Synthesis of poly vinyl chloride/chlorinated polypropylene-active natural substance derivatives for potential packaging materials application. Tannic acid, menthol and lipoic acid.

A novel one step route for the synthesis of tannic acid, lipoic acid and menthol functionalized polyvinyl chloride, PVC, (PVC-Tann, PVC-Lip, PVC-Mnt) and chlorinated polypropylene, PP-Cl, (PP-Mnt, PP-Lip) was applied imparting antioxidative properties to the newly-formed materials. The resulting modified polymers were characterized by stress-strain mechanical measurement, 1H NMR, gel permeation chromatography (GPC) and thermogravimetric (TGA) analysis. Linseed oil, owing to its high linolenic acid content, was used to track the autoxidation process. The chloride functional groups were reacted with the hydroxyl/carboxylic acid of the natural compounds in the presence of a base. Linseed oil was poured into the natural compound functionalized PVC covered Petri dish to undergo autoxidation under white light. Each of the PVC- and PP-Cl-based polymers was active in delaying autoxidation. The PP-Mnt series and PP-Lip polymers all delayed autoxidation by 8 days over the PP-Cl precursor material. The autoxidation process was further confirmed by monitoring peroxide formation in the exposed linseed oil samples through differential scanning calorimeter (DSC) analysis.

Curcuma longa L. Rhizome Extract as a Poly(vinyl chloride)/Graphene Nanocomposite Green Modifier.

In this work, a method to increase the dispersion of graphene (GN) in the matrix of rigid poly(vinyl chloride) (PVC) by using a natural plant extract from Curcuma longa L. (CE) is proposed. Currently, despite the increasing number of reports on the improvement of GN dispersion in PVC blends, still there is a need to find environmentally friendly and economical dispersion stabilizers. We proposed a stabilizer that can be easily obtained from a plant offering thermal stability and high effectiveness. PVC/GN nanocomposites stabilized with the proposed extract were investigated by SEM, AFM (structure), TGA, and Congo red test (thermal properties). Additionally, static and dynamic mechanical properties and electrical resistivity were measured. The use of CE as a graphene dispersant improved its dispersion in the PVC matrix, influenced tensile properties, increased the storage modulus and glass transition temperature, and extended the thermal stability time of nanocomposites. In this work, a CE extract is proposed as an efficient eco-friendly additive for the production of nanocomposites with an improved homogeneity of a nanofiller in the matrix and promising characteristics.

Effects of ferrous iron supplementation on reductive dechlorination of tetrachloroethene and on methanogenic microbial community.

Chloroethenes are common soil and groundwater pollutants. Their dechlorination is impacted by environmental factors, such as the presence of metal ions. We here investigated the effect of ferrous iron on bacterial reductive dechlorination of chloroethenes and on methanogen community. Reductive dechlorination of tetrachloroethene was assayed with a groundwater sample originally containing 6.3 × 103 copies mL-1 of Dehalococcoides 16S rRNA gene and 2 mg L-1 of iron. Supplementation with 28 mg L-1 of ferrous iron enhanced the reductive dechlorination of cis-dichloroethene (cis-DCE) and vinyl chloride in the presence of methanogens. The supplementation shortened the time required for complete dechlorination of 1 mg L-1 of tetrachloroethene to ethene and ethane from 84 to 49 d. Methanogens, such as Candidatus 'Methanogranum', Methanomethylovorans and Methanocorpusculum, were significantly more abundant in iron-supplemented cultures than in non-supplemented cultures (P < 0.01). Upon methanogen growth inhibition by 2-bromoethanesulfonate and in the absence of iron supplementation, cis-DCE was not dechlorinated. Further, iron supplementation induced 71.3% dechlorination of cis-DCE accompanied by an increase in Dehalococcoides 16S rRNA and dehalogenase vcrA gene copies but not dehalogenase tceA gene copies. These observations highlight the cooperative effect of iron and methanogens on the reductive dechlorination of chloroethenes by Dehalococcoides spp.

Sustained Dechlorination of Vinyl Chloride to Ethene in Dehalococcoides-Enriched Cultures Grown without Addition of Exogenous Vitamins and at Low pH.

Trichloroethene (TCE) bioremediation has been demonstrated at field sites using microbial cultures harboring TCE-respiring Dehalococcoides whose growth is cobalamin (vitamin B12)-dependent. Bioaugmentation cultures grown ex situ with ample exogenous vitamins and at neutral pH may become vitamin-limited or inhibited by acidic pH once injected into field sites, resulting in incomplete TCE dechlorination and accumulation of vinyl chloride (VC). Here, we report growth of the Dehalococcoides-containing bioaugmentation culture KB-1 in a TCE-amended mineral medium devoid of vitamins and in a VC-amended mineral medium at low pH (6.0 and 5.5). In these cultures, Acetobacterium, which can synthesize 5,6-dimethylbenzimidazole (DMB), the lower ligand of cobalamin, and Sporomusa are dominant acetogens. At neutral pH, Acetobacterium supports complete TCE dechlorination by Dehalococcoides at millimolar levels with a substantial increase in cobalamin (∼20-fold). Sustained dechlorination of VC to ethene was achieved at pH as low as 5.5. Below pH 5.0, dechlorination was not stimulated by DMB supplementation but was restored by raising pH to neutral. Cell-extract assays revealed that vinyl chloride reductase activity declines significantly below pH 6.0 and is undetectable below pH 5.0. This study highlights the importance of cobamide-producing populations and pH in microbial dechlorinating communities for successful bioremediation at field sites.

Role of dietary fatty acids in liver injury caused by vinyl chloride metabolites in mice.

BACKGROUND: Vinyl chloride (VC) causes toxicant-associated steatohepatitis at high exposure levels. Recent work by this group suggests that underlying liver disease may predispose the liver to VC hepatotoxicity at lower exposure levels. The most common form of underlying liver disease in the developed world is non-alcoholic fatty liver disease (NAFLD). It is well-known that the type of dietary fat can play an important role in the pathogenesis of NAFLD. However, whether the combination of dietary fat and VC/metabolites promotes liver injury has not been studied. METHODS: Mice were administered chloroethanol (CE - a VC metabolite) or vehicle once, 10weeks after being fed diets rich in saturated fatty acids (HSFA), rich in poly-unsaturated fatty acids (HPUFA), or the respective low-fat control diets (LSFA; LPUFA). RESULTS: In control mice, chloroethanol caused no detectable liver injury, as determined by plasma transaminases and histologic indices of damage. In HSFA-fed mice, chloroethanol increased HSFA-induced liver damage, steatosis, infiltrating inflammatory cells, hepatic expression of proinflammatory cytokines, and markers of endoplasmic reticulum (ER) stress. Moreover, markers of inflammasome activation were increased, while markers of inflammasome inhibition were downregulated. In mice fed HPUFA all of these effects were significantly attenuated. CONCLUSIONS: Chloroethanol promotes inflammatory liver injury caused by dietary fatty acids. This effect is far more exacerbated with saturated fat, versus poly-unsaturated fat; and strongly correlates with a robust activation of the NLRP3 inflammasome in the saturated fed animals only. Taken together these data support the hypothesis that environmental toxicant exposure can exacerbate the severity of NAFLD/NASH.

Assessment of urinary thiodiglycolic acid exposure in school-aged children in the vicinity of a petrochemical complex in central Taiwan.

BACKGROUND: School-aged children living in the vicinity of vinyl chloride (VCM)/polyvinyl chloride (PVC) factories may have an increased risk of exposure to hazardous air pollutants. OBJECTIVES: We aimed to evaluate the urinary thiodiglycolic acid (TDGA) level, as TDGA is a major metabolite of VCM, for students at elementary schools near a petrochemical complex in central Taiwan. METHODS: We recruited 343 students from 5 elementary schools based on distance to the VCM/PVC factory. First-morning urine and blood samples were obtained from our subjects from October 2013 to September 2014. Urine samples were analyzed for urinary creatinine and TDGA using LC/MS-MS. Hepatitis virus infection were assessed using blood samples. We determined their vitamin consumption, resident location, parent's employment, and other demographic or lifestyle characteristics using a questionnaire. RESULTS: Median urinary TDGA levels for 316 students at 5 elementary schools from the closest (<.9km) to the farthest (∼8.6km) with respect to the petrochemical complex were 147.6, 95.5, 115.5, 86.8, and 17.3µg/g creatinine, respectively. After adjusting for age, gender, hepatitis virus infection, vitamin B consumption, passive smoking, and home to source distance, we found that urinary TDGA levels for the closest students was significantly higher than those at other schools. Further, median urinary TDGA levels for students during school time were 4.1-fold higher than those during summer vacation. CONCLUSIONS: After adjusting for confounders, urinary TDGA levels for the school-aged children decreased with increasing distances between the elementary schools and the petrochemical complex.

Catalytic destruction of vinyl chloride over an alumina-supported platinum catalyst.

In this study, vinyl chloride (VC), the primary material for manufacturing polyvinyl chloride (PVC), is decomposed via catalytic oxidation (C-OX) using Pt/γ-Al2O3 catalyst. The effects of related major factors such as reaction temperature (T) and gas hourly space velocity on the conversion of VC (X) were examined. The values of T for achieving conversions of 50% and 90% are 504 and 580 K with C-OX, respectively, whereas those without Pt/γ-Al2O3 (i.e., thermal oxidation, T-OX) are 900 and 983 K, respectively, thus indicating that C-OX significantly reduces T for effective oxidation of VC to form CO2, HCl, and Cl2 when compared with T-OX. The mineralizations of carbon in VC to form CO2 are 75.5% and 38% for C-OX and T-OX, respectively, at 90% X. The conversions of chlorine atom in 1,2-dichloroenane (DCEA) to Cl in HCl and Cl2 are approximately 42% and 50.8% for C-OX and T-OX, respectively, at 90% X. These results indicate that the Pt/γ-Al2O3 catalyst exhibits remarkable performance for the mineralizations to form CO2 even though a proportion of chlorine atoms are adsorbed on the Pt surface. The Eley-Rideal model can be used to describe the experimental results, thus yielding activation energy and frequency factor values of 49.0 kJ mol(-1) and 1.77 × 10(6) s(-1), respectively. The obtained information and kinetic parameters are useful for the rational design and operation of C-OX process for the abatement of VC.

Vinyl chloride monomer (VCM) induces high occurrence of neural tube defects in embryonic mouse brain during neurulation.

The aim of this study was to explore the direct embryonic teratogenicity of vinyl chloride monomer (VCM), especially the toxic effects on the early development of the nervous system and its underlying mechanisms. Pregnant mice at embryonic day 6.5 (E6.5) were injected with different doses of VCM (200, 400 and 600 mg/kg) and embryos were harvested at E10.5. Our results showed that doses higher than 400 mg/kg of VCM increased the incidence of malformed embryos, especially the neural tube defects (NTDs). In addition, high-dose of VCM decreased mitotic figure counts in the neuroepithelium and enhanced the percentage of cells in G0/G1 phase, while they were reduced in S phase. The more VCM was injected into mice, the fewer positive PCNA cells were seen and the more positive TUNEL cells were observed in the neuroepithelium. Moreover, significant increases in the levels of caspase-3 protein were observed in NTD embryos. Our results demonstrate that during early pregnancy, exposure to doses higher than 400 mg/kg of VCM increases the incidence of malformations and particularly the rate of NTDs. High-dose of VCM inhibits the proliferation of neural cells and induces cell apoptosis, leading to an imbalance in the ratio of proliferation and apoptosis. Meanwhile, the apoptosis of neuroepithelial cells might be accelerated by the activation of the caspase-3 pathway, and it might be a reason for NTDs.

Harnessing microbial activities for environmental cleanup.

Human activities have released large amounts of toxic organic and inorganic chemicals into the environment. Toxic waste streams threaten dwindling drinking water supplies and impact terrestrial, estuarine and marine ecosystems. Cleanup is technically challenging and the costs based on traditional technologies are exceeding the economic capabilities of even the richest countries. Recent advances in our understanding of the microbiology contributing to contaminant transformation and detoxification has led to successful field demonstrations. Hence, harnessing the activity of naturally occurring bacteria, particularly the power of anaerobic reductive processes, is a promising approach to restore contaminated subsurface environments, protect drinking water reservoirs and to safeguard ecosystem health.

Factors that contribute to biomarker responses in humans including a study in individuals taking Vitamin C supplementation.

It is possible in many situations to identify humans exposed to potentially toxic materials in the workplace and in the environment. As in most human studies, there tends to be a high degree of interindividual variability in response to chemical insults. Some non-exposed control individuals exhibit as high a level of damage as some exposed individuals and some of these have levels of damage as low as many of the controls. Thus, it is only the mean values of the groups that can substantiate an exposure-related problem; the data on an individual basis are still of limited use. While human lymphocytes remain the most popular cell type for monitoring purposes, sperm, buccal, nasal, epithelial and placental cells are also used. However, for interpretation of responses, the issue of confounding factors must be addressed. There are endogenous confounding factors, such as age, gender, and genetic make-up and exogenous ones, including lifestyle habits (smoking, drinking, etc.) There are biomarkers of exposure, effect/response and susceptibility and the last may be influenced by the genotype and polymorphism genes existing in a population. From our own studies, confounding effects on cytogenetic damage and ras oncoproteins will be considered in relation to workers exposed to vinyl chloride and petroleum emissions and to volunteers taking Vitamin C supplementation. Smoking history, exposure and duration of employment affected the worker studies. For petroleum emissions, so did gender and season of exposure. For the non-smoking volunteer Vitamin C supplementation study, cholesterol levels, plasma Vitamin C levels, lipid peroxidation products and DNA damage in the Comet assay were also measured. Gender affected differences in Vitamin C levels, antioxidant capacity and the number of chromosome aberrations induced by bleomycin challenge in vitro. The results were the same for both high and low cholesterol subjects. The relationship between biomarkers and the various factors which affect them is complex. Sometimes the variables are not completely independent of each other.

Factors contributing to biomarker responses in exposed workers.

"...[Th]e proper study of mankind is man" (Pope, circa 1733/1734). Human monitoring fits this notion and monitoring after exposure to genotoxic agents is now an established discipline. It is possible in many situations to identify humans exposed to potentially toxic materials in the workplace and the environment. Responses are often measured in peripheral lymphocytes because these cells can be acquired by a generally socially and ethically acceptable, minimally invasive route. In the early 1960s, chromosome damage in these cells was one of the first endpoints to be used as a biomarker and benzene was one of the first chemicals investigated. Although a causal relationship between chromosome damage and cancer has not been proven, it has been suggested to have some prognostic significance for future cancer onset. With other genetic biomarkers this is as yet not the case, but there are now many biomarkers for different areas of toxicology. Other well-established genetic biomarkers include the detection of hprt mutations, micronuclei and sister chromatid exchanges. However, for interpretation of responses, the issue of confounding factors must be addressed. As in most human studies, there tends to be a high degree of interindividual variability in response to chemical insults. Some non-exposed control individuals exhibit as high a level of damage as some exposed individuals and some of these have levels of damage as low as many of the controls. Thus, it is only the mean values of the groups that can substantiate an exposure related-problem; the data on an individual basis are still of limited use. While human lymphocytes remain the most popular cell type for monitoring purposes, sperm, buccal, nasal, epithelial and placental cells are also used. Confounding factors affect responses in all cell types. There are endogenous confounding factors such as age, sex, genetic make-up and exogenous confounding factors including lifestyle habits such as smoking, drinking, etc. There are biomarkers of exposure, effect and susceptibility and the last may be influenced by the genotype and polymorphism genes existing in a population. From our own studies, confounding effects will be considered in relation to workers exposed to vinyl chloride and petroleum emissions. The relationship between the biomarkers and various factors which influence them is complex. Sometimes the variables are not completely independent of one another.

Oligomers in plastics packaging. Part 1: Migration tests for vinyl chloride tetramer.

Vinyl chloride (VC) tetramer has been studied as a representative oligomer that has the potential for migration from plastics packaging. Poly(vinyl chloride) (PVC) bottles for retail beverages were analysed by a process of dissolution followed by gas chromatography. Tetramer levels ranged from 70 to 190 mg/kg in the plastic. When these bottles were tested for migration into the simulants distilled water, 3% acetic acid, 15% ethanol and olive oil, no tetramer migration was detected at a limit of 5-10 micrograms/kg. Since, of the low molecular weight oligomers, the tetramer had the highest concentration in the PVC plastics, it is concluded that the other VC oligomers of higher molecular weight, would not migrate above this limit of detection either.

Characterization of an H2-utilizing enrichment culture that reductively dechlorinates tetrachloroethene to vinyl chloride and ethene in the absence of methanogenesis and acetogenesis.

We have been studying an anaerobic enrichment culture which, by using methanol as an electron donor, dechlorinates tetrachloroethene (PCE) to vinyl chloride and ethene. Our previous results indicated that H2 was the direct electron donor for rductive dechlorination of PCE by the methanol-PCE culture. Most-probable-number counts performed on this culture indicated low numbers (< or equal to 10(4)/ml)) of methanogens and PCE dechlorinators using methanol and high numbers (> or equal to 10(6)/ml)) of sulfidogens, methanol-utilizing acetogens, fermentative heterotrophs, and PCE dechlorinators using H2. An anaerobic H2-PCE enrichment culture was derived from a 10(-6) dilution of the methanol-PCE culture. This H2-PCE culture used PCE at increasing rates over time when transferred to fresh medium and could be transferred indefinitely with H2 as the electron donor for the PCE dechlorination, indicating that H2-PCE can serve as an electron donor-acceptor pair for energy conservation and growth. Sustained PCE dechlorination by this culture was supported by supplementation with 0.05 mg of vitamin B12 per liter, 25% (vol/vol) anaerobic digestor sludge supernatant, and 2 mM acetate, which presumably served as a carbon source. Neither methanol nor acetate could serve as an electron donor for dechlorination by the H2-PCE culture, and it did not produce CH4 or acetate from H2-CO2 or methanol, indicating the absence of methanogenic and acetogenic bacteria. Microscopic observatios of the pruified H2-PCE culture showed only two major morphotypes: irregular cocci and small rods.

Immunoaffinity clean-up combined with 32P-postlabelling analysis of 1,N6-ethenoadenine and 3,N4-ethenocytosine in DNA.

Immunoaffinity gels able to bind 1,N6-ethenodeoxyadenosine 3'-monophosphate (3'-epsilon dAMP) and 3,N4-ethenodeoxycytidine 3'-monophosphate (3'-epsilon dCMP) were prepared. These gels retained their specific binding capacity for 3'-epsilon dAMP or 3'-epsilon dCMP in the presence of a large excess (> 2 mg per column) of unmodified 3'-deoxynucleotide monophosphates. 3'-epsilon dAMP and 3'-epsilon dCMP were 32P-postlabelled in the presence of [gamma-32P]ATP and T4 polynucleotide kinase to give either 3',5'-[5'-32P]-bisphosphates or 5'-[32P]monophosphates. 3',5'-[5'-32P]Bisphosphates were recovered from the labelling mixture by immunoprecipitation and quantitated by Cerenkov counting (method A). The detection limit of this procedure was 1 fmol with an efficiency of 80% for both ethenonucleotides. Alternatively, 5'-[32P]epsilon dAMP and 5'-[32P]epsilon dCMP were analysed by two-dimensional TLC on PEI cellulose and autoradiography (method B). The detection limit of method B was 50 amol of ethenonucleotide. Methods A and B are complementary and can quantify the formation and repair of 3'-epsilon dAMP and 3'-epsilon dCMP in DNA from rats exposed to a low level of vinyl chloride.

[Scleroderma and scleroderma-like diseases caused by environmental pollutants]. / Sklerodermie und Sklerodermie-ähnliche Erkrankungen durch Umweltsubstanzen.

For the stimulation of research on scleroderma and the prophylaxis of occupational scleroderma-like diseases and the prevention of iatrogenic injuries, respect., it is important to know the inducing environmental substances. Plastics (vinyl chloride, epoxy resins), solvents (chlorinated, aromatic and aliphatic hydrocarbons), drugs (bleomycin, pentazocine), cocaine (abuse) and contaminated rapeseed oil are more or less able to induce scleroderma-like diseases. Vinyl chloride disease is the best known among these. The toxic oil syndrome represents the most inglorious example of the recent time. Paraffin and silicon can act as adjuvants and induce a progressive systemic sclerosis. In our studies it could be shown, that silica is able to induce not only a silicosis, but also a true progressive systemic sclerosis after long term exposure. Acknowledgment of such cases as an occupational disease is justified and regulated by law in the German Democratic Republic.

Migration from packaging materials into foodstuffs--a need for more fundamental information.

During recent years considerable legislative attention has been focused on food packaging materials, especially plastics, and in a number of countries extensive legislation has been formulated. Such legislation often takes the form of a positive list of permitted substances accompanied either by compositional limits or migration limits in foods or stimulant liquids. In the UK this approach has not been followed owing to the general lack of fundamental information on which to base such a system. Instead, the UK has opted for a basic legislative framework supported by informal controls which rely to a large extent on close co-operation between Industry and Government. It is recognized, however, that in future years there is likely to be a move towards more extensive legislation on packaging materials in the UK, particularly as a result of the EEC's harmonization programme. It is imperative that any future legislation is placed on a sound scientific footing and affords adequate protection for the consumer. The Government of the UK is, therefore, currently sponsoring a number of studies aimed at providing this necessary basic information.

Epidemiology of brain tumours in man and their relationship with chemical agents.

The 2000 or so deaths that result each year in England and Wales from brain tumours, as defined by ICD 191, represent approximately 0.3-0.4% of all deaths, with a slightly greater incidence in men than in women. Because of the low incidence of mortality from other causes in childhood, brain cancer accounts for 3.5% of all deaths in the 1-14-year age group. Mortality from brain cancer increased considerably between 1931 and 1961 but this is probably explained by changes in disease classification and improvements in diagnostic techniques. Because of the relatively low incidence of brain cancer in man, cohort studies need to be large in order to accrue sufficient cases for meaningful interpretation. Large cohort studies may run the risk of diluting a high-risk group of workers with lesser or non-exposed individuals. These considerations have encouraged the investigation of brain cancer by case-control studies and the interpretation of these must take into account possible sources of bias. At present the evidence for any chemical causation of brain cancer in man is inconclusive.

Extrapolation of the evidence on teratogenicity of chemicals between humans and experimental animals: chemicals other than drugs.

Epidemiologic literature regarding the possible association between malformations and 23 exposures or occupations other than pharmaceutical products, was analysed. The qualitative level of scientific evidence was classified into four categories: high (ethanol, methylmercury, PCBs, laboratory work), limited (anesthetic gases, carbon monoxide), low (hexachlorophene, LSD, nitrous oxide, smelter work, tobacco), and inadequate (all other exposures). Human data for exposures belonging to categories "high" and "limited" were quantitatively compared to results of animal teratogenicity tests of the relevant chemicals. Ethanol, methylmercury, and PCBs have caused malformations in experimental animals, and the effective doses have ranged from 0.2 to 8.0 times the effective human doses. Ethanol and PCBs caused similar types of lesions in some animal species as have been observed in humans.