Sustainable energy sources are of great importance, and will become even more important in the future. Gasification of biomass is an important process for utilization of biomass, as a renewable energy carrier, to produce fuels and chemicals. Density functional theory (DFT) calculations were used to investigate i) the effect of co-adsorption of water and CO on the Ni(111) catalysed water splitting reaction, ii) water adsorption and dissociation on Ni(111), Ni(100) and Ni(110) surfaces, as well as iii) formyl oxidation and dissociation, iv) hydrocarbon combustion and synthesis, and v) the water gas shift (WGS) reaction on these surfaces. The results show that the structures of an adsorbed water molecule and its splitting transition state are significantly changed by co-adsorption of a CO molecule on the Ni(111) surface. This leads to less exothermic reaction energy and larger activation barrier in the presence of CO which means that far fewer water molecules will dissociate in the presence of CO. For the adsorption and dissociation of water on different Ni surfaces, the binding energies for H2O and OH decrease in the order Ni(110) > Ni(100) > Ni(111), and the binding energies for O and H atoms decrease in the order Ni(100) > Ni(111) > Ni(110). In total, the complete water dissociation reaction rate decreases in the order Ni(110) > Ni(100) > Ni(111). The reaction rates for both formyl dissociation to CH + O and to CO + H decrease in the order Ni(110) > Ni(111) > Ni(100). However, the dissociation to CO + H is kinetically favoured. The oxidation of formyl has the lowest activation energy on the Ni(111) surface. For combustion and synthesis of hydrocarbons, the Ni(110) surface shows a better catalytic activity for hydrocarbon combustion compared to the other surfaces. Calculations show that Ni is a better catalyst for the combustion reaction compared to the hydrocarbon synthesis, where the reaction rate constants are small. It was found that the WGS reaction occurs mainly via the direct pathway with the CO + O → CO2 reaction as the rate limiting step on all three surfaces. The activation barrier obtained for this rate limiting step decreases in the order Ni(110) > Ni(111) > Ni(100). Thus, the WGS reaction is fastest on the Ni(100) surface if O species are present on the surfaces. However, the barrier for desorption of water (as the source of the O species) is lower than its dissociation reaction on the Ni(111) and Ni(100) surfaces, but not on the Ni(110) surface. Therefore the direct pathway on the Ni(110) surface will dominate and will be the rate limiting step at low H2O(g) pressures. The calculations also reveal that the WGS reaction does not primarily occur via the formate pathway, since this species is a stable intermediate on all surfaces. All reactions studied in this work support the Brønsted-Evans-Polanyi (BEP) principles.

The rapid urbanization and industrialization has led to an increase of disposal petroleum hydrocarbons (PHC) and trace elements (TE) into the environment. These pollutants are considered as the most toxic contaminants in the world due to their persistence in the environment, and the long range of toxicological effects for living beings. Recent concerns regarding the environmental contamination have initiated the development of several remediation technologies, including physical, chemical, and biological approaches. In this thesis, gentle soil remediation options (GRO) were investigated at different scales for the reclamation of PHC and TE co-contaminated soil. In the first part of this thesis, laboratory experiments were performed to characterize PHC and TE contaminated soil as well as the indigenous microorganisms (bacteria and fungi) present inside these contaminated soil. It was found that the studied aged contaminated soil had a negative effect on earthworm’s development and L. sativum biomass. Moreover, a high respiration of microorganisms attributed to the transformation/ mineralization of organic matter or/and organic pollutants was observed. This presence of viable microorganisms suggested an adaptation of microorganisms to the contaminant. Further results showed that the long-term exposure of soil microorganisms to high PHC concentration and the type of isolation culture media did not influence the ability of isolates to effectively degrade PHC. However, phylogenic affiliation had a strong on PHC biodegradation. In the second part of this thesis, preliminary studies in greenhouse were assessed to investigate the ability of M. sativa assisted by compost in the greenhouse aided-phytoremediation of PHC and TE. It was found that compost incorporation into the soil promoted PHC degradation, M. sativa growth and survival, and phytoextraction of TE. Residual risk assessment after the phytoremediation trial also showed a positive effect of compost amendment on plant growth and earthworm development. Pilot scale ecopile experiment carried out in the third part of this thesis allow a reduction of up to 80% of PHC and 20% of metals after 17 months. This research demonstrated that M. sativa and H. annus were suitable for phytodegradation of PHC and phytoextraction of TE.  Results from this thesis are helpful for further full-scale phytoremediation studies.

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Alkylphenanthrenes such as retene (7-isopropyl-1-methylphenanthrene) are aquatic contaminants commonly found in anthropogenically-, industrially-, and petroleum-contaminated environments, and have been implicated in crude oil toxicity. In the early life stages (ELS) of fish, exposures to alkylphenanthrenes produce signs of toxicity typical of those observed in exposures to halogenated aromatic hydrocarbons, particularly to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). TCDD, the most toxic congener, serves as the basis of the current mechanism-based risk assessment model. The model assumes that congeners that produce TCDD-like toxicity share a common mode of action and act additively. The mechanism of TCDD-like toxicity is assumed to be mediated by the aryl hydrocarbon receptor (AhR), a ligand-activated transcription factor involved in the xenobiotic response (e.g., induction of cytochrome P450 1A enzymes; CYP1A) and in normal development. CYP1A enzymes are not involved in the mechanism of TCDD toxicity. Alkylphenanthrenes toxic to the ELS of fish are AhR ligands, but in contrast to TCDD, are readily metabolized by CYP1A enzymes. The byproducts of CYP1A metabolism have been implicated in retene toxicity. However, the target tissue of retene and the direct roles of AhR and CYP1A in retene toxicity are unknown, but are expected to be similar to those of TCDD. The results presented in this thesis suggest that in the ELS of fish: (1) the primary target of retene is the cardiovascular system (Chapters 2 & 5); (2) retene toxicity is stage-specific (Chapter 2); (3) the mechanism of retene toxicity is mediated by AhR2, and is independent of CYP1A enzymes (Chapter 5); (4) multiple CYP1A-independent toxicities can result from exposures to different mixtures of CYP1A inducing (retene) and CYP1A inhibiting (alpha-naphthoflavone or 2-aminoanthracene) PAHs (Chapters 3 & 4); and (5) multiple concentration-dependent mechanisms of toxicity (i.e., synergism and response addition) can occur in co-exposures of a CYP1A inducer (retene) with a range of CYP1A inhibitor (alpha-naphthoflavone) concentrations (Chapter 3). Thus, retene toxicity is mechanistically similar to that of TCDD toxicity, suggesting alkylphenanthrenes can be included in the current risk assessment model. However, the observed variable mixture toxicities and species differences in retene toxicity raise questions about the effectiveness of this model. / Thesis (Ph.D, Biology) -- Queen's University, 2009-01-13 12:10:31.373

Diss. (sammanfattning) Stockholm : Karol. inst., 2003. / Härtill 5 uppsatser.

Thesis (Ph. D.)--University of Washington, 2005. / Vita. Includes bibliographical references (leaves 200-205).

Le bisphénol A (BPA) est un perturbateur endocrinien couramment employé dans l’industrie agroalimentaire, en particulier pour les matériaux en contact des denrées alimentaires. Son utilisation dans la fabrication de polycarbonates et de résines époxy, recouvrant la face interne des boîtes de conserve et des canettes, en fait un contaminant ubiquitaire de l’alimentation humaine. L’augmentation de l’exposition humaine à ce contaminant a été corrélée avec la récurrence de certains troubles comme l’intolérance alimentaire, l’obésité ou le diabète de type 2. Ces dernières années, une attention particulière a été portée sur sa capacité à perturber différentes fonctions physiologiques, dont celle du système immunitaire, après exposition périnatale à des niveaux environnementaux pertinents pour l’Homme. Dans une première étude, nous avons montré qu’une exposition périnatale au BPA à 50 µg/kg de poids corporel/jour induit une diminution de l’activité anti-microbienne corrélée à une chute de l’expression du lysozyme dans l’iléon de la descendance femelle. La perméabilité intestinale de ces individus augmente en association avec le niveau d’IFN- dans les muqueuses du côlon. De plus, nous observons une diminution des plasmocytes à IgA associée à une perte de sécrétion d’IgA dans les fèces, démontrant un défaut de la fonction barrière et des défenses de l’intestin chez la descendance BPA. De manière intéressante, une diminution de la fréquence des ILC3 intestinaux est observée chez ces individus, avec une augmentation du niveau d’IgG sanguin dirigé contre une E.coli commensale. Ces effets sont associés à un défaut de maturation et de capacité migratoire des cellules de la lamina propria (LP) et de la rate. L’exposition périnatale au BPA provoque une augmentation de la sécrétion d’IFN- et d’IL-17 après re-stimulation in vitro CD3/CD28 des cellules de la LP, et une réponse de type Th17 dans la rate. Réunis, ces effets confortent la capacité du BPA, lors d’une exposition périnatale, à induire une intolérance alimentaire chez la descendance femelle. Dans une seconde étude, nous avons mis en évidence que l’exposition périnatale au BPA, à la même dose, induit des perturbations de l’homéostasie du système immunitaire intestinal et systémique chez la descendance mâle au jour 45, via une diminution de la fréquence des Th1 et Th17 dans la LP et une augmentation de la réponse Th1 et Th17 dans la rate. Ces impacts apparaissent en parallèle avec une altération de la sensibilité au glucose, une diminution de la sécrétion d’IgA dans les fèces et un appauvrissement des bifodobacteria dans le microbiote intestinal de ces individus. L’ensemble de ces évènements précède l’infiltration de macrophages M1 pro-inflammatoires dans le tissu adipeux péri-gonadique, en association avec une diminution de la sensibilité à l’insuline et une augmentation du poids corporel apparaissant avec le vieillissement (jour 170) chez la descendance BPA. Cette étude longitudinale a permis de proposer une séquence d’évènements aboutissant à un phénotype obèse et au T2D lors d’une exposition périnatale au BPA, et ainsi de comprendre le rôle du système immunitaire en lien avec le microbiote intestinal dans le développement de ces désordres métaboliques. Enfin, nous émettons l’hypothèse que les bisphénols S et F, deux analogues structuraux du BPA, peuvent disposer de capacités immunomodulatrices équivalentes à celles du BPA, susceptibles de provoquer les mêmes troubles chez la descendance. Nous avons testé cette hypothèse de manière préliminaire chez la descendance femelle après exposition périnatale au BPS et au BPF. Des résultats préliminaires d’études in vitro sur ces deux composés en comparaison au BPA sont également apportés. Ce travail de thèse contribue à accroître les connaissances relatives aux effets immunotoxiques des bisphénols dans le contexte de l’origine développementale des pathologies chroniques de l’adulte (DOHaD). / The endocrine disruptor bisphenol A (BPA) is commonly found in food industry, more precisely in food contact packaging. BPA is used to manufacture polycarbonate plastics and epoxy resins lining food and beverage cans, becoming an ubiquitous contaminant in human food. The extent of human exposure to this chemical is thought to be correlated with the occurrence of disorders like food intolerance, obesity and type-2 diabetes (T2D). During last years, a particular interest have been raised about its ability to disrupt various physiological functions, including immune system, after perinatal exposure at relevant environmental doses for Human. In the first study, we showed that perinatal exposure to BPA (50 µg/kg body weight/day) decreased anti-microbial activity and ileal lysozyme expression in the female mouse offspring. In those mice, we observed an increased gut permeability, in association with an increase of colonic IFN- level. Moreover, we observed a decrease of IgA+ cells with a loss of IgA secretion into faeces, depicting intestinal barrier and defense function defects in BPA female offspring. Interestingly, a decrease of the intestinal ILC3 frequency associated with an increase of IgG against commensal E.coli in sera have been observed in these individuals. These effects were linked to a defect of maturation and migratory ability of dendritic cells from lamina propria (LP) and spleen. Perinatal exposure to BPA also increased IFN- and IL-17 secretions after in vitro stimulation in the gut and elicited Th17 response in the spleen. Altogether, these effects support the ability of a perinatal exposure to BPA to induce oral intolerance with ageing in female offspring. Secondly, we showed that perinatal exposure to BPA at the same dose led to intestinal and systemic immune system homeostasis disturbances in male mouse offspring at day 45, through a decrease of Th1 and Th17 frequencies in the LP and an increase of Th1 and Th17 response in spleen. These effects were associated with an altered glucose sensibility, a decrease of faecal IgA secretion and a fall of bifidobacteria in the microbiota of these individuals. These BPA-mediated events precede infiltration of pro-inflammatory M1 macrophages in gonadal white adipose tissue, together with a decreased insulin sensitivity and an increased weight gain. This longitudinal study allowed us to better understand the sequential events linked to perinatal exposure to BPA that lead to obesity and T2D, and highlighted the role of immune system linked to gut microbiota in the development of these metabolic disorders. Finally, we hypothesized that two structural analogs of BPA –i.e., Bisphenol S and F- can display similar immune-modulatory effects that could lead to similar developmental disturbances than BPA in exposed-offspring. This hypothesis was tested in a preliminary experiment in female mouse offspring perinatally exposed to BPS and BPF. We also provided preliminary results of these two compounds, compared to BPA, from an in vitro study. This thesis contributes to the increase knowledge about the immunotoxic effects of bisphenol compounds in the context of the Developmental Origins of Health and Disease (DOHaD).

No description available.

Diesel #2 is used to heat nearly 400,000 dwellings in Virginia. Home heating oil released from leaking underground tanks located adjacent to homes and residing in unsaturated soil adjacent to houses poses a potentially serious health risk. Specifically, the migration of hazardous vapors into buildings, known as vapor intrusion, can negatively impact indoor air quality in homes and public buildings (USEPA 2015). In this look-back study, we assessed the potential for petroleum vapor intrusion by sampling soil vapor at 25 previously remediated spill sites. Residual contaminants, in particular total petroleum hydrocarbons (TPH) and naphthalene, were detected in approximately 1/3 of the samples. Concentration levels were correlated to site variables (building type, remediation time, physiographic region) including previous abatement measures. Spill category as assigned by the remediation contractor was investigated in conjunction with these three site variables. Remediation time was the most promising predictive site variable, with visible trends downward in DEQ Category 2 sites with increased remediation time. Higher contaminant concentrations were found near basement-style dwellings, which we hypothesize is due to the wall of the basement blocking horizontal migration of contaminants and the flow of oxygen to the release source zone. We found that many sites exceeded the sub-slab risk target threshold in naphthalene concentration, which has negative implications on previous abatement strategy efficacy. / Master of Science

Effects of man made pollutants on an ecosystem are initiated at the cellular level where a prime determinant for survival of an organism is its ability to metabolise and excrete toxic chemicals or their metabolites, thereby preventing cellular toxicity or damage to germ cell DNA. Cytochrome P450 (CYP) enzymes are responsible (in concert with the remainder of the Ah battery enzymes) for the metabolism of numerous xenobiotics and endogenous compounds, including the metabolic activation of most environmental toxic chemicals and carcinogens. Genetic polymorphisms which affect performance of these enzymatic detoxification systems may alter tolerance to pollutants and thus survival in polluted environments. Alterations in the susceptibility of individuals and the development of resistant populations has arisen by forced selection of populations with variant genes, resulting in increased detoxification capacity. There is evidence for such scenarios of variations in activities of pollutant biotransforming enzymes of fish contributing to survival in polluted estuarine environments and several chemically resistant populations have been identified in the USA and Europe. In fish it has been demonstrated that CYP1A enzyme activity is required to activate some carcinogenic xenobiotics to a metabolic state in which they can form DNA adducts. The mechanism of reduced CYP1A expression in highly contaminated populations may therefore represent resistance to chemical stressors. European flounder (Platichthys flesus) from some waterways which have a long history of severe sedimentary contamination do not show elevated levels of CYP1A. The aim of the current study was to investigate whether any heritable differences were apparent between offspring from parents inhabiting long-term polluted and pristine areas. Flounder were obtained from a highly polluted estuary in the UK and crossed with fish from a relatively pristine environment. Offspring were raised in communal tanks in order to standardise environmental conditions, and allow investigations into the genetic variation of CYP1A. To allow identification of offspring to parental fish, polymorphic microsatellite loci were isolated and characterised for the flounder. Novel cDNA probes to transcription factors in the detoxification pathway (AhR2 and ARNT2) were cloned for flounder, and RT-PCR / Southern blot methods were developed for quantitation of gene transcript levels. A novel method of CYP1A quantification using real-time PCR was developed. PAH and PCB exposure trials were carried out on mixed batch offspring, and CYP1A gene transcript levels assessed using Northern blot and real-time PCR techniques. Offspring were genotyped to their parents using the microsatellites obtained, and CYP1A transcript levels were correlated with clean and polluted areas. CYP1A was further correlated to transcription factor expression, and data are presented. Following exposure to the commercial PCB mixture, Aroclor 1254, CYP1A transcript levels were found to be significantly lower in families whose parents originated from a polluted area. This observation indicates that there is a possible genetic component to variation in CYP1A levels, and that these fish may have acquired a heritable tolerance to polluted areas. The lack of induction, or correlation with CYP1A levels, of AhR2 and ARNT2 expression indicates a possible AhR independent pathway for the metabolism of PCBs in the flounder. © Tom Dixon 2003 http://www.tomdixon.org