Thesis (Ph. D.)--West Virginia University, 2008. / Title from document title page. Document formatted into pages; contains xiv, 240 p. : ill. (some col.). Includes abstract. Includes bibliographical references (p. 95-104).

Thesis (M.S.)--Youngstown State University, 2009. / Includes bibliographical references (leaves 63-68). Also available via the World Wide Web in PDF format.

Thesis (M.S.)--Youngstown State University, 2009. / Includes bibliographical references (leaves 38-42). Also available via the World Wide Web in PDF format.

Thesis (Ph. D.)--University of Missouri-Columbia, 2003. / Typescript. Vita. Includes bibliographical references (leaves 101-107). Also available on the Internet.

Thesis (Ph. D.)--University of Missouri-Columbia, 2003. / Typescript. Vita. Includes bibliographical references (leaves 101-107). Also available on the Internet.

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The measurement of Polycyclic Aromatic Hydrocarbons (PAHs) in flames is essential for the understanding of soot formation. In comparison to conventional aromatics-sampling techniques, a new technique was proposed that involves fewer manual operations and no hazardous extraction solvents. Apparatus and experimental procedures of the newly proposed adsorptive-sampling and desorptive-extraction technique for aromatic-hydrocarbon measurements were established in this study. The capabilities and limitations of this new technique were assessed in terms of limits of detection, sampling locations and data repeatability. The accuracy of this technique was also evaluated. Aromatic-hydrocarbon species concentrations were measured in laminar co-flow diffusion flames of ethylene (C2H4) and synthetic paraffinic kerosene (SPK). The results obtained from the ethylene flame were compared to its numerical simulation, with the goal of achieving agreement within an order of magnitude. The differences between simulated values and experimental measurements, along with the limitations of the technique, were used as an indication of the accuracy of the technique.

The measurement of Polycyclic Aromatic Hydrocarbons (PAHs) in flames is essential for the understanding of soot formation. In comparison to conventional aromatics-sampling techniques, a new technique was proposed that involves fewer manual operations and no hazardous extraction solvents. Apparatus and experimental procedures of the newly proposed adsorptive-sampling and desorptive-extraction technique for aromatic-hydrocarbon measurements were established in this study. The capabilities and limitations of this new technique were assessed in terms of limits of detection, sampling locations and data repeatability. The accuracy of this technique was also evaluated. Aromatic-hydrocarbon species concentrations were measured in laminar co-flow diffusion flames of ethylene (C2H4) and synthetic paraffinic kerosene (SPK). The results obtained from the ethylene flame were compared to its numerical simulation, with the goal of achieving agreement within an order of magnitude. The differences between simulated values and experimental measurements, along with the limitations of the technique, were used as an indication of the accuracy of the technique.

Heavy Fuel Oil (HFO) is a petroleum product and emerging contaminant used as fuel by cargo ships, cruise liners, and oil tankers. As a high-frequency, low volume commodity shipped by pipeline, train, truck, and ship, it is at high risk for small-scale spills in terrestrial, aquatic, and marine environments. There are few reports characterizing HFOs and quantifying the contaminants therein, but previous studies have shown that the most toxic classes of compounds in petroleum products are polycyclic aromatic hydrocarbons (PAHs). This project seeks to address that by analyzing HFO 7102, the specific HFO spilled in Wabamun Lake, Alberta in August 2005. Through an Effects-Driven Fractionation and Analysis, HFO 7102 was successively fractionated by physical and chemical means. First, a low-temperature vacuum distillation separated the oil into three fractions by volatility. The most toxic of these (lowest median toxic concentration, or LC50), F3, underwent a series of solvent extractions to remove asphaltenes and waxes. The remaining PAH-rich extract (F3-1) was further separated using open column chromatography into non-polar, mid-polar, and polar fractions with groupings approximately by number of aromatic rings. At each stage, fractions and sub-fractions were characterized by GC-MS for compositional analysis and bioassays were conducted with rainbow trout embryos. In this fashion, toxicity thresholds were developed for all fractions and the components of HFO 7102 associated with toxicity were identified and quantified. The F3 fraction was six times more toxic than the whole oil. While the wax fraction (F3-2) was shown to be non-toxic, the remaining PAH-rich extract (F3-1) accounted for all of the toxicity in F3. Future work may be done to determine the relative toxicity of the last fractions generated and identify a range of PAH responsible for fish toxicity. It is expected that the F3-1-2 fraction will be most toxic, as it contains nearly all of the three-ring and most of the four-ring PAH. These size classes of PAH have been associated with chronic toxicity to fish embryos in studies of crude oil. Further separations may be attempted to identify a more specific range of toxic compounds, such as by degree of alkylation. / Thesis (Master, Chemistry) -- Queen's University, 2012-07-31 11:31:15.238

<p>Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous environmental contaminants formed from the incomplete combustion of fossil fuels and are found in the environment as complex mixtures. PAHs are developmentally toxic to fish, causing yolk sac edema, hemorrhaging, craniofacial malformations and cardiac defects including impaired heart looping, elongated heart, decreased blood flow, and pericardial effusion. Previous research has shown that many of the toxic effects of PAHs are mediated through the aryl hydrocarbon receptor (AHR), which upregulates phase I and II metabolic genes, but the underlying mechanisms of PAH-induced toxicity are not yet known. The primary goal of this dissertation was to better understand the molecular mechanisms by which PAH mixtures cause developmental toxicity in fish. To this end, the zebrafish (Danio rerio) was used as a developmental model. Simple mixtures consisting of a PAH that is an AHR agonist (benzo[a]pyrene or benzo[k]fluoranthene) and a PAH that is a cytochrome P450 1 (CYP1) inhibitor (fluoranthene) were used in these experiments along with the dioxin-like compound 3,3',4,4',5-pentachlorobiphenyl (PCB-126). Morpholino gene knockdown was used to examine the role of specific genes in response to PAHs, gene expression changes in response to PAH exposures were examined via QPCR, quantification of pericardial effusion was used as a metric for cardiac toxicity, and CYP1 activity was measured as an indication of AHR pathway induction. First, PAH mixtures consisting of an AHR agonist (BkF) and a CYP1 inhibitor (FL) induced cardiac toxicity that was preceded by upregulation of CYP1 and redox-responsive gene expression, and these effects were dependent upon the AHR2. Second, knockdown of glutathione s-transferase pi class 2 (GSTp2), part of phase II metabolism, exacerbated PAH-induced toxicity but did not affect PCB-126-induced toxicity. Third, knockdown of another isoform of the AHR, AHR1, exacerbated PAH- and PCB-126-induced toxicity and increased CYP1 activity but did not affect CYP expression in response to these agonists. Simultaneous knockdown of AHR1A and AHR2 did not exacerbate nor ameliorate PAH-induced toxicity but did prevent PCB-126-induced toxicity. Fourth, to examine AHR2-dependent and AHR2-independent gene induction in zebrafish hearts in response to PAHs, microarrays were used. Gene expression changes caused by PAHs were largely AHR2-dependent and consisted of genes involved in cell adhesion, oxidation-reduction, and TGF-&beta signaling processes as well as genes involved in heart structure and function. These findings help to elucidate how PAHs elicit deformities during development and highlight differences between PAHs and other AHR agonists. Additionally, these experiments have identified other genes in addition to AHR2 that are involved in mediating or responding to the toxicity of PAHs.</p> / Dissertation