Graduate Thesis Or Dissertation
 

Effects of Pesticide Exposure on Honey Bee Health : Impacts of Pesticide Interactions and Exposure Through Multiple Routes

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  • Honey bees (Apis mellifera) are responsible for approximately $17 billion in crop production per year in the United States, and are arguably the most important pollinators in the nation. The future of crop pollination and production is threatened by widespread national honey bee colony losses, which have averaged approximately 30% per year over the past decade. Many factors contribute to colony mortality, but the particular impacts of pesticides are still poorly understood. Here, we investigated the impacts of pesticides under conditions that have not been examined in previous research. Our research focused on the effects of an interaction between the neonicotinoid imidacloprid and the fungicide chlorothalonil, and effects of exposure through multiple routes. To understand the potential impacts of pesticide interactions, we exposed whole colonies to imidacloprid, chlorothalonil, or combination of both chemicals through a pollen diet for one month. We found that many of our response variables were unaffected by our treatments, and that outliers influenced the outcome of several analyses. Brood area and prophenoloxidase activity were significantly affected by different treatments when outliers were excluded, although these differences were no longer significant after the multiple comparisons confidence interval adjustment. Similarly, the number of non-pollen foragers returning to the colonies was affected by the interaction between imidacloprid and time, chlorothalonil and time, and both chemicals and time, when outliers were removed. The interactions indicated that seven weeks after the end of the exposure period, both imidacloprid and chlorothalonil reduced the number of non-pollen foragers returning to the colonies. Imidacloprid and chlorothalonil also reduced the number of total foragers returning to the colonies overall. Our results indicate that colonies may be affected by pesticide exposure long after the exposure period, and that bees exposed to pesticides early in life may be detrimentally affected by that exposure at later stages. To determine whether pesticide exposure through multiple routes has a greater effect on bees than single-route exposure, we conducted a laboratory experiment in which we exposed bees to imidacloprid through pollen diet, sugar syrup, or both routes. We found that exposure through sugar syrup increased the midgut proteolytic enzyme activity overall, as well as glucose oxidase activity after four weeks of exposure. Exposure through sugar syrup, as well as exposure through both routes, increased glucose oxidase activity when outliers were included and excluded from the analysis, respectively. Mortality differed significantly between bees exposed to imidacloprid through sugar syrup and those exposed through both matrices, but none of the treatments were significantly different from the control group. We also found that bees in different treatment groups consumed different amounts of sugar syrup and pollen. Our results indicate the importance of conducting laboratory experiments that better reflect field-realistic pesticide exposure by both incorporating effects over a longer period of exposure, and exposure through multiple routes. In summary, our results provide new knowledge and insights on how pesticides impact long-term colony health. Future research must thoroughly examine statistical procedures, outliers, and statistical power, and must also determine interactions between pesticides and pathogens under different conditions, such as different types of pesticide application, honey bee subspecies, nutritional conditions, season, etc. Discerning the variability in results when these conditions vary will provide a fuller understanding of the true impacts of pesticides on colony health.
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