Thesis (Ph. D.)--Joint Program in Oceanography (Massachusetts Institute of Technology, Dept. of Earth, Atmospheric, and Planetary Sciences; and the Woods Hole Oceanographic Institution), 2000. / Includes bibliographical references (p. 207-219). / Processes affecting organic carbon distribution and composition can control the speciation of organic contaminants such as polychlorinated biphenyls (PCBs) and ultimately determine their residence time in a particular environment. In marine systems, the microbial loop influences organic carbon dynamics by recycling a significant fraction of dissolved and particulate organic matter. The goal of this thesis was to understand how these recycling processes affect chlorobiphenyl (CB) cycling in marine systems by monitoring CB dynamics among organic carbon pools represented by dissolved organic matter, bacterial prey and phagotrophic protozoan grazers. Initially, I studied the extent to which a protozoan grazer (Uronema sp.-10[micro]m ciliate) equilibrated with aqueous PCBs within 2-3 hours. Initial calculations predicted rapid equilibration via passive diffusion. Experimentally, no difference in equilibration time was noted between grazing and non-grazing protozoa, indicating that diffusion was the primary uptake pathway for these organisms. The results were extended to determine the transition size of an organism where the rates of diffusive and ingested uptake are equivalent (100-500[micro]m). Disassociation rate constants were estimated for complexes of CB congeners and dissolved organic carbon (DOC). CB-DOC complexes enhanced the diffusive uptake rate constant for Tenax resin and, by inference, protozoan grazers. In the second phase of this work, concentrations of surfactants, organic carbon and cells were monitored over time in protozoan cultures. The effects of bacterial growth substrate and protozoan species were examined. Surfactants increased during protozoan exponential growth while total DOC concentrations decreased. Production of / (cont.) surface-active material in ciliate cultures was significantly higher than in flagellate cultures, and all protozoan cultures were higher than the bacterial control. Common headspace vessels were then used to compare and contrast the affinity of protozoan and bacterial culture filtrates (<0.2[micro]m) for PCBs relative to a seawater control. Affinities were normalized to bulk DOC and surfactant concentrations to determine underlying relationships among these parameters. Values of equilibrium partition coefficients (K[oc]) ranged from 10⁴·⁶ in Vineyard Sound seawater to 10⁵·⁴ and 10⁵·⁵ in protist cultures, indicating that "grazer-enhanced" DOM was a better sorbent for PCBs than DOM in bacterial controls and Vineyard Sound seawater. / by Elizabeth Belle Kujawinski. / Ph.D.

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Szeto Tsz Kwan Leo. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2005. / Includes bibliographical references (leaves 112-120). / Abstracts in English and Chinese. / Abstract --- p.i / 摘要 --- p.iii / Acknowledgements --- p.v / Table of Contents --- p.vi / List of Tables --- p.ix / List of Figures --- p.x / Abbreviations --- p.xii / Chapter Chapter 1 --- Introduction --- p.1 / Chapter 1.1 --- Heavy metals contaminations in Shing Mun River --- p.1 / Chapter 1.1 --- Importance of copper regulation and role of liverin copper metabolism --- p.6 / Chapter 1.1.1 --- Role of copper --- p.6 / Chapter 1.1.2 --- Toxicity due to unbalanced copper regulation --- p.7 / Chapter 1.1.3 --- Function of liver in copper detoxification --- p.9 / Chapter 1.2 --- Aims and rationale of this research --- p.11 / Chapter Chapter 2 --- Heavy metal concentrations of tilapia samples collected from Shing Mun River --- p.12 / Chapter 2.1 --- Introduction --- p.12 / Chapter 2.1.1 --- Sampling sites - Fo Tan and Siu Lek Yuen Nullah --- p.12 / Chapter 2.1.2 --- Tilapia samples collected from the sites --- p.16 / Chapter 2.1.3 --- Tilapia as a study model --- p.18 / Chapter 2.1.4 --- Bioavailability of heavy metals in water --- p.19 / Chapter 2.1.5 --- Metal content in liver --- p.20 / Chapter 2.1.6 --- Aim of this chapter --- p.20 / Chapter 2.2 --- Materials and Methods --- p.22 / Chapter 2.2.1 --- Collection of control and field samples --- p.22 / Chapter 2.2.2 --- Heavy metal concentrations determination --- p.23 / Chapter 2.2.3 --- Homogenization of liver cells --- p.24 / Chapter 2.2.4 --- Subcellular fractionation --- p.24 / Chapter 2.2.5 --- Determination of copper and zinc content in each subcellular fraction --- p.253 / Chapter 2.3 --- Results --- p.27 / Chapter 2.3.1 --- Physical data --- p.27 / Chapter 2.3.2 --- Metal concentrations in liver and muscle --- p.27 / Chapter 2.3.3 --- Copper and zinc subcellular distribution in liver cell --- p.33 / Chapter 2.4 --- Discussion --- p.36 / Chapter 2.4.1 --- Difference in metal concentration between sites --- p.36 / Chapter 2.4.2 --- Copper contamination in water and fish organ (muscle and liver) from the Shing Mun River --- p.36 / Chapter 2.4.3 --- Comparison of metal content in muscle and liver at Fo Tan site with previous studies --- p.39 / Chapter 2.4.4 --- Copper and zinc concentrations in the liver of tilapia --- p.42 / Chapter 2.4.5 --- Copper and zinc sebcellular distribution in the liver of tilapia --- p.43 / Chapter Chapter 3 --- Column chromatography of hepatic proteins from tilapias --- p.44 / Chapter 3.1 --- Transport of metals from circulatory system to liver --- p.44 / Chapter 3.1.1 --- Copper transporting plasma proteins in vertebrates --- p.44 / Chapter 3.1.2 --- Copper uptake into hepatocytes --- p.45 / Chapter 3.1.3 --- Intracellular metabolism of copper --- p.48 / Chapter 3.1.4 --- Mechanism of copper toxicity following excess accumulation --- p.49 / Chapter 3.1.5 --- Aim of this chapter --- p.50 / Chapter 3.2 --- Materials and Methods --- p.51 / Chapter 3.2.1 --- Purification of liver cytosolic proteins by gel-filtration column chromatography --- p.51 / Chapter 3.2.2 --- Copper content detection in elution --- p.52 / Chapter 3.2.3 --- Analysis of peaks from elution profile using tricine gel SDS PAGE --- p.53 / Chapter 3.3 --- Results --- p.55 / Chapter 3.3.1 --- Gel-filtration liquid chromatography elution profiles --- p.55 / Chapter 3.3.2 --- SDS PAGE analysis of peaks in elution profiles --- p.51 / Chapter 3.4 --- Discussion --- p.54 / Chapter 3.4.1 --- Comparison of gel filtration profiles of sample liver cytosol between sites and sexes --- p.64 / Chapter 3.4.2 --- Possible proteins in peaks found in the gel filtration profiles --- p.64 / Chapter 3.4.3 --- Common copper-indeced proteins --- p.67 / Chapter 3.5 --- Conclusion --- p.70 / Chapter Chapter 4 --- Two-dimensional electrophoresis of hepatic cutosol of tilapias caught from Shing Mun River and copper-treated HEPA T1 cell --- p.72 / Chapter 4.1 --- Introduction --- p.72 / Chapter 4.1.1 --- The need of ´بin vitro' experiment --- p.72 / Chapter 4.1.2 --- Choice of cell line --- p.73 / Chapter 4.1.3 --- Aim of this chapter --- p.74 / Chapter 4.2 --- Materials and Methods --- p.76 / Chapter 4.2.1 --- HEPA T1 cell cultivation --- p.76 / Chapter 4.2.2 --- Copper exposure of HEPA T1 cell --- p.77 / Chapter 4.2.3 --- Subcellular protein extraction of the copper-treated HEPA T1 cells --- p.77 / Chapter 4.2.4 --- Bicinchoninic Acidic (BCA) Protein Assay --- p.79 / Chapter 4.2.5 --- Two-dimensional gel electrophoresis --- p.79 / Chapter 4.3 --- Results --- p.83 / Chapter 4.3.1 --- Graphical presentation of spots observed on 2-dimensional gel of field samples and copper-injected samples --- p.33 / Chapter 4.3.2 --- Graphical presentation of spots detected on 2-dimensional gel of HEPAT1 cells --- p.84 / Chapter 4.3.3 --- Comparison of matched spots on 2-dimensional gels among control and copper-treated HEPAT1 cells --- p.97 / Chapter 4.4 --- Discussion --- p.105 / Chapter 4.4.1 --- Comparison of the spot patterns between field sample and copperOtreated HEPA T1 cells --- p.105 / Chapter 4.5 --- Conclusion --- p.107 / Chapter Chapter 5 --- General Discussions --- p.108 / Chapter 5.2 --- Research Overview --- p.108 / Chapter 5.2 --- Characterization of metal binding proteins from the cytosol of liver of tilapia --- p.109 / REFERENCES --- p.112

by Wong On Nei. / Thesis submitted in: October 2004. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2005. / Includes bibliographical references (leaves 101-116). / Abstracts in English and Chinese. / ABSTRACT --- p.ii / 摘要 --- p.iv / ACKNOWLEDGEMENTS --- p.vi / TABLE OF CONTENTS --- p.vii / LIST OF TABLES --- p.xi / LIST OF FIGURES --- p.xiii / Chapter CHAPTER ONE --- INTRODUCTION --- p.1 / Chapter 1.1 --- Background --- p.1 / Chapter 1.2 --- Lethal and sublethal effects of SS on fish --- p.2 / Chapter 1.2.1 --- Biological effects --- p.2 / Chapter 1.2.2 --- Molecular biomarkers --- p.3 / Chapter 1.2.2.1 --- Acetylcholinesterase activity inhibition assay --- p.4 / Chapter 1.2.2.2 --- Induction of cytochrome P450 mRNA --- p.5 / Chapter 1.2.2.3 --- Induction of metallothionein mRNA --- p.6 / Chapter 1.2.3 --- Study on CYP1A and MT expression / induction --- p.8 / Chapter 1.2.3.1 --- Reverse Transcription (RT) --- p.8 / Chapter 1.2.3.2 --- Polymerase chain reaction (PCR) --- p.8 / Chapter 1.3 --- Objectives --- p.11 / Chapter CHAPTER TWO --- MATERIALS AND METHODS --- p.13 / Chapter 2.1 --- Study sites --- p.13 / Chapter 2.2 --- Sediment --- p.15 / Chapter 2.2.1 --- Sediment samples collection --- p.15 / Chapter 2.2.2 --- Sediment handling --- p.15 / Chapter 2.2.3 --- Sediment dry-wet (w/w) ratio measurement --- p.15 / Chapter 2.2.4 --- Heavy metal content analysis --- p.16 / Chapter 2.2.5 --- Organic content analysis --- p.16 / Chapter 2.3 --- Test organism --- p.17 / Chapter 2.4 --- Bioassays --- p.17 / Chapter 2.4.1 --- 10-day exposure treatments --- p.17 / Chapter 2.4.1.1 --- Experimental setup --- p.17 / Chapter 2.4.1.2 --- Procedure --- p.21 / Chapter 2.4.1.3 --- Tissue sample collection --- p.22 / Chapter 2.4.2 --- 30-day exposure treatments --- p.22 / Chapter 2.4.2.1 --- Behavioural observations --- p.23 / Chapter 2.4.2.2 --- Tissue sample collection --- p.23 / Chapter 2.5 --- Molecular Biomarkers --- p.25 / Chapter 2.5.1 --- Tested samples --- p.25 / Chapter 2.5.2 --- Acetylcholinesterase activity inhibition assay --- p.25 / Chapter 2.5.2.1 --- Acetylcholinesterase activity assay --- p.25 / Chapter 2.5.2.2 --- BioRad Bradford assay --- p.26 / Chapter 2.5.2.3 --- Calculation of specific enzyme activity --- p.26 / Chapter 2.5.3 --- Study on CYP1A and MT expression / induction --- p.27 / Chapter 2.5.3.1 --- Gill and liver tissue samples --- p.27 / Chapter 2.5.3.2 --- Preparation of ribonuclease free reagents and apparatus --- p.27 / Chapter 2.5.3.3 --- Isolation of total RNA --- p.27 / Chapter 2.5.3.4 --- Spectrophotometric analyses of DNA and RNA --- p.28 / Chapter 2.5.3.5 --- First strand cDNA synthesis --- p.28 / Chapter 2.5.3.6 --- Cloning and sequencing of CYP1A and MT gene --- p.29 / Chapter 2.5.3.7 --- RT-PCR co-amplification of CYP1A and 18S rRNA --- p.34 / Chapter 2.5.3.8 --- Real-time RT-PCR --- p.36 / Chapter CHAPTER THREE --- RESULTS --- p.39 / Chapter 3.1 --- Sediment chemistry --- p.39 / Chapter 3.1.1 --- Sediment dry-wet (w/w) ratio --- p.39 / Chapter 3.1.2 --- Heavy metal content of sediments --- p.39 / Chapter 3.1.3 --- Levels of total PCBs and PAHs in sediment --- p.39 / Chapter 3.2 --- Monitoring of test conditions --- p.42 / Chapter 3.3 --- Bioassays --- p.42 / Chapter 3.3.1 --- Survivorship --- p.42 / Chapter 3.3.2 --- Growth --- p.46 / Chapter 3.3.3 --- Feeding rate --- p.51 / Chapter 3.3.4 --- Behaviour --- p.54 / Chapter 3.3.5 --- Sediment clogging --- p.59 / Chapter 3.3.6 --- Body lesions --- p.59 / Chapter 3.3.7 --- Abnormal behaviour --- p.59 / Chapter 3.4 --- Molecular biomarkers --- p.63 / Chapter 3.4.1 --- Acetylcholinesterase activity inhibition assay --- p.63 / Chapter 3.4.2 --- Cloning and sequencing of CYP1A and MT gene --- p.66 / Chapter 3.4.3 --- RT-PCR co-amplification of CYP1A and 18S rRNA --- p.73 / Chapter 3.4.4 --- Real-time RT-PCR --- p.77 / Chapter CHAPTER FOUR --- DISCUSSION --- p.84 / Chapter 4.1 --- Sediment chemistry --- p.84 / Chapter 4.2 --- Biological responses --- p.85 / Chapter 4.3 --- Molecular biomarkers --- p.91 / Chapter 4.3.1 --- Acetylcholinesterase activity inhibition assay --- p.91 / Chapter 4.3.2 --- Cloning and sequencing of CYP1A and MT gene --- p.93 / Chapter 4.3.3 --- RT-PCR co-amplification of CYP1A and 18S rRNA --- p.93 / Chapter 4.3.4 --- Real-time RT-PCR --- p.95 / Chapter 4.4 --- Recommendations --- p.99 / Chapter 4.5 --- Conclusions --- p.100 / REFERENCES --- p.101 / APPENDIX --- p.117

Pak Ah Pan. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2006. / Includes bibliographical references (leaves 149-158). / Abstracts in English and Chinese. / ABSTRACT --- p.ii / 摘要 --- p.vi / ACKNOWLEDGEMENTS --- p.vii / TABLE OF CONTENTS --- p.ix / LIST OF TABLES --- p.xiv / LIST OF FIGURES --- p.xvi / Chapter CHAPTER ONE --- LITERATURE REVIEWS --- p.1 / Chapter 1.1. --- Sediment pollution problems --- p.1 / Chapter 1.2. --- Effects of suspended sediments (SS) on aquatic biota --- p.3 / Chapter 1.3. --- Histopathological biomarkers in fish --- p.7 / Chapter CHAPTER TWO --- INTRODUCTION --- p.20 / Chapter CHAPTER THREE --- MATERIALS AND METHODS --- p.23 / Chapter 3.1. --- Sediments --- p.23 / Chapter 3.1.1. --- Sediment sampling sites --- p.23 / Chapter 3.1.2. --- Sediment collection and handling --- p.25 / Chapter 3.1.3. --- Chemical analysis of sediments --- p.25 / Chapter 3.2. --- Collection and maintenance of fish --- p.26 / Chapter 3.3. --- Sediment bioassays for groupers (E. coioides) --- p.28 / Chapter 3.3.1. --- Preparation of suspended sediments (SS) --- p.28 / Chapter 3.3.2. --- Experimental design --- p.30 / Chapter 3.3.2.1. --- 10-day exposure experiment --- p.30 / Chapter 3.3.2.2. --- 30-day exposure experiment --- p.31 / Chapter 3.3.2.3. --- Time-course and recovery experiment --- p.33 / Chapter 3.3.3. --- Measurement of oxygen consumption and ventilation rates --- p.33 / Chapter 3.4. --- "Tissue sample collection, preparation and examinations" --- p.35 / Chapter 3.4.1. --- Study of sediment clogging --- p.35 / Chapter 3.4.2. --- Scanning electron microscopy (SEM) study --- p.37 / Chapter 3.4.3. --- Histopathological investigations --- p.38 / Chapter 3.4.3.1. --- Histopathology of gills --- p.40 / Chapter 3.4.3.2. --- Histopathology of liver --- p.40 / Chapter 3.4.3.3. --- Histopathology of kidney --- p.41 / Chapter 3.5. --- Sediment bioassays for seabreams (A. schlegeli) --- p.42 / Chapter 3.6. --- Statistical analysis --- p.43 / Chapter CHAPTER FOUR --- RESULTS --- p.44 / Chapter 4.1. --- Chemical analysis of sediments --- p.44 / Chapter 4.2. --- Physicochemical parameters --- p.47 / Chapter 4.3. --- Sediment bioassays for groupers (E. coioides) --- p.49 / Chapter 4.3.1. --- Feeding rate --- p.49 / Chapter 4.3.2. --- Growth rate --- p.49 / Chapter 4.3.3. --- Sediment clogging --- p.53 / Chapter 4.3.4. --- Survival rates --- p.53 / Chapter 4.3.5. --- Oxygen consumption rate and ventilation rate --- p.56 / Chapter 4.3.6. --- SEM study --- p.56 / Chapter 4.3.7. --- Histopathological investigations --- p.64 / Chapter 4.3.7.1. --- Histopathology of gills --- p.64 / Chapter 4.3.7.2. --- Histopathology of liver --- p.82 / Chapter 4.3.7.3. --- Histopathology of kidney --- p.94 / Chapter 4.4. --- Sediment bioassays for seabreams (A. schlegeli) --- p.113 / Chapter 4.4.1. --- Survival rates --- p.113 / Chapter 4.4.2. --- Histopathological investigations of gills and liver --- p.113 / Chapter CHAPTER FIVE --- DISCUSSION --- p.122 / Chapter 5.1. --- Hypoxic effects of SS on histopathology --- p.122 / Chapter 5.2. --- Synergistic effects between SS and chemical --- p.126 / Chapter 5.3. --- Effects of gill impairment on biological responses --- p.131 / Chapter 5.4. --- Reparability of histopathological alterations --- p.135 / Chapter 5.5. --- Species differences in sensitivity to SS --- p.135 / Chapter 5.6 --- Recommendation --- p.136 / Chapter CHAPTER SIX --- CONCLUSION --- p.138 / APPENDICES --- p.140 / REFERENCES --- p.149

by Tse Ching Yee Carol. / Thesis submitted in: September 2005. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2006. / Includes bibliographical references (leaves 75-90). / Abstracts in English and Chinese. / Abstract --- p.ii / 摘要 --- p.iv / Acknowledgments --- p.vi / Table of contents --- p.vii / List of tables X / List of figures --- p.xii / Chapter 1.0 --- Introduction --- p.1 / Chapter 1.1 --- Sediment pollution in Hong Kong --- p.1 / Chapter 1.2 --- Impact of suspended sediment on fish --- p.2 / Chapter 1.3 --- Biochemical responses to pollution --- p.3 / Chapter 1.3.1 --- Aspartate aminotransferase (AST) and alanine aminotransferase (ALT) --- p.4 / Chapter 1.3.2 --- Creatine kinase (CK) --- p.5 / Chapter 1.3.3 --- Ethoxyresorufin O-deethylase (EROD) --- p.6 / Chapter 1.3.4 --- DNA damage --- p.8 / Chapter 1.4 --- Study of recovery --- p.10 / Chapter 1.5 --- Objectives and significances --- p.11 / Chapter 2.0 --- Materials and Methods --- p.13 / Chapter 2.1 --- Study sites --- p.13 / Chapter 2.2 --- Sediments collection and handling --- p.13 / Chapter 2.3 --- Measurement of heavy metals and organic contents of sediment --- p.15 / Chapter 2.4 --- Exposure tests --- p.16 / Chapter 2.4.1 --- Test organisms --- p.16 / Chapter 2.4.2 --- 10- and 30-day exposure experiments --- p.18 / Chapter 2.4.3 --- 20-day exposure and recovery experiment --- p.19 / Chapter 2.5 --- Biochemical responses --- p.19 / Chapter 2.5.1 --- "Aspartate aminotransferase (AST), alanine aminotransferase (ALT) and creatine kinase (CK) activities" --- p.19 / Chapter 2.5.2 --- Ethoxyresorufin O-deethylase activity (EROD) --- p.20 / Chapter 2.5.3 --- DNA damage --- p.21 / Chapter 2.5.4 --- Statistical analysis --- p.22 / Chapter 3.0 --- Results --- p.24 / Chapter 3.1 --- Physical and chemical parameters --- p.24 / Chapter 3.2 --- Pollutants in sediment --- p.24 / Chapter 3.3 --- Mortality --- p.28 / Chapter 3.4 --- Biochemical responses --- p.31 / Chapter 3.4.1 --- 10- and 30-day exposure experiments --- p.31 / Chapter 3.4.2 --- 20-day exposure and recovery experiments --- p.50 / Chapter 4.0 --- Discussion --- p.58 / Chapter 4.1 --- "Sediment pollution at Port Shelter, Mirs Bay and Victoria Harbor" --- p.58 / Chapter 4.2 --- Biochemical responses --- p.59 / Chapter 4.2.1 --- 10- and 30-day exposure experiments --- p.59 / Chapter 4.2.1.1 --- "AST, ALT and CK" --- p.59 / Chapter 4.2.1.2 --- EROD --- p.63 / Chapter 4.2.1.3 --- DNA damage --- p.67 / Chapter 4.2.2 --- 20-day exposure and recovery experiments --- p.69 / Chapter 5.0 --- Recommendations and conclusions --- p.73 / References --- p.75 / Appendix --- p.91

Previous research regarding aquatic acidification has examined the protonation of the carbonate and does not consider calcium to be a limiting factor. This is the first study to suggest that pH may affect the uptake of calcium in crustacean gills. This project describes ion transport mechanisms present in the cell membranes of white river shrimp Litopenaeus setiferus gill epithelium, and the effects of pH on the uptake of calcium by these means. Partially purified membrane vesicles (PPMV) of shrimp gills were prepared through a homogenization process that has been used previously to define ion transport in crab and lobster gill tissues. In the current study, shrimp gill PPMV calcium uptake at 50 µM, and 250 µM was greatest at pH 7.0 (p=0.01, p=0.0001). A valinomycin/K+ induced membrane potential (PD) at pH 7.0 significantly increased (p=0.003) calcium uptake from that observed in the absence of a PD. An induced PD at pH 8.0 significantly increased (p=0.003) calcium uptake from that observed in the absence of a PD, however, was not significantly greater than uptake at pH 7.0 in the presence of a PD (p=0.05). Amiloride (2mM) treatments, and amiloride (2mM) + verapamil (100µM) cocktail treatments showed significant decrease in calcium uptake from the control (p=0.03), however, they were not different from each other. This indicates an electrogenic carrier with two driving forces: calcium concentration, and asymmetric exchange stoichiometry.

Two Oregon reservoirs contaminated by different mercury sources were compared for mercury distribution in sediment and bioaccumulation by fish. The average mercury concentration in the sediment of Cottage Grove reservoir (0.67 �� 0.05 ��g/g dry wt) was higher than for Dorena Reservoir (0.12 �� 0.01 ��g/g dry wt). Sediment mercury in the main tributary of Cottage Grove Reservoir, which drains the tailing of past mercury mining activities, was ten fold higher than mercury in sediment from other reservoir tributaries with no evidence of mining. However, there were no significant differences between sediment mercury concentrations in the tributaries of the Dorena Reservoir, which has no mercury mining history within its watershed. Three fish species (largemouth bass, bluegill, crappie) from Cottage Grove Reservoir had significantly higher levels of mercury than the same species from Dorena Reservoir. These results indicated that a point source, Black Butte Mine, contributed amounts of mercury in excess of natural deposits based on differences in bioaccumulation among fish populations from these two systems. Cottage Grove Reservoir was examined for environmental evidence of point source mercury pollution. High mercury concentrations were found at various points around the suspected source, the Black Butte Mine area. The highest concentration occurred close to the kiln. The mercury concentration in the sediments of a creek below the mine dump was up to ten times higher than that of the sediments of a creek from a watershed adjacent to the watershed of the mine area. Two sediment cores from the deep area were collected to assess for pollution history profiles. These showed mercury loading in Cottage Grove Reservoir was consistent with the past mercury production in Black Butte Mine. Therefore most of mercury in Cottage Grove Reservoir was believed to be of Black Butte Mine origin. Mercury contents in pore water and food web indicated that continuing mercury transportation from the point source create a management problem in Cottage Grove Reservoir. / Graduation date: 1996