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Honey bees are commonly co-exposed to pesticides during crop pollination, including the fungicide captan and neonicotinoid insecticide thiamethoxam. We assessed the impact of exposure to these two pesticides individually and in combination, at a range of field-realistic doses. In laboratory assays, mortality of larvae treated with captan was 80–90% greater than controls, dose-independent, and similar to mortality from the lowest dose of thiamethoxam. There was evidence of synergism (i.e., a non-additive response) from captan-thiamethoxam co-exposure at the highest dose of thiamethoxam, but not at lower doses. In the field, we exposed whole colonies to the lowest doses used in the laboratory. Exposure to captan and thiamethoxam individually and in combination resulted in minimal impacts on population growth or colony mortality, and there was no evidence of synergism or antagonism. These results suggest captan and thiamethoxam are each acutely toxic to immature honey bees, but whole colonies can potentially compensate for detrimental effects, at least at the low doses used in our field trial, or that methodological differences of the field experiment impacted results (e.g., dilution of treatments with natural pollen). If compensation occurred, further work is needed to assess how it occurred, potentially via increased queen egg laying, and whether short-term compensation leads to long-term costs. Further work is also needed for other crop pollinators that lack the social detoxification capabilities of honey bee colonies and may be less resilient to pesticides. [ABSTRACT FROM AUTHOR]

Agricultural intensification has been identified as one of the key causes of global insect biodiversity losses. These losses have been further linked to the widespread use of agrochemicals associated with modern agricultural practices. Many of these chemicals are known to have negative sublethal effects on commercial pollinators, such as managed honeybees and bumblebees, but less is known about the impacts on wild bees. Laboratory‐based studies with commercial pollinators have consistently shown that pesticide exposure can impact bee behavior, with cascading effects on foraging performance, reproductive success, and pollination services. However, these studies typically assess only one chemical, neglecting the complexity of real‐world exposure to multiple agrochemicals and other stressors. In the summer of 2020, we collected wild‐foraging workers of the common eastern bumblebee, Bombus impatiens, from five squash (Cucurbita) agricultural sites (organic and conventional farms), selected to represent a range of agrochemical, including neonicotinoid insecticide, use. For each bee, we measured two behaviors relevant to foraging success and previously shown to be impacted by pesticide exposure: sucrose responsiveness and locomotor activity. Following behavioral testing, we used liquid chromatography–tandem mass spectrometry (LC–MS/MS) chemical analysis to detect and quantify the presence of 92 agrochemicals in each bumblebee. Bees collected from our sites did not vary in pesticide exposure as expected. While we found a limited occurrence of neonicotinoids, two fungicides (azoxystrobin and difenoconazole) were detected at all sites, and the pesticide synergist piperonyl butoxide (PBO) was present in all 123 bees. We found that bumblebees that contained higher levels of PBO were less active, and this effect was stronger for larger bumblebee workers. While PBO is unlikely to be the direct cause of the reduction in bee activity, it could be an indicator of exposure to pyrethroids and/or other insecticides that we were unable to directly quantify, but which PBO is frequently tank‐mixed with during pesticide applications on crops. We did not find a relationship between agrochemical exposure and bumblebee sucrose responsiveness. To our knowledge, this is the first evidence of a sublethal behavioral impact of agrochemical exposure on wild‐foraging bees. [ABSTRACT FROM AUTHOR]

Most pesticide research has focussed on risk to managed honeybees, but other managed and wild bees are also exposed to pesticides. Critically, we know little about the magnitude and sources of risk to honeybees compared with other bees during crop pollination.To compare pesticide exposure and risk across wild and managed bees, we sampled the main bee groups present during bloom in 20 apple orchards, including managed honeybees (Apis mellifera), managed bumblebee workers (Bombus impatiens), wild mining bees (Andrena spp. and Andrena [Melandrena] spp.), bumblebee foundress queens (Bombus impatiens) and eastern carpenter bees (Xylocopa virginica). We screened all bees for 92 pesticides and computed a Risk Quotient using available toxicity data (honeybee LD50s), adjusting for differences in toxicity known to scale with body mass. To gain insight into exposure origin, we compared residues in bees to those in focal orchard apple and dandelion flowers.Nearly all bee samples contained pesticides (95%), with the average contamination level ranging from 7.1 ± 2.8 parts per billion (ppb) in B. impatiens workers to 388.4 ± 146.2 ppb in Andrena. Exposure profiles were similar for all bees except A. mellifera, whose unique exposure profile included high levels of the neonicotinoid insecticide thiamethoxam.All bee groups except wild B. impatiens queens had at least one sample exceeding a US Environmental Protection Agency or European Food Safety Authority exposure level of concern. Apis mellifera experienced significantly greater risk than other bee groups, with 63% and 81% of samples exceeding an acute or chronic exposure level of concern, respectively. Risk to honeybees was driven primarily by high thiamethoxam levels not found in focal orchard flowers and likely originating outside the orchard.Synthesis and applications: We find that pesticide exposure and risk differ between honeybees and other managed and wild bees during apple pollination. Furthermore, pesticide exposure is a landscape‐scale phenomenon and therefore measures to reduce exposure must consider the surroundings beyond focal farms. Limiting orchard sprays, while reducing on‐farm exposures, will not protect far‐foraging bees from off‐farm exposures such as thiamethoxam, which we hypothesize is coming from nearby seed‐treated corn fields planted during apple bloom. [ABSTRACT FROM AUTHOR]

Pathogen transport by biotic or abiotic processes (e.g. mechanical vectors, wind, rain) can increase disease transmission by creating more opportunities for host exposure. But transport without replication has an inherent trade‐off, that creating new venues for exposure decreases the average pathogen abundance at each venue. The host dose‐response relationship is therefore required to correctly assess infection risk. We model and analyse two examples—biotic mechanical vectors in plant–pollinator networks, and abiotic‐facilitated long‐distance pathogen dispersal—to illustrate how oversimplifying the dose‐response relationship can lead to incorrect epidemiological predictions. When the minimum infective dose is high, mechanical vectors amplify disease transmission less than suggested by simple compartment models, and may even dilute transmission. When long‐distance dispersal leads to infrequent large exposures, models that assume a linear force of infection can substantially under‐predict the speed of epidemic spread. Our work highlights an important general interplay between dose‐response relationships and pathogen transport. [ABSTRACT FROM AUTHOR]