Resident fishes in coastal estuaries and bays experience multiple abiotic and biotic stressors, including exposure to chemical pollutants such as pesticides. However, the sub-lethal effects of pesticides on the behavior and ecology of fishes remain poorly understood. Therefore, the broad goal of this dissertation was to explore the behavioral and ecological consequences of sub-lethal pesticides on estuarine fishes, in addition to other environmental factors such as habitat structure and parasites. In Chapter 1, I investigated the separate and combined effects of an acute 4 h exposure of the pyrethroid pesticide esfenvalerate and structural habitat complexity on the behavior and predation risk of larval topsmelt, Atherinops affinis. Larvae were exposed to four nominal esfenvalerate concentrations (control, 0.12, 0.59, 1.18 ppb) before placement into 12 L mesocosms with a predator, the three-spine stickleback, Gasterosteus aculeatus. Artificial eelgrass was manipulated to create a uniform and patchy distribution of vegetative structure at a low (500 shoots per m2 ) and high density (1000 shoots per m2 ), in addition to the absence of eelgrass. The capture success of predators and aggregative behavior of prey was quantified during the first 10 min of each trial, and mortality of prey was recorded after 60 min. I observed an increase in the proportion of swimming abnormalities of larvae exposed to esfenvalerate. Surprisingly, prey mortality did not increase linearly with pesticide exposure but increased with habitat structure (density of eelgrass), which may have been a consequence of compensating predator behavior. The degree of prey aggregation decreased with both habitat structure and iv pesticide exposure, suggesting that anti-predator behaviors by prey may have been hampered by the interactive effects of both of these factors. In addition to behavioral consequences, sub-lethal pesticide exposure can predictably alter different physiological endpoints. Acetylcholinesterase (AChE) inhibition has become a common biomarker of organophosphate and carbamate pesticide exposure in fishes. However, the relationship of AChE activity to many ecological behaviors remains poorly understood. In Chapter 2, I exposed California killifish, Fundulus parvipinnis, to three concentrations (control, 1 ppb, 5 ppb) of the organophosphate pesticide, chlorpyrifos, for 4 d. Individual behaviors were recorded and quantified in three consecutive assays, including swimming activity, position in the water column, sociality, foraging, and predator avoidance. Following assays, AChE activity was measured in brain and lateral muscle tissues. AChE was moderately inhibited by 1 ppb chlorpyrifos in brain (35 ± 5% relative to controls) and muscle (25 ± 6%), and significantly inhibited by 5 ppb in brain (85 ± 3%) and muscle (97 ± 1%). Four behaviors were modified by chlorpyrifos exposure: increased surfacing in a novel environment and following a predator attack, decreased sociality, decreased foraging, and decreased distance to a predator following attack. A total 77% of the variation in behavior was described by three principle components, and each component was significantly correlated with AChE inhibition in brain and muscle. This study demonstrates the ecological relevance of the AChE biomarker by linking it to multiple sensitive behaviors that influence individual fitness and population processes. Pesticides are frequently present with multiple additional stressors in coastal and estuarine systems, including parasites. However, little is known regarding the interactive effects of these stressors on the physiology and behavior of resident fishes. In the third and final chapter of my dissertation, I investigated the effects of chlorpyrifos and a common trematode parasite, Euhaplorchis californiensis, on three important traits of California killifish: neurotransmitter activity, release of the stress hormone cortisol, and behavioral modifications. Killifish were collected from a population without E. californiensis, and half of the fish were experimentally infected. Following a 30 d parasite maturation period, infected and uninfected groups were exposed to four concentrations of chlorpyrifos (control, 1, 2, 3 ppb) prior to behavior trials to quantify activity rate, feeding behavior, and anti-predator responses. Rates of water-borne cortisol release were measured non-invasively from each fish prior to infection, one-month postinfection, and following pesticide exposure. AChE activity in the brain and muscle tissue of killifish exposed to the 3 ppb concentration was reduced to 25.43 ± 6.82 % and 39.49 ± 8.30 %, respectively, relative to control fish. Cortisol release was not affected by E. californiensis but was suppressed by each chlorpyrifos level relative to controls. Killifish exposed to the medium (2 ppb) and high (3 ppb) pesticide concentrations exhibited reduced swimming and anti-predator responses. Cortisol and muscle AChE were positively related to swimming activity, while brain AChE was related to foraging behavior. No effects of E. californiensis were observed, possibly because of low parasite densities of experimentally infected fish. Taken together, these studies further establish the potential for sub-lethal pesticide exposure to modify several organismal endpoints in fishes, including neurological, endocrine, and behavioral responses.