Benzene and toluene are known groundwater contaminants . Male CD-I mice were continuously exposed to 0, 31, 166, and 790 mg/ L benzene and 0, 17, 80, and 405 mg/L toluene, respectively, in drinking water for four weeks. Benzene caused a reduction of leukocytes, lymphocytes and erythrocytes, and resulted in a macrocytic anemia. Lymphocyte response to both B- and T-cell mitogens, mixed lymphocyte response to alloantigens, and the ability of cytotoxic lymphocytes to lyse tumor cells were enhanced at the lowest dose of benzene and depressed in the higher dosage animals. Benzene at doses of 166 and 790 mg/L decreased the number of sheep red blood cell (SRBC) -specific plaque-forming cells, the level of serum anti-SRBC antibody, and the activity of interleukin-2 (IL -2). Benzene treatment increased endogenous concentrations of the brain biogenic amines norepinephrine (NE), dopamine (DA) and serotonin (5-HT), and concomitantly, elevated the levels of their respective major metabolites vanillymandelic acid (VMA), 3,4-dihydroxyphenyl acetic acid (DOPAC) and homovanillic acid (HVA), and 5-hydroxyindoleacetic acid (5-HIAA), in several brain regions . In most cases, the changes were dose related; in several instances, maximum effects occurred at the 166 mg/L benzene dose. Toluene did not adversely affect the hematological parameters. Depression of immune function was evident at the highest dose (405 mg/L), except for mitogeneses. Increased neurochemical concentrations caused by toluene displayed a dose-dependent biphasic manner which began at a dose of 17 mg/L, peaked at 80 mg/L, and decreased at 405 mg/L. Toluene treatment had more selective effects on NE, 5-HT ,VMA and 5-HIAA, than DA, DOPAC and HVA. Both compounds, by increasing concentrations of the hypothalamic NE and its major metabolite VMA, stimulated the hypothalamic-pituitary-adrenocortical axis activity, resulting in an elevated plasma adrenocorticotropic hormone and serum corticosterone which had an additive adverse effect on IL-2 synthesis. Toluene, 325 mg/ L, completely inhibited benzene-induced cytopenia and immunosuppression when it was coadministered with benzene (166 mg/L). The low dose of toluene (80 mg/L ) did not antagonize benzene immunotoxicity. Mice given the combined exposures exhibited raised levels of regional neurochemicals when compared to the untreated controls. Increased levels of monoamine metabolites in several brain regions were greater in the combined treatments of benzene and toluene than when either chemical was used alone. The results of the interaction studies support the known metabolic interaction mechanisms of benzene and toluene.

<p>Nitrate is one of the most common groundwater contaminants, with levels commonly exceeding established drinking water limits. In areas of high agricultural or industrial nitrate use, nitrate contaminated groundwater poses a potential health risk. In situ denitrification is the microbially mediated reduction of nitrate to innocuous nitrogen gas compounds and is the principal process for nitrate removal in contaminated aquifers. This process is becoming increasingly recognized for its ability to reduce or eliminate nitrate concentrations in groundwater with minimal site disturbance and cost. Predicting the extent to which denitrification occurs in aquifers as well as the rate, therefore, has become the focus of numerous mathematical models. However, the predictive capabilities of numerical models are constrained because knowledge of the biological processes implicated in denitrification is limited.</p> <p>This report examines the microbial processes involved in <i>in situ</i> denitrification, and then applies this knowledge to assess the capability of a two-dimensional numerical model, NBI02D. NBI02D is a variation of a code, SEAM2D, developed by Widdowson (1988,1992).</p> <p>Model development and model application are presented. The model development overview provides insight to the mathematical methods used to simulate the microbial processes. The model application compares model predictions with data received from a USGS research site on Cape Cod, Massachusetts. Data are derived from a natural gradient experiment in which formate was injected into a carbon-limited aquifer in order to stimulate and accelerate denitrification. NBI02D simulations for the Cape Cod site are developed for model verification and model applicability.</p> / Master of Science