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

Thesis (MTech (Chemistry))--Cape Peninsula University of Technology, 2015. / Immunosensors are analytical devices comprising antibody (Ab) molecules intimately integrated with electronic physicochemical transducers. Abs are responsible for specific recognition of an analyte so called antigen (Ag) while transducers are responsible for the conversion of chemical changes brought about by Ab-Ag interactions into measurable and processable signal. Amongst the many analytical tools, immunosensors have shown outstanding performance in applications in fields such as clinical diagnostics, agricultural purposes and environmental monitoring. They have come in place of the many conventional analytical methods which showed a number of disadvantages; high cost and longer time of operation, and requirement of highly knowledgeable personnel. On the other hand, immunosensors have shown potential to overcome these constraints. Their advantages include possibilities of portability, miniaturization, and simplified procedures. Of the possible fields of immunosensor applications, this study focussed on the environmental aspect. The safety of the environment is good for the well-being even though there are still some environmental threats that exist. Polychlorinated biphenyls (PCBs) have reportedly been found to be some of the potential substances to pose such threats due to their toxic and persistent behaviour. In this study, we have developed an electrochemical immunosensor as an analytical tool for the analysis and monitoring of PCBs. The development was based on the use of silver nanoparticles-doped polyaniline (PANI/Ag NPs) for modification of an electrode as a process for fabrication of the transducer. The PANI/Ag NPs composite was deposited on the glassy carbon (GC) and platinum (Pt) electrodes by oxidative electropolymerization of aniline in the presence of Ag NPs in 1 M HCl using cyclic voltammetry (CV) by ramping the potential from -0.1 to 1.4 V at 50 mV/s. The composite was then characterized and evaluated as a potential material for electrochemical transduction. Evaluation was on electroactivity, which is the main property of interest for materials used in the fabrication of electrochemical devices. The PANI composites were characterized using spectroscopic (FTIR), microscopic (TEM) and electrochemical CV techniques. Results confirmed the formation of PANI in its emeraldine form and the presence of Ag NPs. Characteristic functional groups and peaks of PANI were observed in FTIR and CV respectively. TEM micrograms showed one dimensional nanofibric tubes and crystalline-like structure of the composite. The incorporation of Ag NPs was indicated by the transition from the amorphous (PANI) to crystalline (PANI/Ag NPs) structure accompanied by increase in size as well as smoothness of the tubes. EDS-TEM counts increase of the chlorine (Cl) peaks is due to the closeness of these peaks to those of Ag, thus confirming incorporation of Ag NPs.

No description available.

Polychlorinated biphenyls (PCBs) are persistent, man-made toxicants that are linked to adverse health effects and diseases such as endocrine disruption, diabetes, obesity, cardiovascular effects, and cancer. Since their manufacturing began in 1929 for industrial use, and was banned in 1979, they have bioaccumulated in water, sediment, food, animals, humans and more. PCBs are also found in indoor air of older buildings and as inadvertent byproducts in the manufacture of paints and pigments. The lower chlorinated PCBs, those with fewer than 5 chlorine atoms, are readily metabolized to form hydroxylated PCBs (OH-PCBs) that are further converted to PCB-sulfates in reactions catalyzed by cytosolic sulfotransferases (SULTs). Steroid sulfotransferases SULT1E1 and SULT2A1 participate in regulating the homeostasis of estrogens and androgens, respectively, through the deactivation of active hormones. The estrogen sulfotransferase (SULT1E1) is also a potential key player in adipogenesis. Recent literature has shown that downregulating expression of SULT1E1 in cells derived from humans and mice caused opposite effects, where adipogenesis was inhibited or stimulated, respectively. Adipogenesis is the maturation of preadipocytes into mature adipocytes, which is regulated by peroxisome proliferating-activator γ (PPARγ). Adipocytes are a main component of adipose tissue, which is important for energy homeostasis, organ protection, and thermoregulation. Adipose tissue also secretes various cytokines such as adiponectin. Adipose tissue dysfunction can result from adipocyte dysfunction, which can be caused by alterations in cell signaling. The objective of this dissertation research was to determine if OH-PCBs and PCB-sulfates are inhibitors of SULT1E1 and SULT2A1 and if inhibition of SULT1E1 by OH-PCBs could potentially affect adipogenesis. We hypothesized that PCB metabolites would inhibit SULT1E1 and SULT2A1 and potentially affect adipogenesis in both human and murine cell models. Using purified recombinant human SULT1E1 and SULT2A1, I found that 4’-OH-PCB 3, 4-OH-PCB 8, 4-OH-PCB 11, 4’-OH-PCB 25, and 4-OH-PCB 52 were potent inhibitors of the sulfation of representative substrates (7.0 nM estradiol for SULT1E1 and 1.0 µM dehydroepiandrosterone for SULT2A1, Figures 3-3 and 3-4, respectively). Moreover, 4-OH-PCB 11 and 4-OH-PCB 52 were the most potent inhibitors of SULT1E1 and SULT2A1 with IC50 values of 7.2 nM and 1.5 μM, tables 3-1 and 3-2, respectively. The least potent inhibitor of SULT1E1 was 4’-OH-PCB 3, with an IC50 of 1300 nM. The PCB-sulfates were not potent inhibitors for either enzyme. 4-OH-PCB 11 inhibited the sulfation of estradiol in the cytosol of both pre-adipocytes and fully differentiated adipocytes (Figure 4-9). Immortalized human adipocytes were treated with 10 µM of triclosan (a known inhibitor of SULT1E1), 4’-OH-PCB 3 and 4-OH-PCB 11. Experiments included exposure to these toxicants for 1) 72 hours to preadipocytes, 2) 72 hours to preadipocytes followed by 11-day differentiation, 3) to differentiating adipocytes and for 48 hours post-differentiation. The lipid accumulation levels remained unaffected, as determined by microscopic imaging and quantification using AdipoRed. The mRNA expression levels of prominent adipogenic markers SULT1E1, PPARγ, and AdipoQ were measured using RT-Q-PCR. Changes in SULT1E1 and PPARγ expression were unaffected upon treatment before, during and after adipogenesis when compared to controls. However, the increase in AdipoQ expression was reduced upon treatment with 4-OH-PCB 11 in differentiated adipocytes and in preadipocytes exposed for 72 hours followed by 11-day differentiation (Figure 4-14). This could be an indicator of adipocyte dysfunction that was not manifested by a change in lipid accumulation. Murine 3T3-L1 cells were also treated with 10 µM of triclosan, 4’-OH-PCB 3 and 4-OH-PCB 11 for 48 hours to preadipocytes, during 8-day differentiation and for 48 hours after differentiation. The mRNA expression levels of prominent markers of cardiovascular and adipogenesis functions, ACE2, PPARγ, FABP4, and AdipoQ were measured using RT-PCR. Compared to controls, the increase in AdipoQ expression was reduced following treatment of preadipocytes with triclosan and 4-OH-PCB 11 and subsequent differentiation (Figure 5-11). The increase in PPARγ expression remained either unchanged from controls or slightly stimulated in differentiating and differentiated adipocytes (Figures 5-11 and 5-13). Angiotensin-converting enzyme 2 (ACE2) expression was decreased compared to control values, upon treatment with 4’-OH-PCB 3 (Figure 5-12), while fatty acid binding protein 4 (FABP4) expression was stimulated to the same extent across all treatment groups in differentiating adipocytes (Figure 5-12). The results, overall, show that these OH-PCBs did not affect lipid accumulation in human adipocytes, but they may affect other signaling pathways in adipogenesis. 4-OH-PCB 11 decreased adiponectin expression compared to the increase that was seen in unexposed differentiating human and mouse adipocytes. Adiponectin is secreted from adipose tissue, and this decrease could indicate a form of dysfunction. This finding is consistent with the results of the purified SULT1E1 study, where 4-OH-PCB 11 potently inhibited SULT1E1, but 4’-OH-PCB 3 did not (Figure 3-3 and Table 3-1). Thus, there is a potential for OH-PCBs to disrupt the expression of adiponectin and perhaps other vital adipokines and this could negatively affect adipose tissue function. Future studies will be needed to determine if these effects are indeed mediated by intracellular estradiol and SULT1E1. Moreover, the potential for in vivo disruption of circulating adiponectin by OH-PCBs and other toxicants that inhibit SULTs remains to be studied.

Although the production of polychlorinated biphenyl (PCB) technical mixtures has been banned in the U.S. since the 70’s, they remain ubiquitous in the environment, particularly in indoor and ambient air. Due to the presence of PCB’s in air, inhalation is a significant route of exposure. PCBs released from various building materials have been shown to contaminate the indoor air in homes and schools. In the AESOP Study, an epidemiologic study of PCB exposures among school children and their mothers, PCB28 was found in the serum of over 20% of participants. Data are lacking on the absorption, distribution, metabolism, and excretion (ADME) of inhaled PCBs and on the biological fate and dose-specific toxicological endpoints. In order to inform toxicokinetic modeling for risk-assessment, we are conducting ADME toxicological studies with lung exposure to a representative trichlorobiphenyl, and evaluating the uptake from the lung and the distribution, metabolism, and excretion. Male Sprague-Dawley rats were exposed to [14C]PCB28 via intratracheal instillation at two different doses (42 µg/rat and 4.2 µg/rat). Digestive matter from five separate compartments of the gastrointestinal tract and thirty-six tissue types were excised and measured by scintillation counting. Exhaled air and excreta were also collected and analyzed. Measurements for the high dose were made at 12, 25, 50, 100, 200, 400, 720, and 1440 min, and for the low dose at 2, 12, 50, 200, and 720 min post-exposure. Data show that pulmonary uptake exceeded 99% in both doses. [14C]PCB28 entered the blood stream and distributed quickly to all tissues within minutes of dosing. In the high dose, the majority of radioactivity initially went to the muscle and liver, while in the low dose [14C]PCB28 initially distributed to the muscle, esophagus, and trachea, before being redistributed to the skin and adipose tissue, where it accumulated in both doses. In most tissues, elimination was biphasic, consisting of an initial fast phase with a half-life (t1/2) of 7-93 min (high dose) and t1/2 of 6-60 min (low dose), followed by a slower phase with t1/2 of 5-18 hours (high dose) and t1/2 of 3-18 hours (low dose). The metabolism of PCB28 was not extensive, with the parent compound as the major component in liver, kidney, serum, and adipose tissue. Excretion via urine and feces was limited, with 92% (high dose) and 88% (low dose) of radioactivity remaining in the tissues by the end of the time course, primarily in skin and adipose tissue. Low urinary concentration relative to serum, suggested that parent PCB28 in serum would serve as an accurate biomarker for assessment of exposure to inhaled trichlorobiphenyls. The time course and tissue distribution is comparable to [14C]PCB11, while metabolism and excretion of [14C]PCB28 is much less extensive.