The city of Kalgoorlie in Western Australia has been labeled an “asthma hot spot” attributed to mining activity, prompting further investigation into toxic elements (Lee et al., 2006). Inhalation of nickel-bearing particles is a particular concern due to the presence of a nickel smelter 10km upwind of the city. The toxicological properties of nickel are well-documented, thus the primary objective is the characterization of phases identified as problematic in the lungs. To determine the smelter’s influence on nickel bioaccessibility in the soils throughout the city of Kalgoorlie, surface soil samples were taken from areas within the city and compared to soils near the smelter and outside the city, distant from the smelter. Soils were sieved to isolate the respirable fraction (<10um) potentially associated with lung disease and analyzed using a simulated lung fluid to determine the concentration of nickel soluble in the lungs. The soluble nickel represents the fraction that may be involved in allergic or asthmatic reactions, while the insoluble compounds may be of concern as some are carcinogenic. Further soil characterization was done using a six step sequential extraction and mineralogical analysis to identify nickel-bearing minerals. The influence of the smelter activity on nickel bioaccessibility in the soils within Kalgoorlie is low, but soils near the smelter host significantly higher nickel concentrations and higher bioaccessibility. Respiratory nickel bioaccessibility in soils ranges from 1 to 3% in and outside the city of Kalgoorlie, while the area surrounding the smelter increases to up to 6.8%. In each case, there is a direct correlation between bioaccessibility percent and percent nickel bound in the water-soluble and exchangeable fractions, but the simulated lung fluid dissolves more nickel in each sample than is present in these two fractions, potentially due to the presence of weak chelating agents in the solution. Respiratory bioaccessibility is low in Kalgoorlie soils because nickel occurs primarily in sulfides, with minor oxides and silicates, all relatively insoluble in lung fluid. However, the high concentrations of these compounds could be of concern, as they are potential carcinogens at high concentrations. Lee, Y.P., Cook, A., Thompson, P., Weinstein, P. 2006. Epidemiology. 17(6):283-284 / Thesis (Master, Geological Sciences & Geological Engineering) -- Queen's University, 2008-07-07 10:29:10.129

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No description available.

Hexabromocyclododecane (HBCD) is a brominated flame retardant commonly used in industrial and household products to reduce the spread of fire and the risk of death. Similar to polybrominated diphenyl ethers (PBDEs), HBCD is a ubiquitous and persistent environmental contaminant, highly lipophilic and bioaccumulative, and has been detected throughout various ecosystems and phyla, thus posing potential cause for concern for top consumer species, including birds of prey. Captive adult American kestrels (Falco sparverius) were exposed by diet to HBCD at an estimated daily concentration of 0.8 μg HBCD / μL safflower oil per cockerel (or 800 ng/ g ww / day / pair); their offspring, used in this study, were exposed in ovo only to environmentally relevant HBCD concentrations of 164.13 ± 18.26 ng/g ww or to background concentrations in the control eggs (0.4 ± 0.04 ng/g ww). The in ovo exposed HBCD group of male nestling kestrels showed a reduced corticosterone response. Moreover, in ovo HBCD concentrations were correlated with reduced flying activities of juvenile males during hunting behaviour trials and delayed response times of juvenile female kestrels during predator avoidance behaviour trials, suggesting an ongoing effect of HBCD on corticosterone levels. These findings show that embryonic exposure to environmentally relevant concentrations of technical mixture HBCD influences the corticosterone response, hunting success and avoidance of potential predators in captive American kestrels. / L'Hexabromocyclododécane (HBCD) est un ignifuge bromé couramment utilisé dans les produits industriels et ménagers pour réduire les risques d'incendies et de mortalité. À l'instar des éthers diphényliques polybromés (EDPB), le HBCD est un polluant omniprésent et persistant de l'environnement, fortement lipophile et bioaccumulable, décelé dans divers écosystèmes et phylums et donc potentiellement préoccupant pour les espèces du haut de la chaîne alimentaire, dont les oiseaux de proie. L'étude consiste à exposer par leur alimentation des crécerelles d'Amérique (Falco sparverius) adultes en captivité à une concentration quotidienne estimée de 0,8 mg HBCD / μL d'huile de carthame par coquelet (c.-à-d. 800 ng / g pf/ jour / paire); leur progéniture, utilisée dans cette étude, ont été exposés in ovo à des concentration écologiquement pertinentes de HBCD 164,13 ± 18,26 ng / g pf ou des concentrations de fond (0,4 ± 0,04 ng / g pf) dans le cas des œufs de contrôle . Chez les oisillons mâles du groupe exposé au HBCD in ovo, il y a réduction de la sécrétion de corticostérone. En outre, les concentrations de HBCD in ovo sont corrélées à une réduction des activités de vol chez les mâles juvéniles durant des essais de comportement de chasse et des temps de réaction accrus chez les femelles juvéniles durant des essais de comportement d'évitement de prédateurs, ce qui suggère un effet continu du HBCD sur les niveaux de corticostérone. Ces constatations démontrent que l'exposition embryonnaire à des concentrations écologiquement pertinentes de HBCD dans un mélange technique a une incidence sur le taux de sécrétion de corticostérone, le taux de réussite des activités de chasse et l'évitement de prédateurs potentiels chez la crécerelle d'Amérique.

Bisphenol A (BPA), an estrogenic endocrine disruptor, used in the production of polycarbonate plastics and epoxy resins, is found in drinking containers, food packaging and lining of canned goods. BPA can leach from the plastics into food, water, and the environment and is thus the primary cause for the widespread and continuous exposure of BPA to humans. BPA binds to estrogen receptors (ERs) and has also been shown to bind strongly to estrogen related receptor gamma ERRγ. ERs are expressed in human and mouse embryonic stem cells, indicating a fetal cardiac response to sex hormones occurs early. Furthermore, functional ER, ER ERR are expressed in heart and affect cardiac gene expression and function. The receptors can dimerize and enter the nucleus in order to alter target gene expression by means of modifying DNA methylation patterns. Higher BPA concentrations in urine were associated with an increased prevalence of cardiovascular disease and type 2 diabetes. BPA enters the rodent placenta, accumulates in the fetus and alters the epigenome in reproductive and non-reproductive tissues at levels found in human blood, tissue and urine by altering DNA methylation. Alteration of the epigenome results in changes of protein expression. Changes in calcium homeostasis protein expression leads to cardiac dysfunction. We therefore hypothesize that BPA exposure epigenetically reprograms the fetal/early neonate development of the heart by altering expression of proteins involved in calcium homeostasis, heart structure, and heart function.Pregnant C57BL/6N mice received 0.5, 5, or 200 g/kg/day of BPA starting GD 11. Exposure of the pups continued lifelong for the 0.5 and 5 g/kg/day doses whereas 200μg BPA pups received regular water at weaning. Cardiac function was measured by tail cuff blood pressure, echocardiography and electrocardiography. Physical parameters (body weight (BW) and body length (BL), and anogenital distance (AGD)) were measured monthly until four months. Organ weights were collected at euthanasia. Immunoblots of ventricle homogenates measured specific protein expression.Differences in physiological and cardiac function parameters were observed, indicating lifelong exposure to BPA alters cardiac development and function in the adult. Changes observed in the expression of cardiac genes and DNMT3a, as well as, changes in methylation of individual CpG pairs further indicates that BPA mediates changes via DNA methylation. The majority of changes occurred in BPA exposure levels of 0.5 and 5.0μg/kg/day and most often, an opposite effect was noticed in the 200μg/kg/day BPA treated progeny, suggesting BPA effects may be dose-dependent. / Le bisphénol A (BPA), un perturbateur endocrinien estrogénique est utilisé dans la production de plastiques polycarbonates et de résines époxy trouvés dans les emballages alimentaires et les revêtements de conserves et de canettes. Dû au transfert du BPA des matières plastiques aux aliments, à l'eau et à l'environnement, les humains sont constamment exposés au BPA. Il est connu que le BPA se lie aux récepteurs des estrogènes (RE), plus précisément aux récepteurs d'estrogène gamma RREγ. Les REs sont présents dans les cellules embryonnaires humaines et murines, ce qui indique une réponse fœtale aux hormones sexuelles. Les récepteurs d'estrogène ER, ERβ, ERRγ sont exprimés dans le cœur embryonnaire et peuvent donc affecter l'expression des gènes et la fonction cardiaque. Ces récepteurs se dimèrisent et pénètrent ainsi dans le noyau cellulaire afin de modifier l'expression des gènes cibles en modifiant les motifs de méthylation de l'ADN. Des concentrations plus élevées de BPA dans l'urine ont été associées à une prévalence accrue de maladies cardiovasculaires et de diabète de type 2. Le BPA pénètre le placenta, s'accumule dans le fœtus et modifie la méthylation de l'ADN. Ces modifications de l'épigénome causent des changements à l'expression des protéines, comme à celles responsables de l'homéostasie du calcium ce qui entraîne ensuite une dysfonction cardiaque. Nous avons donc posé l'hypothèse que l'exposition au BPA cause une reprogrammation épigénétique du développement du cœur fœtal en modifiant l'expression de protéines impliquées dans l'homéostasie du calcium, la structure du cœur, et la fonction cardiaque.Des souris C57BL/6N enceintes ont reçues 0.5, 5 ou 200 ug / kg / jour de BPA à partir du jour de gestation 11. L'exposition au BPA a continuée tout au long de la vie des souris pour les doses de 0.5 et 5 ug / kg / jour, alors que les doses de BPA de 200μg ont reçu de l'eau régulière au moment du sevrage. Les fonctions cardiaques ont été mesurées par la pression artérielle de la queue, l'échocardiographie et l'électrocardiographie. Les paramètres physiques (le poids corporel, la longueur du corps, et la distance ano-génitale) ont été mesurés à tous les mois jusqu'à l'âge de quatre mois. Le poids des organes a été prélevé à l'euthanasie. Des immunotransferts des homogénats ventriculaires ont mesurées l'expression des protéines cardiaques d'intérêts.Les paramètres de la fonction physiologique et cardiaque ont démontrés des différences, indiquant que l'exposition constante au BPA modifie le développement et la fonction cardiaque chez l'adulte. Les changements observés dans l'expression des gènes cardiaques et du DNMT3A, ainsi que les changements dans la méthylation de chaque paire CpG indiquent que le BPA modifie les motifs de méthylation de l'ADN. La majorité des changements observés dans les niveaux d'exposition au BPA de 0.5 et 5.0μg/kg/jour sont inversés lorsque que le niveau de BPA augmente à 200μg/kg/jour, ce qui suggère que les effets du BPA peuvent être dépendants de la dose.

<p>&quot / The aim of the study was to use in vitro human whole blood cultures to screen the water samples collected from the Eerste/Plankenbrug river system for cytotoxicity and inflammatory activity and for the first time investigate the impact on the cell- mediated and humoral immune pathways. Water samples were collected fronm the sites during the dry summer season and rainy winter season. Blood was collected from the healthy male volunteers and diluted with RPMI 1640. For cytotoxicity and inflammatory activity 2.5ul of blood for 18-20 hrs at 37 C... This study shows that waster from the Plankenbrug River is heavily polluted by contaminants from both the agricultural area and informal settlement of Kayamandi. These contaminants can be potentially immunotoxic during the summer season and they can result in inflammatory diarrheal disease and immunosuppression in exposed individuals...&quot / </p>

1,2-dichloroethane (DCA) is one of the most widely used and produced chemicals of the modern world. It is used as a metal degreaser, solvent, chemical intermediate as well as a fuel additive. This carcinogen is toxic to both terrestrial and aquatic ecosystems and accidental spills and poor handling has resulted in contamination of the environment. Thus far several bacteria in the Northern hemisphere have been identified that are capable of utilizing this compound as a sole carbon and energy source. This report focuses on the isolation and characterization of bacterial isolates from the Southern hemisphere that are capable of degrading DCA as well as the global distribution of the DCA catabolic route. Samples obtained from waste water treatment plants were batch cultured in minimal medium containing DCA and repeatedly sub-cultured every five days over a 25 day period. A halogen release assay was performed in order to determine whether individual isolates possessed dehalogenase activity. Confirmation of DCA utilization by bacterial isolates positive for dehalogenase activity was done by sub-culturing back into minimal medium containing DCA. Enzyme activities were confirmed with cell free extracts using all of the intermediates in the proposed DCA degradative pathway and compared to a known DCA degrading microorganism. Biochemical tests and 16SrDNA sequencing indicated that all the South African isolates belonged to the genus Ancylobacter and were different from each other. Based on enzyme activities, it was found that the South African isolates may possess a similar degradative route as other DCA degrading microorganisms. Primers based on genes involved in DCA degradation were synthesized and PCR analysis was performed. It was found that all isolates possessed an identical hydrolytic dehalogenase gene whereas the other genes in the pathway could not be PCR amplified. Southern hybridization using probes based on known genes indicated that some of the isolates had homologous genes. Pulsed field gel electrophoresis (PFGE) and random amplified polymorphic DNA (RAPD) analysis indicated that the five South African isolates of Ancylobacter aquaticus are distinguishable from each other. This study is the first report indicating that microbes from different geographical locations use similar metabolic routes for DCA degradation. The first gene of the pathway (dhlA) has undergone global distribution which may be due to widespread environmental contamination. / Thesis (Ph.D)-University of KwaZulu-Natal, Westville, 2009.

The foetal toxicity of the methyl isocyanate metabolites trimethylamine (TMA) and S-(N-methylcarbamoyl)glutathione (SMG) was studied in mice. Administration of TMA but not SMG during pregnancy decreased foetal weight and selectively inhibited the postnatal growth of male offspring. Both TMA and SMG were teratogenic to mouse embryos in culture. TMA caused a dorsal-rostral split in the head and SMG produced distortion and separation of somites; both agents decreased the growth of embryos. The inhibition of embryonic growth by TMA could not be antagonized by antioxidants or growth factors. The embryotoxic effects of SMG could be antagonized by glutathione (GSH). TMA inhibited the incorporation of $ sp3$H-thymidine, $ sp3$H-uridine and $ sp3$H-leucine into their respective macromolecules; SMG inhibited the incorporation of $ sp3$H-thymidine. Uptake by the yolk sac placenta and incorporation into embryonic proteins of $ sp3$H-leucine-labelled proteins but not of free $ sp3$H-leucine was inhibited by TMA at concentrations which did not inhibit lysosomal degradation of proteins. SMG inhibited the uptake and incorporation of both free $ sp3$H-leucine and $ sp3$H-leucine-labelled proteins. The inhibition of receptor-mediated uptake by SMG could be antagonized by GSH. The data suggest that TMA, and SMG produce embryotoxicity mainly by an inhibition of uptake mechanisms of the yolk sac placenta.

Cadmium and mercury are among the most toxic metals and can be a serious threat to human health. A clear understanding how cells respond, especially in terms of genetically controlled responses to these two metals, is required in order to develop appropriate prevention and treatment procedures that can protect humans from toxic exposure to these metals. Therefore, this study is aimed at elucidating the genetically programmed response to cadmium and mercury exposure in HeLa cells. Two different approaches were employed for this study. Differential expression patterns of mRNAs were studied by differential display reverse transcriptase-polymerase chain reaction (DDRT-PCR) and changes in protein composition of HeLa cells were monitored by two-dimensional (2D) gel electrophoresis. The results showed that transcripts of particular genes were altered by cadmium and/or mercury exposure. These gene are aspartyl/asparginyl beta-hydroxylase (asph), monocyte to macrophage differentiation associated antigen (MMD), and ribosomal protein S24 (rpS24) genes. In addition, some protein spots from 2D gels were found to be altered in their levels as a result of cadmium and/or mercury exposure. The possible roles of asph, MMD and rpS24 genes in response to cadmium and mercury are discussed and further studies are suggested.

No description available.