Environmental factors such as chemical contamination can have immunomodulatory effects on the immune response of fish and may be contributing to the decline in salmonid populations by augmenting disease susceptibility. Xenobiotics can interfere with the immune system at several levels of complexity, and different immune cells and processes have variable sensitivity to pollutants. For this reason, a suite of tests is required to evaluate immunomodulatory mechanisms. In this thesis, I formulated and calibrated an assay for the detection of humoral immunity for chinook salmon (Oncorhynchus tshawvtscha). Subsequently, I used this technique in conjunction with other immune and endocrine assays to detect effects of embryonic exposure to o,p'-DDE, a known environmental estrogen. The technique combines exposure of whole animals or leukocyte cultures to immunomodulatory agents/conditions with in vitro mitogenic activation of B-lymphocytes. The proportion of leukocytes undergoing blastogenesis following in vitro stimulation with lipopolysaccaride (LPS) was quantified by flow cytometric analysis of forward and side scatter properties. In addition, I used a fluorescein isothiocyanate labeled anti-rainbow trout surface immunoglobin monoclonal antibody (anti-RBT SIgM-FITC) to determine the ability of the lymphoblasts to express surface immunoglobin (SIgM) through flow cytometry. I used the assay to evaluate the effects of short-term exposures to o,p'-DDE during early life history stages on the long-term immune competence of fall chinook salmon. Immersion of chinook salmon eggs in 10 ppm o,p'-DDE for 1 h at fertilization followed by 2 h at hatch caused significant reductions in the ability of splenic leukocytes to undergo blastogenesis and express SIgM upon in vitro stimulation with LPS one year after treatment (ANOVA, P<0.05). The concentration of o,p'-DDE in fry treated with 10 ppm o,p'-DDE was 0.92 ��g g����� lipid one month post first feeding. The chemical persisted through development and, one year after exposure, levels in juvenile muscle tissue were 0.94 ��g g����� lipid. Mortality rate, time to hatch, fish size, sex ratios, gonadal development, plasma estradiol and 11-ketotestosterone concentrations were not affected by treatment with o,p'-DDE. In addition, neither plasma lysozyme concentration, nor mitogenic response of splenic leukocytes to concanavallin A or polyinosinic-polycytidylic acid were influenced by the treatment. A short period of exposure to an estrogenic chemical during early periods of development induced long term effects on humoral immune competence of chinook salmon. I discuss the possibility that the xenobiotic is exerting its activity through steroid-mediated pathways. / Graduation date: 2002