Substantial environmental contamination has occurred from coal tar creosote and pentachlorophenol (C5P) in wood preserving solutions. The present studies focused on the characterization and remediation of these contaminants. The first objective was to delineate a sequence of biological changes caused by chlorinated phenol (CP) exposure. In Clone 9 cells, short-term exposure to 10 ?M C5P decreased pH, GJIC, and GSH, and increased ROS generation. Long-term exposure caused mitochondrial membrane depolarization (25 ?M), increased intracellular Ca2+ (50 ?M), and plasma membrane depolarization (100 ?M). Cells were affected similarly by C5P or 2,3,4,5-C4P, and similarly by 2,3,5-C3P or 3,5-C2P. Endpoints were affected by dose, time, and the number of chlorine substituents on specific congeners. Thus, this information may be used to identify and quantify unknown CPs in a mixture to be remediated. Due to the toxic effects observed due to CP exposure in vitro, the objective of the second study was to develop multi-functional sorbents to remediate CPs and other components of wood preserving waste from groundwater. Cetylpyridinium-exchanged low pH montmorillonite clay (CP-LPHM) was bonded to either sand (CP-LPHM/sand) or granular activated carbon (CP-LPHM/GAC). Laboratory studies utilizing aqueous solution derived from wood preserving waste indicated that 3:2 CP-LPHM/GAC and CP-LPHM/sand were the most effective formulations. In situ elution of oil-water separator effluent indicated that both organoclay-containing composites have a high capacity for contaminants identified in wood preserving waste, in particular high molecular weight and carcinogenic PAHs. Further, GAC did not add substantial sorptive capacity to the composite formulation. Following water remediation, the final aim of this work was to explore the safety of the parent clay minerals as potential enterosorbents for contaminants ingested in water and food. Calcium montmorillonite and sodium montmorillonite clays were added to the balanced diet of Sprague-Dawley rats throughout pregnancy. Based on evaluations of toxicity and neutron activation analysis of tissues, no significant differences were observed between animals receiving clay supplements and control animals, with the exception of slightly decreased brain Rb in animals ingesting clay. Overall, the results suggest that neither clay mineral, at relatively high dietary concentrations, influences mineral uptake or utilization in the pregnant rat.

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.

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

Thesis (Ph. D.)--McMaster University (Canada), 1990. / Source: Dissertation Abstracts International, Volume: 52-10, Section: B, page: 5244. Supervisor: D.R. McCalla.

Thesis (M.S.)--University of Texas at El Paso, 2008. / Title from title screen. Vita. CD-ROM. Includes bibliographical references. Also available online.

Thesis (M.S.) -- Mississippi State University. Department of Chemistry. / Title from title screen. Includes bibliographical references.

Thesis (Ph. D.)--University of Kentucky, 2004. / Title from document title page (viewed Jan. 7, 2005). Document formatted into pages; contains ix, 141p. : ill. Includes abstract and vita. Includes bibliographical references (p. 128-139).

Thesis (M.S.)--West Virginia University, 2004. / Title from document title page. Document formatted into pages; contains vii, 71 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references (p. 64-70).