Vinyl Chloride Concentrations Research Articles

Toxic action/toxicity

ABSTRACTSome six or so physiological systems, essential to normal mammalian life, are involved in poisoning; an intoxication that causes severe injury to any one of them could be life threatening. Reversible chemical reactions showing Scatchard‐type binding are exemplified by CO, CN− and cyclodiene neurotoxin insecticide intoxications, and by antigen‐antibody complex formation. Haemoglobin (Hb) molecular biology accounts for the allosteric co‐operativity and other characteristics of CO poisoning, CN− acts as a powerful cytochrome oxidase inhibitor, and antigen binding in a deep antibody cleft between two domains equipped with epitopes for antigen‐binding groups explains hapten‐specific immune reactions. Covalent chemical reactions with second‐order (SN2) kinetics characterize Hg and Cd poisonings, the reactions of organophosphates and phosphonates with acetylcholinesterase and neurotoxic esterase and the reaction sequence whereby Paraquat accepts electrons and generates superoxide under aerobic conditions. Indirect carcinogens require cytochrome P450 activation to form DNA adducts in target‐organ DNA and cause cancer, but a battery of detoxifying enzymes clustered with the P450 system must be overcome. Thus, Smetabolism competes ineffectively with target DNA for reactive vinyl chloride (VC) metabolites, epoxide hydrolase is important to the metabolism and carcinogenicity of aflatoxins and polycyclic aromatic hydrocarbons (benzo[a]pyrene, etc.), and the non‐toxic 2‐naphthylhydroxylamine N‐glucuronide acts as a transport form in 2‐naphthylamine bladder cancer. VC liver‐cancer pathogenesis is explicable in terms of the presence of the glutathione S‐transferase detoxifying system in hepatocytes and its absence from the fibroblastic elements, and of the VC concentrations reaching the liver by different administrative routes. In VC carcinogenicity, chemical reactions give imidazo‐cyclization products with nucleoside residues of target DNA, and in benzene leukaemia, Z,Z‐muconaldehyde forms cyclic products containing a pyrrole residue linked to purine. Increased HbCO concentrations reduce the O2‐carrying capacity of the blood, and the changed shape of the O2‐Hb dissociation curve parallels disturbance in O2 unloading. CN− acts on electron transport and paralyses respiration. In telodrin poisoning, preconvulsive glutamine formation abstracts tricarboxylic acid intermediates incommensurately with normal cerebral respiration. Antigen‐antibody complexing depletes the antibody titre, available against infection. At high doses of Cd, Cd‐thionein filtered through the kidneys is reabsorbed and tubular lesions produced. Some organophosphate insecticides promote irreversible acetylcholinesterase phosphorylation and blockade nerve function, and others react with neurotoxic esterase to cause delayed neuropathy. The evidence for Paraquat pulmonary poisoning suggests a radical mechanism involving three interrelated cyclic reaction stages. The action of N‐ and O6 (O substituent in 6‐position of the purine) demethylases explains deletion mechanisms for DNA‐alkyl adducts. DNA‐directed synthesis in the presence of ultimate carcinogens provides for an estimation of misincorporations, which implicate the same transversions as those found by direct mutagenicity testing. Chemical carcinogens recognize tissue‐sensitive cells and modify their heritable genetic complement.Oncoproteins encoded by activated oncogenes signal the transformation of normal cells into cancer cells. The importance of the H‐ras oncogene and p53 tumour‐suppressor gene is stressed. Antidotal action is analysed; for example, parenteral glutamine administration to telodrin‐intoxicated rats restores the depleted cerebral glutamate level and prevents seizures. Glutamate acts as anticonvulsant in petit mal epilepsy. In general, therefore, the reaction of the toxicant‐related substance with the relevant target‐tissue macromolecule accounts for the biochemical/biological events at a cellular level and also the symptoms in the living mammal. This mechanism is analogous to mechanisms for diseases such as arthritis and Parkinsonism.

Toxic action/toxicity.

Some six or so physiological systems, essential to normal mammalian life, are involved in poisoning; an intoxication that causes severe injury to any one of them could be life threatening. Reversible chemical reactions showing Scatchard-type binding are exemplified by CO, CN- and cyclodiene neurotoxin insecticide intoxications, and by antigen-antibody complex formation. Haemoglobin (Hb) molecular biology accounts for the allosteric co-operativity and other characteristics of CO poisoning, CN- acts as a powerful cytochrome oxidase inhibitor, and antigen binding in a deep antibody cleft between two domains equipped with epitopes for antigen-binding groups explains hapten-specific immune reactions. Covalent chemical reactions with second-order (SN2) kinetics characterize Hg and Cd poisonings, the reactions of organophosphates and phosphonates with acetylcholinesterase and neurotoxic esterase and the reaction sequence whereby Paraquat accepts electrons and generates superoxide under aerobic conditions. Indirect carcinogens require cytochrome P450 activation to form DNA adducts in target-organ DNA and cause cancer, but a battery of detoxifying enzymes clustered with the P450 system must be overcome. Thus, S-metabolism competes ineffectively with target DNA for reactive vinyl chloride (VC) metabolites, epoxide hydrolase is important to the metabolism and carcinogenicity of alfatoxins and polycyclic aromatic hydrocarbons (benzo[a]pyrene, etc.), and the non-toxic 2-naphthylhydroxylamine N-glucuronide acts as a transport form in 2-naphthylamine bladder cancer. VC liver-cancer pathogenesis is explicable in terms of the presence of the glutathione S-transferase detoxifying system in hepatocytes and its absence from the fibroblastic elements, and of the VC concentrations reaching the liver by different administrative routes. In VC carcinogenicity, chemical reactions give imidazo-cyclization products with nucleoside residues of target DNA, and in benzene leukaemia, Z,Z-muconaldehyde forms cyclic products containing a pyrrole residue linked to purine. Increased HbCO concentrations reduce the O2-carrying capacity of the blood, and the changed shape of the O2-Hb dissociation curve parallels disturbance in O2 unloading. CN- acts on electron transport and paralyses respiration. In telodrin poisoning, preconvulsive glutamine formation abstracts tricarboxylic acid intermediates incommensurately with normal cerebral respiration. Antigen-antibody complexing depletes the antibody titre, available against infection. At high doses of Cd, Cd-thionein filtered through the kidneys is reabsorbed and tubular lesions produced. Some organophosphate insecticides promote irreversible acetylcholinesterase phosphorylation and blockade nerve function, and others react with neurotoxic esterase to cause delayed neuropathy. The evidence for Paraquat pulmonary poisoning suggests a radical mechanism involving three interrelated cyclic reaction stages. The action of N- and O8 (O substituent in 6-position of the purine) demethylases explains deletion mechanisms for DNA-alkyl adducts. DNA-directed synthesis in the presence of ultimate carcinogens provides for an estimation of misincorporations, which implicate the same transversions as those found by direct mutagenicity testing. Chemical carcinogens recognize tissue-sensitive cells and modify their heritable genetic complement. Oncoproteins encoded by activated oncogenes signal the transformation of normal cells into cancer cells. The importance of the H-ras oncogene and p53 tumour-suppressor gene is stressed. Antidotal action is analysed; for example, parenteral glutamine administration to telodrin-intoxicated rats restores the depleted cerebral glutamate level and prevents seizures. Glutamate acts as anticonvulsant in petit mal epilepsy. In general, therefore, the reaction of the toxicant-related substance with the relevant target-tissue macromolecule accounts for the biochemical/biological events at a cellular level a

Modeling the kinetics of vinyl chloride cometabolism by an ethane-grown Pseudomonas sp.

Pseudomonas sp strain EA1 was isolated under aerobic conditions using ethane as the sole organic carbon and electron donor source, with an observed yield of 0.99 mg total suspended solids/mg ethane (0.85 mg volatile suspended solids / mg ethane) and a maximum specific growth rate of 0.015 d(-1). When grown on ethane, EA1 cometabolizes vinyl chloride (VC) at a maximum rate of 0.350 micromol/mg volatile suspended solids/d and with a half saturation constant of 0.62 microM VC. The rate of VC use by EA1 is twice as high when ethane is also provided, even though consumption of ethane is almost completely inhibited until VC is consumed. The presence of ethane also reduces the total amount of VC cometabolized. A model was developed that adequately describes the batch kinetics of VC cometabolism in the presence and absence of ethane, as well as ethane metabolism in the presence and absence of VC. Terms are included that increase the initial rate of VC use in the presence of ethane (according to the ratio of initial ethane concentration to the half saturation coefficient) but decrease the total amount of VC cometabolized. Parameter estimates for the model were obtained using a step-wise experimental approach, with varying initial concentrations of VC and ethane. Strain EA1 completely dechlorinates VC in the presence and absence of ethane. Measurements of soluble chemical oxygen demand indicate that approximately 50% of the VC consumed is mineralized, with the balance released as soluble, nonchlorinated products. Ethene is not used as a substrate by EA1 but it does inhibit ethane metabolism and VC cometabolism. In mixtures containing all three compounds, more VC is degraded and at a faster rate compared to VC plus ethene. The results suggest that ethane-enhanced biodegradation of VC may contribute to VC removal at the aerobic fringe of groundwater plumes undergoing reductive dechlorination.

Reduction of Vinyl Chloride in Metallic Iron−Water Systems

Batch experiments examining the kinetics and mechanism of vinyl chloride (VC) reduction by metallic iron in aqueous systems were performed. The effects of various iron loadings, VC concentrations, pH conditions, temperatures, and Fe(II)/Fe(III) chelating agents (1,10-phenanthroline, 2,2‘-dipyridyl, and nitrilotriacetic acid) on reduction kinetics were examined. Ethylene was the major carbon-containing product of VC reduction under all conditions examined, indicating hydrogenolysis. The reaction was pseudo-first-order with respect to aqueous VC concentration. The amount of VC adsorption on iron surfaces was estimated from the rapid initial loss of VC from solution, and the resultant sorption isotherm was linear over the concentration range examined. The first-order kinetics and the linear sorption for VC suggest that the portion of VC sorption to surface reactive sites relative to nonreactive sorption sites is constant, unlike the behavior observed for the higher chlorinated ethenes. The activation energy ...

Metabolic Activation of Vinyl Chloride by Rat Liver Microsomes: Low-Dose Kinetics and Involvement of Cytochrome P450 2E1

The metabolism and pharmacokinetics of vinyl chloride (VC) have been extensively studied in rodents and humans, but the maximum velocity ( V max) and Michaelis constant ( K m) for the activation of VC by microsomal monooxygenases in vitro have not yet been determined. Using a new sensitive assay, the epoxidation of VC by rat liver microsomes (adult Sprague–Dawley) at concentrations from 1 ppm to 10 6 ppm in the gas phase was measured. In the assay, the reactive VC metabolites chloroethylene oxide and 2-chloroacetaldehyde were trapped with excess cAMP, yielding 1, N 6-etheno-cAMP (ϵcAMP) which was quantitated by HPLC fluorimetry. The trapping efficiency of electrophilic VC metabolites by cAMP was close to 10%. The specificity of the method was confirmed by purification of ϵcAMP on an immunogel. The VC concentration in the gas phase was measured by GC/flame ionization detection, while in the aqueous phase it was calculated from the partition coefficient between air and the microsomal suspension. Activation of VC by rat liver microsomes followed Michaelis–Menten kinetics with K m = 7.42 ± 0.37 (±SD) μM and V max = 4674 ± 46 pmol · mg protein −1 · min −1. Inhibitor studies and immunoinhibition assays showed that VC was activated by cytochrome P450 (CYP) 2E1 down to 1 ppm in the air phase. Based on the metabolic parameters determined, the uptake of VC by rats in vivo can be accurately predicted.

Decomposition of ethyl chloride and vinyl chloride in an electron beam generated plasma reactor

An electron beam generated plasma reactor is used to decompose low concentrations of ethyl chloride (EC) and vinyl chloride (VC) in atmospheric pressure air streams. The energy requirements for 90% decomposition of each compound are reported as a function of inlet concentration. VC decomposition is enhanced by chlorine radical reactions. Both the EC and VC reactions seem to be inhibited by electron scavenging decomposition products. A simple analytic expression is used for fitting decomposition data where inhibition effects are important.

A risk assessment of chlorinated aliphatics in bioremediated soils

AbstractNatural microbes living in contaminated subsurface media can be enhanced to degrade large concentrations of contaminating compounds at a faster rate than the microbes could degrade under natural conditions. A feasibility study demonstrating this principle was performed on‐site in southern Louisiana to evaluate the effectiveness of two microbial degradation remediation methods used to decrease the human carcinogenic risks associated with exposure to ethylene dichloride and vinyl chloride concentrations in contaminated clay and sludge soils at the site. The results of the study are compared to an acceptable Louisiana Department of Environmental Quality closure level to evaluate in‐situ microbial enhancement in chlorinated aliphatic‐contaminated sludge and clay soils as a remediation/cleanup alternative in similar industrial situations.

Byproduct Formation During the Reduction of TCE by Zero‐Valence Iron and Palladized Iron

AbstractTrichloroethene (TCE) was reduced with zero‐valence iron and palladized iron in zero‐head‐space extractors. Progress of the reaction in these batch studies was monitored with purge‐and‐trap gas chromatography and a flame ionization detector. When a 5 ppm initial concentration of TCF. reacts with zero‐valence iron, approximately 140 ppb of vinyl chloride persists for as long as 73 days. The concentration of vinyl chloride (approximately If) ppb) remaining with palladized iron is approximately an order of magnitude less than when zero‐valence iron is the reductant. These data suggest that volatile byproducts may be under‐represented in oilier published data regarding reduction with zero‐valence metals. These results also demonstrate that the reduction of TCE with palladized iron (0.05 percent palladium) is more than an order of magnitude faster than with zero‐valence iron. Wilh a 5:1 solution‐to‐solid ratio the TCE half‐life with zero‐valence iron is 7.41 hours. but is only 0.59 hours with the palladized iron.

Impact of Turbidity on TCE and Degradation Products in Ground Water

AbstractElevated particulate concentrations in ground water samples can bias contaminant concentration data. This has been particularly problematic for metal analyses where artificially increased turbidity levels can affect metals concentrations and confound interpretation of the data. However, few studies have been conducted to determine the impact of particulates on trichloroethylene (TCE), cis‐dichloroethylene (c‐DCE), and vinyl chloride concentrations.Laboratory batch studies and field investigations were conducted to evaluate the effects of suspended solids on VOC concentrations in ground water samples analyzed by purge‐and‐trap gas chromatography. Three different solids were used to assess the effects of suspended particulates. The solids were aquifer material from a field site in North Carolina and two reference clay minerals (kaolinite and Namontimorillonite). During the laboratory portion of this study, the solids were used to determine effects on TCE concentrations under controlled laboratory conditions.The same solids were used in a field study to compare the laboratory results with field results. Solids were added to the sample vials prior it) sample collection to intentionally increase turbidity levels in the water samples. Results of the study indicate essentially no decrease in TCE, c‐DCH, or vinyl chloride concentrations due to increased turbidity levels.

Small-Column Microcosm for Assessing Methane-Stimulated Vinyl Chloride Transformation in Aquifer Samples

A small-column microcosm was designed and operated to evaluate the potential for in-situ vinyl chloride (VC) biotransformation by a methane-stimulated culture. Microcosms consisted of 15-mL test tubes filled with aquifer material and fitted with a fluid exchange system to allow sequential batch testing. Aquifer material was aseptically obtained from two locations at a chloroethene-contaminated Superfund site in St. Joseph, Ml. In microcosm tests, influent VC concentrations ranged from 1 to 17 mg/L (15-275 μM) with methane concentrations of 0.5-4.0 mg/L (30-250 μM) and dissolved oxygen concentrations of about 29 mg/L (900 μM). Stimulation of an active methane-utilizing population occurred within 60 days, and VC transformation was observed in all of the methane-fed microcosms. A maximum amount of VC transformation, independent of influent VC concentration, was observed for each methane concentration used. Significant differences in VC transformation ability was found in the aquifer samples from the two locations. Transformation yields (T y ) of up to 3.5 mg of VC transformed/mg of methane utilized (0.9 mol of VC/mol of CH 4 ) were found atone location compared to a maximum of 1.0 mg of VC/mg of CH 4 (0.26 mol of VC/mol of CH 4 ) at the other. Up to 16 mg/L VC (250 μM) was transformed with an addition of 4 mg/L methane (250 μM) with no significant toxic effects observed. The microcosms performed well throughout the study, providing consistent repeatable results.

Anaerobic Transformation of Chlorinated Aliphatic Hydrocarbons in a Sand Aquifer Based on Spatial Chemical Distributions

We estimated the distribution of chlorinated aliphatic hydrocarbons (CAHs) from groundwater samples collected along three transects in a sand aquifer. Trichloroethylene (TCE) leaked and contaminated the aquifer probably more than a decade before we collected the measurements. The data show significant concentrations of TCE, cis‐l,2‐dichloroethylene (c‐DCE), vinyl chloride (VC), and ethene. We attributed DCE, VC, and ethene to the reductive dehalogenation of TCE. The CAH concentrations varied significantly with depth and correlate with sulfate and methane concentrations. Anoxic aquifer conditions exist with methane present at relatively high concentrations at depth. High concentrations of TCE correspond with the absence of methane or low methane concentrations, whereas products of TCE dehalogenation are associated with higher methane concentrations and low sulfate concentrations. Indications are that the dechlorination of TCE and DCE to VC and ethene is associated with sulfate reduction and active methanogenesis. TCE dechlorination to DCE is likely occurring under the less reducing conditions of sulfate reduction, with further reductions to VC and ethene occurring under methanogenic conditions. We estimated that about 20% of TCE has dechlorinated to ethene. The analysis of the data enhanced our knowledge of natural in situ transformation and transport processes of CAHs.

The microbial growth of Mycobacterium aurum L1 on vinyl chloride with respect to inhibitory and limiting influence of substrate and oxygen

Vinyl chloride (VC) can be biodegraded aerobically by the strain Myobacterium aurum L1 to CO2 and HCl. The influence of VC and oxygen concentrations on microbial growth and VC utilization rate was examined in fed-batch experiments in a stirred tank reactor (STR) and a bubble column (BC). VC and oxygen show limiting and inhibitory effects. The kinetics can be described by a double Haldane model. The kinetic parameters were determined by a numerical optimization using the Simplex method.

Aerobic Mineralization of Trichloroethylene, Vinyl Chloride, and Aromatic Compounds by Rhodococcus Species

Two Rhodococcus strains which were isolated from a trichloroethylene (TCE)-degrading bacterial mixture and Rhodococcus rhodochrous ATCC 21197 mineralized vinyl chloride (VC) and TCE. Greater than 99.9% of a 1-mg/liter concentration of VC was degraded by cell suspensions. [1,2-C]VC was degraded by cell suspensions, with the production of greater than 66% CO(2) and 20% C-aqueous phase products and incorporation of 10% of the C into the biomass. Cultures that utilized propane as a substrate were able to mineralize greater than 28% of [1,2-C]TCE to CO(2), with approximately 40% appearing in C-aqueous phase products and another 10% of C incorporated into the biomass. VC degradation was oxygen dependent and occurred at a pH range of 5 to 10 and temperatures of 4 to 35 degrees C. Cell suspensions degraded up to 5 mg of TCE per liter and up to 40 mg of VC per liter. Propane competitively inhibited TCE degradation. Resting cell suspensions also degraded other chlorinated aliphatic hydrocarbons, such as chloroform, 1,1-dichloroethylene, and 1,1,1-trichloroethane. The isolates degraded a mixture of aromatic and chlorinated aliphatic solvents and utilized benzene, toluene, sodium benzoate, naphthalene, biphenyl, and n-alkanes ranging in size from propane to hexadecane as carbon and energy sources. The environmental isolates appeared more catabolically versatile than R. rhodochrous ATCC 21197. The data report that environmental isolates of Rhodococcus species and R. rhodochrous ATCC 21197 have the potential to degrade TCE and VC in addition to a variety of aromatic and chlorinated aliphatic compounds either individually or in mixtures.

Evaluating the Adequacy of Maximum Contaminant Levels as Health-Protective Cleanup Goals: An Analysis Based on Monte Carlo Techniques

At many sites in the United States, health-based remediation goals for contaminated groundwater have been set at levels far below USEPA′s drinking water standards (i.e., maximum contaminant levels or MCLs). This is due to the fact that, while the USEPA must often consider technical and economic factors (e.g.. cost of compliance, risk/benefit analysis) when setting MCLs for public water systems, cleanup goals for contaminated groundwater are often based solely on conservative "point" estimates of exposure. One of the more recent refinements in the risk assessment process is the use of ranges of exposure estimates or "probability density functions" (PDFs), rather than fixed point estimates, to estimate exposure and chemical uptake. This approach provides a more thorough description of the range of potential risks, rather than a single "worst-case" value, and allows one to understand the conservatism inherent in assessments based on regulatory default parameters. This paper uses a number of PDFs and the Monte Carlo technique to assess whether the USEPA′s MCLs for drinking water are sufficiently low to protect persons exposed to these levels. A case study involving daily exposure to tapwater containing MCL concentrations of tetrachloroethylene, chloroform, bromoform, and vinyl chloride is presented. Several direct and indirect exposure pathways are evaluated, including inhalation and dermal contact while showering, direct ingestion, and inhalation of emissions from household fixtures and appliances. PDFs for each exposure factor are based on the most recent and applicable data available. Our analysis indicates that the estimated increased cancer risks at the 50th and 95th percentile of exposure are within the range of increased cancer risks typically considered acceptable at Superfund sites ( 10 −4-10 −6), These results suggest that, at least for some chemicals, groundwater need not be cleanedup to concentrations less than drinking water standards (i.e., MCLs) to protect human health.

Vinyl Chloride Biodegradation with Methanotrophic Attached Films

Methanotrophic degradation of vinyl chloride (VC) is investigated using a laboratory‐scale methanotrophic attached‐film expanded‐bed (MAFEB) bioreactor. This study provides a basis for applying a microbial cometabolizing reaction to practical treatment of toxic chlorinated compounds. The MAFEB reactor was operated at 20°C with influent VC concentrations ranging from 1,800 to 9,600 μg/L and bed hydraulic retention times ranging from 3.7 to 7.6 h. VC effluent concentrations during steady continuous operation ranged from 3 to 140 μg/L, with most values less than 26 μg/L, resulting in removal efficiencies of 96.3% to 99.8%. The maximum continuous‐flow VC degradation rate observed at 20°C was 2.5 mg VC per gram volatile solids (VS) per day [2.5 mg VC/(g VS d)] or 30 mg VC per liter expanded bed per day 30mgVC/Lebd), under substrate‐limited conditions. During semibatch runs at 35°C, vinyl chloride degradation rates up to 60 mg VC/ (g VS d) or 1g/(Lebd) were observed. Degradation rates increased with temperature between 20°C and 35°C, approximately doubling every 10°C. Dissolved methane concentrations above 0.5 mg/L inhibited VC degradation, with no VC degradation observed with 8 mg/L dissolved methane. The methane consumed during VC degradation was about 40gCH4/gVC. Toxic effects were observed after prolonged exposure of the methanotrophic culture to high concentrations of VC.

Mechanism and microstructure in the free‐radical polymerization of vinyl chloride: Head‐to‐head addition revisited

AbstractThe recent realization that 1,2‐dichloroethyl branches occur in poly(vinyl chloride) (PVC) has now led to a full description of the chemical consequences of head‐to‐head addition during the free‐radical polymerization of vinyl chloride (VC). A kinetic analysis of the relevant reaction scheme is developed here and then verified with the aid of literature values for the branch concentrations of PVC samples prepared by polymerization at subsaturation VC pressures. The analysis allows the following conclusions to be drawn: (1) Kinetically free chlorine atoms are not formed from polymeric ‐CHCl‐CH‐CH2Cl or ‐CH2‐CH‐CHCl‐CH2Cl radicals. Loss of chlorine from these radicals results exclusively, instead, from β scission reactions that transfer chlorine directly to the monomer and are kinetically second‐order, overall. (2) The monomer transfer constant that pertains to the transfer occurring after head‐to‐head addition is, indeed, a true constant that is independent of the concentration of VC. (3) In conventional bulk or suspension VC polymerizations, the rates of the propagation reactions are not controlled by diffusion, even at conversions of ca. 90%. (4) A second type of monomer transfer process probably is responsible for the reductions in polymer molecular weight that result from polymerization at subsaturation VC pressures. This transfer pathway involves the inter‐ and/or intramolecular abstraction of methylene hydrogen from the polymer by the ordinary head‐to‐tail macroradicals. The resultant β‐chloroalkyl radicals then transfer chlorine to VC by β scission.

Characterization of a Mycobacterium sp. and a Xanthobacter sp. for the removal of vinyl chloride and 1,2-dichloroethane from waste gases

Mycobacterium aurum L1 and Xanthobacter autotrophicus GJ10 were characterized with respect to their potential use in the biological treatment of waste gases containing vinyl chloride (VC) and 1,2-dichloroethane (DE). VC at a concentration of 125 g m −3 in the gas phase was not toxic but DE at 22 g m −3 already resulted in a decreased growth rate. Kinetic properties of washed cells were determined and chemostat cultures were run to optimize the medium for VC removal. Using a mixed culture of the two strains, simultaneous removal and mineralization of VC and DE was demonstrated. The affinity constants of growing cells found for the two substrates are, however, significantly higher than the maximal allowable concentrations of VC and DE in waste gases.

Emulsion copolymerization of vinyl chloride with butyl acrylate

AbstractThe emulsion copolymerization of vinyl chloride and butyl acrylate initiated by ammonium peroxodisulfate at 60°C in the presence of an anionic emulsifier was investigated. Random copolymers of butyl acrylate and vinyl chloride covering several sets of monomer compositions were synthesized by emulsion copolymerization conducted to both low and high conversions. The rate of butyl acrylate polymerization at medium conversion was found to be proportional to the 0,5 and 1,0 power of the butyl acrylate concentration for the system with and without vinyl chloride. The overall rate of poymerization was found to decrease with increasing vinyl chloride concentration in the monomer feed. The particle size increases with increasing vinyl chloride monomer concentration in the monomer feed and conversion. The decrease in molecular weight of butyl acrylate/vinyl chloride copolymer is accompanied with the incease of vinyl chloride concentration in the monomer feed and of conversion. The results are discussed in terms of radical desorption, particle nucleation and the dependence of the equilibrium monomer concentration on the reactor pressure.

Carcinogens in rubber production in the Soviet Union.

In a preliminary phase of a broad research project on cancer among workers in a rubber footwear plant in Moscow, exposure to several known or potential carcinogens was assessed. There were high dust contents bearing both toxic substances and carcinogens. The highest concentrations of benzo[a]pyrene (500-14,400 micrograms) were found on the soot used as a filler, and the maximum N-dimethylnitrosamine (DMNA) level was measured in thiram (150-23,868 micrograms.kg-1). Air samples from the vulcanization process and the pressing of rubber goods showed BaP levels of up to 1.43 micrograms.m-3. In the work area where polyvinyl chloride was used, the mean vinyl chloride concentration was 0.21 (SE 0.06) mg.m-3. The mean value of the acrylonitrile concentrations in the workroom area was 0.19 (SE 0.07) mg.m-3. Very high levels of DMNA and N-diethylnitrosamine were measured in the preparatory shop in the winter.

A Field Evaluation of In‐Situ Biodegradation of Chlorinated Ethenes: Part 3, Studies of Competitive Inhibition

AbstractResults are presented that demonstrate the in‐situ biotransformation of vinyl chloride (VC), trans‐l,2‐dichloroethylene (t‐DCE), cis‐l,2‐dichloroethylene (c‐DCE), and trichloroethylene (TCE) by an enhanced population of methane‐utilizing (methanotrophic) bacteria. Biostimulation was accomplished by introducing dissolved methane and oxygen into a shallow, confined aquifer, to encourage the growth of the native methanotrophic bacteria. Biotransformation of the target compounds ensued immediately after the commencement of methane utilization, and reached steady‐state values within three weeks. The approximate extents of transformation achieved in the two meter biostimulated zone were as follows: VC, 95%; t‐DCE, 90%; c‐DCE, 50%; and TCE, 20%. The biotransformation of VC and t‐DCE was observed to be competitively inhibited by methane. Cyclic variations in methane concentration caused by the alternate pulse injection of dissolved methane into the test zone caused oscillations of the aqueous concentrations of VC and t‐DCE. When formate and methanol were substituted for methane as alternative electron donors, inhibition ceased (no oscillations), and concentrations were reduced to levels achieved during periods when no methane was present, confirming the inhibition by methane. Higher transformation rates were achieved temporarily, i.e., for several days, through the addition of formate or methanol. When electron donor addition was terminated, the concentration of target compounds rapidly increased, indicating that the transformation promptly ceased. Although these experiments indicated that methane competitively inhibits transformation rates, this competition is a second‐order effect: methane as substrate for growth was also required for transformation of VC, t‐DCE, c‐DCE, and TCE by methanotrophs.