Water resources in South Africa are scarce, and should therefore be protected against pollutants, also from persistent organic pollutants (POPs). This is emphasised by the Stockholm Convention on POPs, which aims at reducing and ultimately eliminating POPs. South Africa signed and ratified the treaty, and it became international law on 17 May 2004. POPS are highly stable, toxic, hydrophobic and lipophilic compounds, with the ability to accumulate in biological tissues. Previous research had shown that dioxin-like POPS are present in the aquatic environments of South Africa, with the highest concentrations of these substances measured in industrialised areas of South Africa. The present study aimed at investigating the extent of polychlorinated dibenzo-para-dioxin (PCDD), polychlorinated dibenzo-furan (PCDF) and polychlorinated biphenyl (PCB) pollution in the Vaal Triangle, by targeting aquatic sediments and biota. Sediment samples were collected from the Blesbok Spruit, Taaibos Spruit, Leeu Spruit and Suikerbosrand River, and fish tissue samples were collected from Blesbok Spruit and Suikerbosrand River, to determine bio-accumulation. The samples were extracted with organic solvents, cleaned-up and fractionated. Raw extracts and fractions were analysed with the H4IIE-luc reporter gene bio-assay. This bio-assay is a rapid, sensitive and relatively cost-effective method, which measures the effects of dioxin-like compounds on rat hepatoma cells, transfected with firefly luciferase gene. Selected samples were analysed with gas chromatographylmass spectrometry (GCIMS) to confirm results. Only one site had quantifiable amounts of dioxin-like substances in the sediment, measured to be 52.35 ng/kg [Effective Concentration 50 (EC 50)]. This value exceeds many of the European and USA quality guidelines, proposed for sediments. No dioxin-like substances were found in fish tissues. The absence of PCDD/Fs and PCBs in aquatic sediments and fish tissues from the Vaal Triangle area might be due to the climatic conditions of the area, dilution effects in streams, and degradation of these compounds by UV-radiation and microbial organisms. / Thesis (M. Environmental Science (Water Science))--North-West University, Potchefstroom Campus, 2007.

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

The metabolism and distribution of three commonly occurring PCB congeners, 4,4'-dichlorobiphenyl (4-DCB), 2,2',3,3',6,6'-hexachlorobiphenyl (236-HCB) and 2,2',4,4',5,5'-hexachlorobiphenyl (245-HCB), each displaying different structural features, were investigated at their principal metabolic site, the hepatocyte. Hepatocytes, isolated from male Sprague-Dawley rats (200-250 g) by collagenase perfusion, were suspended in medium 199 and maintained at 37°C in a gyratory shaker. The radiolabeled ¹⁴C-PCB congeners were added to the hepatocyte suspensions as a DMSO-albumin mixture. Each congener was rapidly taken up by the cells with less than 10% of the congener remaining in the medium. The congeners accumulated within the hepatocytes without being fully metabolized. Metabolism followed first order Michaelis-Menten kinetics for 20 min and plateaued by 90 min at which point only 32% of 4-DCB (0.01-100 uM) and 60% of 236-HCB (0.01-100 uM) was metabolized, while 245-HCB (0.1-200 uM) was not metabolized. Readdition of congener once metabolism had plateaued resulted in a reinitiation of metabolism with the same proportion of metabolites produced indicating that product inhibition was not the cause for the plateau. A partitioning of the PCB congeners within subcellular compartments and binding to cytosolic proteins influenced the extent of metabolism by decreasing the availability of congener for the drug metabolizing enzymes, cytochrome P-450. Spectral binding studies further revealed that the ability of a PCB congener to bind to the cytochrome P-450 system correlated with the extent of metabolism observed, with 236-HCB 4-DCB 245-HCB. The metabolic potential of the PCB congeners was influenced by both the affinity of the congener for cytochrome P-450 and the partitioning of congener within the hepatocyte, and not by product inhibition.

All major pollution incidents in contemporary Japan have spawned victims' protest movements. This dissertation is a case study of one such movement which emerged in the late 1960s among thousands of persons poisoned by polychlorinated biphenyls (PCBs) that had accidentally leaked into their cooking oil. The study describes the evolution of victims' response to the disaster, beginning with the initial outbreak of symptoms, their efforts to uncover the cause of these symptoms and to receive appropriate medical treatment, and their organization of a movement to seek redress in the form of an apology from the manufacturer of the oil, reform by industry and government, and compensation. Victims utilized a variety of tactics before finally resorting to litigation in attempts to achieve their goals. Theirs was the largest pollution case ever tried in Japan. The final section of the study focuses on a major leader of the victims' movement, Kamino Ryuzo. A spokesman for the victims, Kamino, a retired miner and Christian convert, became a kind of anti-pollution ideologue. An account of his intellectual and religious odyssey and of the unique tactics forged by his family to cope with their predicament provides a perspective on victims' movements not found elsewhere. The study concludes that victims became their own advocates only after the government and industry failed to accept responsibility for pollution; that the victims went to court only reluctantly after all other avenues for redress were closed to them; and that, although they won their case, they felt it was a Pyrrhic victory, because they failed to attain all their goals, such as reform of industrial policy. Research is based on participation-observation, interviews, written materials produced by pollution victims and their supporters, and published newspaper accounts.

Polychlorinated Biphenyls (PCBs) are hazardous and toxic chemicals to both humans and animals. In the late 1960’s PCBs were discovered to be a harmful pollutant which could cause environmental contamination due to its slow degradation and even trace amounts of PCBs were regarded as toxic to both human and animals. Oil spills are a frequent occurrence at Eskom substations which could contain PCBs. The contaminated sediments which are easily carried away by rain and wind can further contaminate the environment and aquatic bodies. Eskom currently disposes of soil and ballast stones contaminated with PCBs by thermal destruction. This is a costly process as PCBs are regarded as hazardous materials and needs to be safely transported and disposed of at a licensed disposal facility. Based on literature, ozone has been used on a laboratory scale to treat soil contaminated with PCBs with the addition of chemicals such as hexane and acetone which assist in breaking down PCBs. The objective of this study was to evaluate whether ozone without the addition of chemicals could reduce the levels of PCBs present in contaminated soil. In this study, two soil samples and one ballast stone sample were contaminated with 50 ppm, 200 ppm and 600 ppm of PCBs and then exposed to 0.4, 0.5 and 0.6 l/min of ozone for a period of 60 minutes to examine the effects of increasing ozone flow rates on PCB destruction in soil. The results of the experimental tests showed that ozone gas reduced the concentration of PCBs in the soil and ballast stone samples for the different total gas flow rates. The literature study identified that the final products of the ozonation of PCBs are carbon dioxide and water and that any products formed after this process could possibly be degraded by the soil natural microorganisms. Calculations based on the Shin et al. (2004) model proved that ozone was in excess after the ozonation process. The results of the experiments also confirmed this, as the PCB residuals were similar for all three total gas flows, which showed that there was no dependence on the gas flow rates hence, ozone was in excess. The experimental data was then trended with zero, first and second order reaction equations, which showed that the best fit was obtained with the firstorder reaction equation. It is recommended that ozone be used for the treatment of PCB contaminated soil at Eskom substations. / Thesis (M.Sc.Eng.)-University of KwaZulu-Natal, Durban, 2011.

PCBs are persistent organic pollutants that have intentionally and unintentionally (through contamination) been added to mineral insulating oil to improve its insulating and cooling properties within electrical equipment. The Stockholm Convention on Persistent Organic Pollutants (2001) orders the eradication of PCBs from use by 2025. Sodium based dechlorination is a PCB destruction process that is non-thermal, relatively cost effective and allows for the recovery of a reusable end product. A comparative benefits study, contained in chapter 2 of this dissertation, describes the increased financial and environmental impact associated with incinerating large volumes of PCB contaminated mineral oil. The results of the comparative analysis indicate a cost ratio of 1: 2.5, in favour of sodium dechlorination. In addition to the financial benefit, the sodium based PCB dechlorination process is versatile and can be either batched or skid mounted and is typically combined with an oil regeneration step, allowing for transformers to be treated onsite and whilst energised. Eskom is currently considering obtaining the mobile dechlorination unit for the purpose of conducting dechlorination and regeneration on its PCB contaminated transformers while energised. Mineral insulating oil is considered a strategic asset within most industries. Eskom uses mainly uninhibited mineral oil in its older transformers and the effects of PCB dechlorination on the natural inhibitor content of the oil is uncertain. The objective of this study was to investigate the effects of sodium dechlorination on the oxidation stability and thereby indirectly the natural inhibitor content of uninhibited naphthenic based mineral oil. The study involved the dechlorination, regeneration and subsequent chemical analyses of PCB contaminated oils in the PCB ranges <50ppm, 50 to 500 ppm and >500 ppm as stipulated by the Stockholm Convention on Persistent Organic Pollutants (2001). The study confirmed the reduction in oxidation stability and thereby the natural inhibitor content of the mineral oil after sodium dechlorination. Based on the results obtain a preliminary algorithm was established to predict the reduction in oxidation stability after sodium dechlorination, as a function of the PCB concentration prior to dechlorination. This will provide an indirect indication of the rate of natural inhibitor depletion of the oil, based on its exposure to the sodium dechlorination reagents and process conditions. / Thesis (M.Sc.Eng.)-University of KwaZulu-Natal, Durban, 2010.

The purpose of this paper was to combine available peer-reviewed literature on PCB phytoremediation and make direct comparisons using ANCOVA statistics in order to determine if and what plants are presently a viable option for the remediation of PCB contaminated soils. Pumpkin (Curbita pepo cv Howden) consistently had the top root and shoot concentrations, as well as total plant accumulation. Their consistency shows that they can be reliable in the field and the most viable option. Tall fescue and sedge were also top contenders. Due to the small sample size for many plants and accounting for several confounding variables, very few of plant species and groups showed to be significantly better at PCB accumulation. PCB phytoremediation can be used in conjunction with other technologies or as an early action plan to begin decreasing PCB concentration levels as well as contain the PCBs, thereby preventing any release.

A research report submitted to the Faculty of Science, University of the Witwatersrand, in partial fulfilment of the requirements for the degree of Master of Science in Environmental Sciences Johannesburg, 2017. / PCBs are chemical compounds which were synthesised in the laboratory in the 1920s. They are classified under the category of POPs. They were mainly used in electrical equipments and transformers as the insulating material. PCBs were released to the environment in the form of oil spillages, combustion of PCB-containing equipments and others. Its production was banned in the 1970s after its toxic, persistent, bioaccumulative and carcinogenic behaviour was discovered. This study was conducted to determine and monitor the level of PCB in soil contaminated by oil spillages from pole mounted transformers in Polokwane, Limpopo, South Africa after sites have been remediated. Seventy eight soil samples were collected from five sites. The QuEChERS extraction method and GC-MS was used to extract and analyse PCBs. The PCB congeners targeted in this study are PCB-180, PCB-158 and PCB-101. The concentration of PCB-180 ranges between 10.02 and 78.30 μg kg -1, PCB-158 ranges between 3.89 and 45.36 μg kg -1 and PCB-101 ranges between 2.42 and 39.12 μg kg -1. The PCB congener with the highest concentration at all sites is PCB-180 followed by PCB-158 while PCB-101 has the least concentration; this order is consistent in all sampling sites. PCB concentrations after bioremediation were found to be extremely higher than concentrations before bioremediation which suggest that the bioremediation process was not efficient including actual analytical methods used. In comparison to the range of the PCB levels reported in literature, the PCB concentration determined from this study is found within a higher range. The PCBs concentration at all five sites was found to be below the legal limits. / LG2018