No description available.

No description available.

A method has been developed that can photoreduce polychlorinated biphenyl (PCB) to biphenyl with great speed and efficiency as well as at relatively low cost. This process uses visible light, generated by ordinary incandescent light bulbs, which is absorbed by a common dye sensitizer. The dye molecules, when excited by the absorption of light, can promote a chemical reaction between polychlorinated biphenyls and a hydrocarbon gas such as propane. In this chemical reaction, hydrogen is abstracted from the hydrocarbon gas molecule and is substituted for chlorine on the PCB molecule in a stepwise fashion, which ultimately yields the major reaction product biphenyl. This reaction occurs in a polar aprotic solvent at room temperature and is accelerated by the presence of an alkali metal hydroxide. The final residence of the chlorine appears to be a salt which precipitates from the reaction mixture. This procedure could be applied to the treatment of PCB contaminated transformer oils, soils, and landfill leachates. / M.S.

Thesis (M.Sc.)--Memorial University of Newfoundland, 2005. / Restricted until October 2006. Bibliography: leaves 99-106.

Polychlorinated biphenyls (PCBs) are persistent organic pollutants. Due to their properties, PCBs accumulate in the food-chain and post a threat to the health of human beings and wildlife. Hydroxylated PCBs (OH-PCBs) are oxidative metabolites of PCBs and are more hydrophilic than their parent PCBs. One of the best approaches to break down these contaminants is through bioremediation, which is an environmental friendly process that uses microorganisms to restore natural environment. Towards this goal, we have investigated the toxicity and accumulation of PCBs and OH-PCBs in a Gram-negative bacterium, Escherichia coli. We have also determined the role played by a primary multidrug efflux transporter AcrB on the accumulation of PCBs and OH-PCBs in bacterial cell. We found that one of the PCBs tested was toxic to E. coli, while different OH-PCBs have different levels of toxicity; the acrB knockout strain accumulated significantly more PCBs and OH-PCBs than the wild-type strain, suggesting that these compounds are substrates of the efflux pump; higher cytoplasmic concentrations of OH-PCBs were also observed in the acrB knockout strain using the biosensors. Based on these observations, we conclude that both PCBs and OH-PCBs are substrates of protein AcrB. Therefore the efflux activities of multidrug resistant pumps in Gram-negative bacteria should be considered while designing bioremediation approaches.

Thesis (M.S. in environmental science)--Washington State University, May 2009. / Title from PDF title page (viewed on May 28, 2009). "School of Earth and Environmental Sciences." Includes bibliographical references (p. 56-63).

The research presented herein provides information on coelomocyte (leukocyte) collection, function and immunotoxicity from polychlorinated biphenyls (PCB) in the earthworm Lumbricus terrestris. Research was undertaken as part of an overall goal to develop a well-documented and scientifically valid non-mammalian surrogate immunoassay with the earthworm Lumbricus terrestris to assess immunotoxic potential of xenobiotics. The principal objectives were to: (1) Develop an extrusion model for analyzing immunotoxicity of xenobiotics; (2) determine if coelomocytes can be collected repeatedly without obvious harm to the earthworm or change in immune response of the coelomocytes harvested and (3) validate the response sensitivity profiles of a panel of biomarkers {differential and total cell counts, erythrocyte rosette (ER) and secretory rosette (SR) formation with, and phagocytosis of antigenic rabbit red blood cells} in earthworms after acute exposure to a known mammalian and L. terrestris immunotoxin, the PCB Aroclor 1254.

Polychlorinated biphenyls (PCBs) are nongenotoxic hepatic tumor promoters. PCBs have been shown to cause oxidative stress, but the exact mechanism by which PCBs exert their tumor promoting activity is not clear. In our study, PCB-153, a non-coplanar congener, caused a transient increase in hepatic NF-B DNA binding activity and cell proliferation, while PCB-77, a coplanar congener, showed no effect. Our second study using a mouse model that was deficient in the p50 subunit of NF-kB (p50-/-) showed that NF-kB contributes to the changes in hepatocyte proliferation and apoptosis in response to PCB-153 treatment: a single dose of PCB-153 increased hepatic NF-B activity and cell proliferation in wild type mice, but not in the p50-/- mice; longer-term treatment with PCB-153 increased cell proliferation in p50-/- mice, but this increase was less than that in the wild type. In addition, p50-/- livers had more apoptosis than in the wild type, and PCB-153 inhibited apoptosis in the p50-/- livers. p50-/- livers had less cyclin D1 protein than the wild type, but that the mRNA levels were same. Bcl-xL protein was not changed by PCB-153, and wild type and p50-/- mice had the same level of Bcl-xL protein. In the third study, PCB-77 caused an increase in hepatic NF-kB DNA binding activity and cell proliferation during the promotion stage, and this increase was blocked by dietary supplementation of vitamin E, but the number and volume of placental glutathione S-transferase (PGST)-positive foci were slightly, though insignificantly, increased in the same animals. The apparent conflict could be due to different effect in different cells: high level vitamin E significantly inhibited PCB-77-induced cell proliferation in normal hepatocytes, while this inhibitory effect was much less in the PGST-positive hepatocytes. In conclusion, our studies show that a non-coplanar PCB can cause an increase in hepatic NF-kB DNA binding activity in rats and mice, and this increase contributes to the change in cell proliferation and apoptosis. Dietary vitamin E supplementation did not show protective effect on the formation of altered hepatic foci that were promoted by PCBs, although vitamin E supplementation decreased PCBs-induced hepatic NF-kB activation and cell proliferation.

Chronically contaminated killifish from Newark Bay (NB) NJ, and New Bedford Harbor (NBH) MA, have developed resistance to halogenated aromatic hydrocarbons that bind to and activate the aryl hydrocarbon receptor (AHR). To study the mechanisms of resistance, adult killifish were exposed to halogenated and non-halogenated AHR ligands and enzymatic and toxicological endpoints were measured in adult and embryonic fish. The chlorinated and non-chlorinated AHR ligands 3,34,4-tetrachlorobiphenyl (PCB77) and benzo-a-pyrene (B[a]P) induced cytochrome P450 1A (CYP1A) in reference site, but not in NB killifish. Expression of CYP3A (not part of the AHR gene battery) was inducible only in Flax Pond killifish. Basal expression of the phase II enzyme glutathione-s-transferase (GST) was higher in NB killifish. These results suggest that NB killifish are resistant to CYP1A induction by chlorinated and non-chlorinated AHR ligands. Higher basal GST activity observed in NB killifish could be protective against toxicity caused by contaminants found in this site. Activation of AHR and induction of CYP1A, by AHR ligands has been associated with the toxic effects caused by these chemicals. To determine the association between resistance to CYP1A induction and the toxicity caused by AHR ligands, CYP1A activity, developmental deformities and reactive oxygen species (ROS) production were measured in reference site and contaminated (NB and NBH) killifish embryos exposed to AHR ligands. 3,34,45-pentachlorobiphenyl (PCB126) and 3-methylcholantherene (3-MC) induced CYP1A, and ROS production in reference site embryos. NB and NBH embryos were resistant to PCB126 induction of CYP1A, but responded to 3-MC. Killifish embryos from NB and NBH were resistant to PCB126 induced deformities. PCB126 and 3-MC did not increase ROS production in NB or NBH killifish embryos. Alpha-naphthoflavone (ANF) (an AHR/CYP1A inhibitor) blocked PCB126 mediated deformities and CYP1A induction in reference site embryos, but increased ROS production. The P450 inhibitor, piperonyl butoxide (PBO) was able to block PCB126 mediated induction of CYP1A activity and ROS production. These results suggest that PCB126 induced deformities are dependent on activation of AHR and CYP1A induction. In chronically contaminated killifish populations, loss of sensitivity to coplanar PCBs and PAHs could be through reduced expression of AHR, or altered DNA sequence or methylation status of the CYP1A gene promoter. Hepatic AHR expression, measured by photoaffinity labeling, was lower in NB killifish than reference site animals, suggesting that NB killifish express less AHR protein. DNA sequence analysis did not reveal considerable differences between contaminated and reference site populations, however additional DNA fragments were observed in some promoters but not in others. The methylation of the CYP1A promoters was studied using methylation sensitive restriction enzymes and no differences were detected between reference site and NB killifish. Treatment with the DNA methyltransferase inhibitor AzaC did not restore CYP1A induction by PCB126 in NB killifish. These studies suggest that resistance to activation of AHR and induction of xenobiotic activating enzymes (CYP1A and CYP3A) in combination with increased expression of conjugating enzymes (GST) protects chronically contaminated killifish against these chemicals.

PCBs are among the most problematic marine contaminants. Converging towards the oceans via the rivers and the atmosphere, they concentrate in sediments where they become a permanent threat to organisms living at their contact. PCBs are extremely resistant, bioaccumulated and some congeners are considered as highly toxic. The North Sea is considered as a highly contaminated area ; however little information is available regarding the impact of PCBs on key benthic organisms of this region. Ubiquist, abundant and generally recognized as a good bioindicator species, the common NE Atlantic sea star Asterias rubens (L.) is an ecosystem-structuring species in the North Sea and was chosen as an experimental model. The present study focused on the characterization of PCB bioaccumulation in A. rubens exposed through different routes (seawater, food, sediments) and on subsequent biological responses, at immune and sucellular levels. The considered responses were respectively (i) the production of reactive oxyggen species (ROS) by sea stars amoebocytes, which constitutes the main line of defence of echinoderms against pathogenic challenges and (ii) the induction of a cytochrome P450 immunopositive protein (CYP1A IPP) which, in vertebrates, is involved in PCB detoxification. Experimental exposures carried out have shown that A. rubens efficiently accumulates PCBs. Exposure concentrations were always adjusted to match those encountered in the field. PCB concentrations reached in sea stars during the experiments matched the values reported in field studies ; therefore our experimental protocol was found to accurately simulate actual field situations. Uptake kinetics were related to the planar conformation of the considered congeners : non-coplanar PCB uptake was described using saturation models, whereas coplanar PCBs (c-PCBs) were bioaccumulated according to bell-shaped kinetics. Non-coplanar congeners generally reached saturation concentrations whithin a few days or a few weeks, which means that sea stars can be used to pinpoint PCB contamination shortly after occurrence. On the other hand, c-PCB concentrations reached a peak followed by a sudden drop, indicating the probable occurrence of c-PCB-targeted metabolization processes in sea stars. Our experimental studies also demonstrated that seawater was by far the most efficient route for PCB uptake in sea stars and that even if PCB levels in seawater are extremely low compared to sediment-associated concentrations, seawater constitutes a non-negligible route for PCB uptake in marine invertebrates. Among the different body compartments, bodywall displayed the highest bioaccumulative potency and can therefore be considered as particularly interesting for field biomonitoring applications. Rectal caeca, which play a central role in digestion and excretion processes in sea stars, have also rised particular interest as results suggest these organs could be involved in the elimination of PCB 77 degradation products. The field work carried out during the present study showed that PCB concentrations measured in A. rubens tissues reflect environmental levels of certain congeners. As it was the case in experimental conditions, A. rubens differentially accumulated PCB congeners according to their planarity. Strong relationships were found between concentrations measured in sediments and those determined in sea stars body wall for certain non-coplanar congeners (e.g. 118 and 138), thus allowing to consider A. rubens as a suitable bioindicator species for medium-chlorinated PCB congeners. On the other hand, sea stars appeared to be able to regulate -to a certain extent- their content in coplanar PCBs. This implies that (i) A. rubens cannot be strictly considered as an indicator organism for c-PCBs and (ii) c-PCBs probably affect essential aspects of sea star biology, potentially leading to deleterious effects. The present study addressed effects of PCB exposure on A. rubens biology, in both experimental and field conditions. In experimental conditions, PCBs were found to significantly alter ROS production by sea stars amoebocytes. This alteration also occurred in a congener-specific way : c-PCBs were found to significantly affect, and probably impair sea stars immune system, whereas non-coplanar congeners had no effect. In the field, the PCB contribution to immunotoxicity could not be determined because none of our studies considered ROS production along with c-PCB concentration measurements. However, the levels of ROS production by sea stars amoebocytes measured in field and experimental conditions were found to potentially lead to altered immunity, and therefore to impair sea stars defence against pathogenic agents. A specially designed ELISA was used to measure CYP1A IPP in experimental and field conditions. Experimental work has shown that the induction of this protein was related to PCB exposure in a congener-specific fashion : c-PCBs alone were found to strongly induce the production of CYP1A IPP according to a dose-dependent relationship. These results have highlighted many similarities between the dioxin-like responsiveness of CYP1A IPP induction in sea stars and that occurring in vertebrates. This strongly suggests similarities in the toxicity-triggering mechanism of dioxins and c-PCBs. In the field, CYP1A IPP induction was found to be significantly related to PCB levels determined in bottom sediments. It can thus be considered as a valuable biomarker. Further research is however needed to better characterize the influence of physico-chemical and physiological parameters on CYP1A induction to refine the interpretation of the information gathered via this biomarker. Results obtained in our study have lead to questionning international regulations applying to PCB biomonitoring in the marine environment. For instance, we strongly suggest that the selection of congeners to be systematically considered should be revised to include c-PCBs. Indeed, in our experiments PCB toxicity was almost always attributable to the sole c-congeners. Historically, determination of c-PCB concentrations was extremely difficult due to analytical limitations ; however, nowadays, these problems have been overcome and do no more justify their exclusion from monitoring studies. Although A. rubens appeared to be quite resistant to PCB contamination, levels measured in sea stars from the southern North Sea can possibly affect their immune and endocrine systems in a subtle way, but with relatively low risk for this species at the short-term. However, this does not mean that other species in this region undergo similarly low risks, or that sea star-structured ecosystems may not become affected in the long-term