soil contamination countermeasures act since 2017, due to the presence of chloroethylene in soil leachate and groundwater. As a consequence, chloroethylene concentrations must be accurately determined to ensure the safety of drinking water, chloroethylene standard solutions with reliable concentrations had not been available because chloroethylene is difficult to handle due to its boiling point of − 13 °C. Here, we developed a quantitative 1H nuclear magnetic resonance (1H-qNMR) method to measure chloroethylene concentration in a standard solution in CD3OD. Sampling temperature must be between − 80 °C and − 21 °C, and the NMR tube headspace volume ratio must be lower than 23% to reduce the volatilization of chloroethylene. We used the signal of CD2HOD present in the standard solution as an internal standard because chloroethylene was volatilized during the addition of another internal standard. The chloroethylene concentration in the standard solution was accurately determined as 117.7 ± 1.4 mg kg−1. [ABSTRACT FROM AUTHOR]

Vinyl chloride (VCM) or chloroethylene is reactive in the gaseous state and its adsorption with pristine armchair (5,5) carbon nanotube (CNT) and silicon carbide nanotube (SiCNT) has been studied. Germanium (Ge) element as an impurity has been introduced to silicon carbide structure (i.e. SiCGeNT) so as to increase the reactivity of the surface of SiCNT and thus increase the sensitivity of the adsorbent during the adsorption process. The B3LYP-D3(GD3BJ) hybrid functional has been used to optimize the isolated nanostructures and vinyl chloride as well as their clusters (gas/nanotube). In addition, energy single-point calculations were performed using ωB97XD, PBE0, B3LYP-D3(GD3BJ), and M06-2X functionals. The selected basis function is 6-311G(d), which is a good approximation to cover the integration space with respect to the constituent atoms of the molecules studied in this research. Wave function analysis including non-covalent interaction (NCI), natural bond orbital (NBO), and quantum theory of atoms in molecules (QTAIM), have also been done to reveal the intermolecular interactions nature. The results of these analyses, which are calculated using B3LYP-D3(GD3BJ)/6-311G(d) level of theory, are in agreement with each other and emphasize that among the mentioned nanotubes, silicon carbide nanotube doped with Ge element is more sensitive with respect to gas adsorption. Therefore, it will be a good option to design and build a nanosensor. [Display omitted] • The interactions of VCM with CNT, SiCNT, and SiCGeNT are studied. • To study the adsorption processes, the results of an NBO analysis are analyzed. • To unravel the nature of intermolecular interactions a QTAIM analysis is applied. • NCI analysis was performed to consider the non-covalent interactions. [ABSTRACT FROM AUTHOR]

The carcinogenicity of vinyl chloride in humans was recognized in 1974 based on observations of hepatic angiosarcomas in highly exposed workers. A multiplicity of endpoints has been demonstrated. The primary target organ, the liver, displays differential susceptibilities of hepatocytes and sinusoidal cells, which are modified by factors of age and dose. There is consistency in organotropism between experimental animals and humans. Vinyl chloride is a pluripotent carcinogen, predominantly directed toward hepatic endothelial (sinusoidal) cells, and second toward the parenchymal cells of the liver. The similarity of results between experimental animals and humans is a solid basis of an amalgamation of experimental and epidemiological risk estimates. Vinyl chloride requires metabolic activation for carcinogenicity and mutagenicity, and toxicokinetics are a key to interpret the dose response. Practically the entire initial metabolism of vinyl chloride is oxidative. At higher exposure concentrations this is nonlinear, and metabolic saturation of metabolism in rats is reached at about 250 ppm. This is consistent with the plateau of hepatic angiosarcoma incidence in rat bioassays. Physiologically based pharmacokinetic/toxicokinetic (PBPK) models have been developed and successfully applied within the frame of human cancer risk assessments. The major DNA adduct induced by vinyl chloride (~ 98% of total adducts in rats), 7-(2-oxoethyl)guanine, is almost devoid of promutagenic activity. The clearly promutagenic “etheno” adducts N 2 ,3-ethenoguanine and 3, N 4 -ethenocytosine each represent ~ 1% of the vinyl chloride DNA adducts in rats, and 1, N 6 -ethenoadenine is found at even lower concentrations. Etheno adducts appear to have a long persistence and are repaired by glycosylases. Vinyl chloride represents a human carcinogen for which a series of mechanistic events connects exposure with the carcinogenic outcome. These include (1) metabolic activation (to form chloroethylene oxide), (2) DNA binding of the reactive metabolite (to exocyclic etheno adducts), (3) promutagenicity of these adducts, and (4) effects of such mutations on protooncogenes/tumor suppressor genes at the gene and gene product levels. In rat hepatocytes, a further event is a biomarker response. Cancer prestages (enzyme-altered foci), as quantitative biomarkers, provide a tool to study dose response even within low dose ranges where a carcinogenic risk cannot be seen in cancer bioassays directly. Such biomarker responses support a linear nonthreshold extrapolation for low-dose assessment of carcinogenic risks due to vinyl chloride. Published risk estimates based on different sets of data (animal experiments, epidemiological studies) appear basically consistent, and on this basis an angiosarcoma risk of ~ 3 × 10 -4 has been deduced by extrapolation, for exposure to 1 ppm vinyl chloride over an entire human working lifetime. An important point that should be considered in regulatory standard settings is the presence of a physiological background of those etheno DNA adducts, which are also produced by vinyl chloride. Likely reasons for this background are oxidative stress and lipid peroxidation. In essence, fundamentals of the hepatocarcinogenicity of vinyl chloride appear now well established, providing a solid scientific basis for regulatory activities. [ABSTRACT FROM AUTHOR]