Abstract:This study measured part of the in-hive pesticide exposome by analyzing residues from live in-hive bees, stored pollen, and wax in migratory colonies over time and compared exposure to colony health. We summarized the pesticide burden using three different additive methods: (1) the hazard quotient (HQ), an estimate of pesticide exposure risk, (2) the total number of pesticide residues, and (3) the number of relevant residues. Despite being simplistic, these models attempt to summarize potential risk from multi… Show more
“…Cyfluthrin alone accounted for 48% and 25% of total contact and oral pesticide risk in the study, respectively (Table 1). Considering that >150 additional insecticide, fungicide and herbicide compounds have been found in beebread1435, but weren’t screened for in our study, our data may in fact overestimate the proportion of pesticide risk that comes from during-bloom sprays.…”
Honey bees provide critical pollination services for many agricultural crops. While the contribution of pesticides to current hive loss rates is debated, remarkably little is known regarding the magnitude of risk to bees and mechanisms of exposure during pollination. Here, we show that pesticide risk in recently accumulated beebread was above regulatory agency levels of concern for acute or chronic exposure at 5 and 22 of the 30 apple orchards, respectively, where we placed 120 experimental hives. Landscape context strongly predicted focal crop pollen foraging and total pesticide residues, which were dominated by fungicides. Yet focal crop pollen foraging was a poor predictor of pesticide risk, which was driven primarily by insecticides. Instead, risk was positively related to diversity of non-focal crop pollen sources. Furthermore, over 60% of pesticide risk was attributed to pesticides that were not sprayed during the apple bloom period. These results suggest the majority of pesticide risk to honey bees providing pollination services came from residues in non-focal crop pollen, likely contaminated wildflowers or other sources. We suggest a greater understanding of the specific mechanisms of non-focal crop pesticide exposure is essential for minimizing risk to bees and improving the sustainability of grower pest management programs.
“…Cyfluthrin alone accounted for 48% and 25% of total contact and oral pesticide risk in the study, respectively (Table 1). Considering that >150 additional insecticide, fungicide and herbicide compounds have been found in beebread1435, but weren’t screened for in our study, our data may in fact overestimate the proportion of pesticide risk that comes from during-bloom sprays.…”
Honey bees provide critical pollination services for many agricultural crops. While the contribution of pesticides to current hive loss rates is debated, remarkably little is known regarding the magnitude of risk to bees and mechanisms of exposure during pollination. Here, we show that pesticide risk in recently accumulated beebread was above regulatory agency levels of concern for acute or chronic exposure at 5 and 22 of the 30 apple orchards, respectively, where we placed 120 experimental hives. Landscape context strongly predicted focal crop pollen foraging and total pesticide residues, which were dominated by fungicides. Yet focal crop pollen foraging was a poor predictor of pesticide risk, which was driven primarily by insecticides. Instead, risk was positively related to diversity of non-focal crop pollen sources. Furthermore, over 60% of pesticide risk was attributed to pesticides that were not sprayed during the apple bloom period. These results suggest the majority of pesticide risk to honey bees providing pollination services came from residues in non-focal crop pollen, likely contaminated wildflowers or other sources. We suggest a greater understanding of the specific mechanisms of non-focal crop pesticide exposure is essential for minimizing risk to bees and improving the sustainability of grower pest management programs.
“…Honey bees often are simultaneously exposed to natural toxins from plants and microorganisms, pesticides and environmental contaminants, as well as apicultural drugs applied by beekeepers . Some studies list pesticide exposure as a possible contributor to high yearly loss rates in managed bee populations …”
“…Since queens are fed a strict diet of worker glandular secretions (i.e, they do not consume potentially contaminated flower products) [13][14][15], they are normally buffered from direct oral xenobiotic exposure [16,17]. However, pesticides (including miticides, fungicides, herbicides, and insecticides) accumulate in wax [18,19] and thus can pose a contact exposure hazard to queens. A cumulative hazard quotient (HQ)…”
Background: Queen failure is a persistent problem in beekeeping operations, but in the absence of overt symptoms it is often difficult, if not impossible, to ascertain the root cause. Stressors like heat-shock, cold-shock, and sublethal pesticide exposure can reduce stored sperm viability and lead to cryptic queen failure. Previously, we suggested candidate protein markers indicating heat-shock in queens, which we investigate further here, and tested new stressors to identify additional candidate protein markers.Results: We found that heat-shocking queens for upwards of one hour at 40 °C was necessary to induce significant changes in the two strongest candidate heat-shock markers, and that relative humidity significantly influenced the degree of activation. In blind heat-shock experiments, we tested the efficiency of these markers at assigning queens to their respective treatment groups and found that one marker was sufficient to correctly assign queens 75% of the time. Finally, we compared cold-shocked queens at 4 °C and pesticide-exposed queens to controls to identify candidate markers for these additional stressors, and compared relative abundances of all markers to queens designated as 'healthy' and 'failing' by beekeepers.Conclusions: This work offers some of the first steps towards developing molecular diagnostic tools to aid in determining cryptic causes of queen failure. Further work will be necessary to determine how long after the stress event a marker's expression remains changed and how accurate these could be in the field.
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