Impact of pesticides on non-target invertebrates in agricultural ecosystems.

In fact, less than 1% of applied pesticides reach their target pests, while the remainder pollute the neighboring environment and adversely impact human health as well as non-target organisms in agricultural ecosystem. Pesticides can contribute to the loss of agrobiodiversity, which are essential to maintaining the agro-ecosystem's structure and functioning in order to produce and secure enough food. This review article examines the negative effects of pesticides on non-target invertebrates including earthworms, honeybees, predators, and parasitoids. It also highlights areas where further research is needed to address unresolved issues related to pesticide exposure, aiming to improve conservation efforts for these crucial species. These organisms play crucial roles in ecosystem functioning, such as soil health, pollination, and pest control. Both lethal and sub-lethal effects of pesticides on the selected non-target invertebrates were discussed. Pesticides affect DNA integrity, enzyme activity, growth, behavior, and reproduction of earthworms even at low concentrations. Pesticides could also induce a reduction in individual survival, disruption in learning performance and memory, as well as a change in the foraging behavior of honeybees. Additionally, pesticides adversely affect population growth indices, reproduction, development, longevity, and consumption of predators and parasitoids. As a result, pesticides must pass adequate ecotoxicological risk assessment to be enlisted by regulatory authorities. Therefore, it is important to adopt integrated pest management (IPM) strategies that minimize pesticide use and promote the conservation of beneficial organisms in order to maintain agrobiodiversity and sustainable agricultural systems. Furthermore, adopting precision agriculture and organic farming lessen these negative effects as well.less than.

A field realistic model to assess the effects of pesticides residues and adulterants on honey bee gene expression.

While studies on the sublethal effects of chemical residues in beeswax on adult honey bees are increasing, the study protocols assessing the impacts on honey bee brood in realistic conditions still need to be investigated. Moreover, little is known about the residue's effect on gene expression in honey bee brood. This study reports the effects of chlorpyriphos-ethyl, acrinathrin and stearin worker pupae exposure through contaminated or adulterated beeswax on the gene expression of some key health indicators, using a novel in vivo realistic model. Larvae were reared in acrinathrin (12.5, 25, 10 and 100 ppb) and chlorpyriphos-ethyl (5, 10, 500 and 5000 ppb) contaminated or stearin adulterated beeswax (3, 4, 5, 6 and 9%) in newly formed colonies to reduce the influence of external factors. On day 11, mortality rates were assessed. Honey bee pupae were extracted from the comb after 19 days of rearing and were analysed for the gene expression profile of four genes involved in the immune response to pathogens and environmental stress factors (Imd, dorsal, domeless and defensin), and two genes involved in detoxifications mechanisms (CYP6AS14 and CYP9Q3). We found no linear relation between the increase in the pesticide concentrations and the brood mortality rates, unlike stearin where an increase in stearin percentage led to an exponential increase in brood mortality. The immune system of pupae raised in acrinathrin contaminated wax was triggered and the expression of CYP6AS14 was significantly upregulated (exposure to 12.5 and 25 ppb). Almost all expression levels of the tested immune and detoxification genes were down-regulated when pupae were exposed to chlorpyrifos-contaminated wax. The exposure to stearin triggered the immune system and detoxification system of the pupae. The identification of substance-specific response factors might ultimately serve to identify molecules that are safer for bees and the ecosystem's health.

Combined effects of three insecticides with different modes of action on biochemical responses of the solitary bee Osmia bicornis.

Bees are simultaneously exposed to a variety of pesticides, which are often applied in mixtures and can cause lethal and sublethal effects. The combined effects of pesticides, however, are not measured in the current risk assessment schemes. Additionally, the sublethal effects of pesticides on a variety of physiological processes are poorly recognized in bees, especially in non-Apis solitary bees. In this study, we used a full-factorial design to examine the main and interactive effects of three insecticide formulations with different modes of action (Mospilan 20 SP, Sherpa 100 EC, and Dursban 480 EC) on bee biochemical processes. We measured acetylcholinesterase (AChE), glutathione S-transferase (GST) and esterase (EST) activities, as well as a nonenzymatic biomarker associated with energy metabolism, i.e., ATP level. All studied endpoints were affected by Sherpa 100 EC, and the activities of AChE and EST as well as ATP levels were affected by Dursban 480 EC. Moreover, complex interactions between all three insecticides affected ATP levels, showing outcomes that cannot be predicted when testing each insecticide separately. The results indicate that even if interactive effects are sometimes difficult to interpret, there is a need to study such interactions if laboratory-generated toxicity data are to be extrapolated to field conditions.

Uncovering hidden dangers: The combined toxicity of abamectin and lambda-cyhalothrin on honey bees.

Studying the toxic effects of pesticides on bees has consistently been a prominent area of interest for researchers. Nonetheless, existing research has predominantly concentrated on individual toxicity assessments, leaving a gap in our understanding of mixed toxicity. This study delves into the individual and combined toxic effects of abamectin (ABA) and lambda-cyhalothrin (LCY) on honey bees (Apis mellifera) in laboratory settings. We discovered that ABA (96 h-LC50 value of 0.079 mg/L) exhibited greater acute toxicity to honey bees compared to LCY (96 h-LC50 value of 9.177 mg/L). Moreover, the mixture of ABA and LCY presented an acute antagonistic effect on honey bees. Additionally, our results indicated that exposure to LCY, at medium concentration, led to a reduction in the abundance of gut core bacterium Snodgrassella. However, an increase in the abundance of Bifidobacterium was noted when exposed to a medium concentration of LCY and its mixture with ABA. Transcriptomic analysis revealed significant regulation of certain genes in the medium concentration of all three treatments compared to the control group, primarily enriching in metabolism and immune-related pathways. Following chronic exposure to field-relevant concentrations of ABA, LCY, and their mixture, there were significant alterations in the activities of immunity-related enzyme polyphenol oxidase (PPO) and detoxification enzymes glutathione S-transferase (GST) and carboxylesterase (CarE). Additionally, the expression of four genes (abaecin, cyp9e2, cyp302a1, and GstD1) associated with immune and detoxification metabolism was significantly altered. These findings suggest a potential health risk posed by the insecticides ABA and LCY to honey bees. Despite exhibiting acute antagonistic effect, mixed exposure still induced damage to bees at all levels. This study advances our knowledge of the potential adverse effects of individual or combined exposure to these two pesticides on non-target pollinators and offers crucial guidance for the use of insecticides in agricultural production.

Comparing Sensitivity of Different Bee Species to Pesticides: A TKTD modeling approach.

Risk assessment for bees is mainly based on data for honey bees; however, risk assessment is intended to protect all bee species. This raises the question of whether data for honey bees are a good proxy for other bee species. This issue is not new and has resulted in several publications in which the sensitivity of bee species is compared based on the values of the 48-h median lethal dose (LD50) from acute test results. When this approach is used, observed differences in sensitivity may result both from differences in kinetics and from inherent differences in species sensitivity. In addition, the physiology of the bee, like its overall size, the size of the honey stomach (for acute oral tests), and the physical appearance (for acute contact tests) also influences the sensitivity of the bee. The recently introduced Toxicokinetic-Toxicodynamic (TKTD) model that was developed for the interpretation of honey bee tests (Bee General Uniform Threshold Model for Survival [BeeGUTS]) could integrate the results of acute oral tests, acute contact tests, and chronic tests within one consistent framework. We show that the BeeGUTS model can be calibrated and validated for other bee species and also that the honey bee is among the more sensitive bee species. In addition, we found that differences in sensitivity between species are smaller than previously published comparisons based on 48-h LD50 values. The time-dependency of the LD50 and the specifics of the bee physiology are the main causes of the wider variation found in the published literature. Environ Toxicol Chem 2024;43:1431-1441. © 2024 The Authors. Environmental Toxicology and Chemistry published by Wiley Periodicals LLC on behalf of SETAC.

Exploring the antibiofilm effects on Escherichia coli biofilm associated with colon cancer and anticancer activities on HCT116 cell line of bee products.

The association between dysbiotic microbiota biofilm and colon cancer has recently begun to attract attention. In the study, the apitherapeutic effects of bee products (honey, bee venom, royal jelly, pollen, perga and propolis) obtained from the endemic Yigilca ecotype of Apis mellifera anatoliaca were investigated. Antibiofilm activity were performed by microplate assay using crystal violet staining to measure adherent biofilm biomass of Escherichia coli capable of forming biofilms. Bee venom showed the highest inhibition effect (73.98%) at 50% concentration. Honey, perga and royal jelly reduced biofilm formation by >50% at all concentrations. The antiproliferation effect on the HCT116 colon cancer cell line was investigated with the water­soluble tetrazolium salt­1 assay. After 48 h of honey application at 50% concentration, cell proliferation decreased by 86.51%. The high cytotoxic effects of royal jelly and bee venom are also remarkable. Additionally, apoptotic pathway analysis was performed by ELISA using caspase 3, 8 and 9 enzyme-linked immunosorbent assay kits. All bee products induced a higher expression of caspase 9 compared with caspase 8. Natural products that upregulate caspase proteins are promising therapeutic targets for proliferative diseases.

Genotoxic effect of two environmentally safe doses of cadmium on the hepato-nephrocytic system of Bombus atratus forager workers.

Eusocial bees are declining due to anthropogenic actions. Individuals can be exposed to contaminants like Cd, which have been found in pollen. Thus, we evaluated the potential genotoxicity of Cd to the hepato-nephrocitic system of Bombus atratus foraging workers exposed to environmentally safe doses of Cd (0.001 mg/kg and 0.003 mg/kg) during 72 h. To assess the genotoxicity of Cd, we conducted an alkaline comet assay. Doses of 0.001 mg/kg of Cd caused comets of levels 2 and 3, and 0.003 mg/kg of Cd induced comets of level 4, while controls exhibited regular nucleoids. Also, 0.003 mg/kg doses caused higher Damage Index, Damage Frequency, and Total Damage. Our results bring new evidence that 0.003 mg/kg Cd exerted genotoxicity to the HNS cells of B. atratus, probably affecting secondary metabolism and the detoxification capability of bees.

Combined pesticides in field doses weaken honey bee (Apis cerana F.) flight ability and analyses of transcriptomics and metabolomics.

Imidacloprid, chlorpyrifos, and glyphosate rank among the most extensively employed pesticides worldwide. The effects of these pesticides and their combined on the flight capability of Apis cerana, and the potential underlying mechanisms remain uncertain. To investigate these effects, we carried out flight mill, transcriptome, and metabolome experiments. Our findings reveal that individual acute oral treatments with pesticides, specifically 20 µL of 10 ng/g imidacloprid (0.2 ng per bee), 30 ng/g chlorpyrifos (0.6 ng per bee), and 60 ng/g glyphosate (1.2 ng per bee), did not impact the flight capability of the bees. However, when bees were exposed to a combination of two or three pesticides, a notable reduction in flight duration and distance was observed. In the transcriptomic and metabolomic analyses, we identified 307 transcripts and 17 metabolites that exhibited differential expression following exposure to combined pesticides, primarily associated with metabolic pathways involved in energy regulation. Our results illuminate the intricate effects and potential hazards posed by combined pesticide exposures on bee behavior. These findings offer valuable insights into the synergistic potential of pesticide combinations and their capacity to impair bee behavior. Understanding these complex interactions is essential for comprehending the broader consequences of pesticide formulations on honey bee populations.

Honey bee queen health is unaffected by contact exposure to pesticides commonly found in beeswax.

Honey bee queen health is crucial for colony health and productivity, and pesticides have been previously associated with queen loss and premature supersedure. Prior research has investigated the effects of indirect pesticide exposure on queens via workers, as well as direct effects on queens during development. However, as adults, queens are in constant contact with wax as they walk on comb and lay eggs; therefore, direct pesticide contact with adult queens is a relevant but seldom investigated exposure route. Here, we conducted laboratory and field experiments to investigate the impacts of topical pesticide exposure on adult queens. We tested six pesticides commonly found in wax: coumaphos, tau-fluvalinate, atrazine, 2,4-DMPF, chlorpyriphos, chlorothalonil, and a cocktail of all six, each administered at 1, 4, 8, 16, and 32 times the concentrations typically found in wax. We found no effect of any treatment on queen mass, sperm viability, or fat body protein expression. In a field trial testing queen topical exposure of a pesticide cocktail, we found no impact on egg-laying pattern, queen mass, emergence mass of daughter workers, and no proteins in the spermathecal fluid were differentially expressed. These experiments consistently show that pesticides commonly found in wax have no direct impact on queen performance, reproduction, or quality metrics at the doses tested. We suggest that previously reported associations between high levels of pesticide residues in wax and queen failure are most likely driven by indirect effects of worker exposure (either through wax or other hive products) on queen care or queen perception.

New bioassay cage methodology for in vitro studies on Varroa destructor and Apis mellifera.

Varroa destructor Anderson and Trueman, is an ectoparasitic mite of honey bees, Apis mellifera L., that has been considered a major cause of colony losses. Synthetic miticides have been developed and registered to manage this ectoparasite, however, resistance to registered pyrethroid and organophosphate Varroacides have already been reported in Canada. To test toxicity of miticides, current contact-based bioassay methods are designed to evaluate mites and bees separately, however, these methods are unlikely to give an accurate depiction of how miticides interact at the colony level. Therefore, the objective of this study was to develop a bioassay cage for testing the toxicity of miticides on honey bees and Varroa mites simultaneously using amitraz as a reference chemical. A 800 mL polypropylene plastic cage holding 100-150 bees was designed and officially named "Apiarium". A comparison of the effects of three subsequent dilutions of amitraz was conducted on: Varroa mites placed in glass vials, honey bees in glass Mason jars, and Varroa-infested bees in Apiariums. Our results indicated cumulative Varroa mortality was dose-dependent in the Apiarium after 4 h and 24 h assessments. Apiarium and glass vial treatments at 24 h also had high mite mortality and a positive polynomial regression between Varroa mortality and amitraz dose rates. Moreover, chemical application in the Apiarium was less toxic for bees compared to the Mason jar method. Considering these results, the Apiarium bioassay provides a simple, cheap and reliable method for simultaneous chemical screening on V. destructor and A. mellifera. Furthermore, as mites and bees are tested together, the Apiarium simulates a colony-like environment that provides a necessary bridge between laboratory bioassay testing and full field experimentation. The versatility of the Apiarium allows researchers to test a multitude of different honey bee bioassay experiments including miticide screening, delivery methods for chemical products, or development of new mite resistance-testing methodology.

Exposure to low doses of pesticides induces an immune response and the production of nitric oxide in honeybees.

Honeybees are essential pollinators of many agricultural crops and wild plants. However, the number of managed bee colonies has declined in some regions of the world over the last few decades, probably caused by a combination of factors including parasites, pathogens and pesticides. Exposure to these diverse biotic and abiotic stressors is likely to trigger immune responses and stress pathways that affect the health of individual honeybees and hence their contribution to colony survival. We therefore investigated the effects of an orally administered bacterial pathogen (Pseudomonas entomophila) and low-dose xenobiotic pesticides on honeybee survival and intestinal immune responses. We observed stressor-dependent effects on the mean lifespan, along with the induction of genes encoding the antimicrobial peptide abaecin and the detoxification factor cytochrome P450 monooxygenase CYP9E2. The pesticides also triggered the immediate induction of a nitric oxide synthase gene followed by the delayed upregulation of catalase, which was not observed in response to the pathogen. Honeybees therefore appear to produce nitric oxide as a specific defense response when exposed to xenobiotic stimuli. The immunity-related and stress-response genes we tested may provide useful stressor-dependent markers for ecotoxicological assessment in honeybee colonies.

Social disruption: Sublethal pesticides in pollen lead to Apis mellifera queen events and brood loss.

Eusocial Apis mellifera colonies depend on queen longevity and brood viability to survive, as the queen is the sole reproductive individual and the maturing brood replenishes the shorter-lived worker bees. Production of many crops rely on both pesticides and bee pollination to improve crop quantity and quality, yet sublethal impacts of this pesticide exposure is often poorly understood. We investigated the resiliency of queens and their brood after one month of sublethal exposure to field relevant doses of pesticides that mimic exposure during commercial pollination contracts. We exposed full size colonies to pollen contaminated with field-relevant doses of the fungicides (chlorothalonil and propicanizole), insecticides (chlorypyrifos and fenpropathrin) or both, noting a significant reduction in pollen consumption in colonies exposed to fungicides compared to control. While we found no difference in the total amount of pollen collected per colony, a higher proportion of pollen to non-pollen foragers was detected in all pesticide exposed colonies. After ceasing treatments, we measured brood development, discovering a significant increase in brood loss and/or cannibalism across all pesticide exposed groups. Sublethal pesticide exposure in general was linked to reduced production of replacement workers and a change in protein acquisition (pollen vs. non-pollen foraging). Fungicide exposure also resulted in increased loss of the reproductive queen.

Effects of developmental exposure to pesticides in wax and pollen on honey bee (Apis mellifera) queen reproductive phenotypes.

Stressful conditions during development can have sub-lethal consequences on organisms aside from mortality. Using previously reported in-hive residues from commercial colonies, we examined how multi-pesticide exposure can influence honey bee (Apis mellifera) queen health. We reared queens in beeswax cups with or without a pesticide treatment within colonies exposed to treated or untreated pollen supplement. Following rearing, queens were open-mated and then placed into standard hive equipment in an "artificial swarm" to measure subsequent colony growth. Our treated wax had a pesticide Hazard Quotient comparable to the average in beeswax from commercial colonies, and it had no measurable effects on queen phenotype. Conversely, colonies exposed to pesticide-treated pollen had a reduced capacity for viable queen production, and among surviving queens from these colonies we observed lower sperm viability. We found no difference in queen mating number across treatments. Moreover, we measured lower brood viability in colonies later established by queens reared in treated-pollen colonies. Interestingly, royal jelly from colonies exposed to treated pollen contained negligible pesticide residues, suggesting the indirect social consequences of colony-level pesticide exposure on queen quality. These findings highlight how conditions during developmental can impact queens long into adulthood, and that colony-level pesticide exposure may do so indirectly.

Sub-lethal effects of the consumption of Eupatorium buniifolium essential oil in honeybees.

When developing new products to be used in honeybee colonies, further than acute toxicity, it is imperative to perform an assessment of risks, including various sublethal effects. The long-term sublethal effects of xenobiotics on honeybees, more specifically of acaricides used in honeybee hives, have been scarcely studied, particularly so in the case of essential oils and their components. In this work, chronic effects of the ingestion of Eupatorium buniifolium (Asteraceae) essential oil were studied on nurse honeybees using laboratory assays. Survival, food consumption, and the effect on the composition of cuticular hydrocarbons (CHC) were assessed. CHC were chosen due to their key role as pheromones involved in honeybee social recognition. While food consumption and survival were not affected by the consumption of the essential oil, CHC amounts and profiles showed dose-dependent changes. All groups of CHC (linear and branched alkanes, alkenes and alkadienes) were altered when honeybees were fed with the highest essential oil dose tested (6000 ppm). The compounds that significantly varied include n-docosane, n-tricosane, n-tetracosane, n-triacontane, n-tritriacontane, 9-tricosene, 7-pentacosene, 9-pentacosene, 9-heptacosene, tritriacontene, pentacosadiene, hentriacontadiene, tritriacontadiene and all methyl alkanes. All of them but pentacosadiene were up-regulated. On the other hand, CHC profiles were similar in healthy and Nosema-infected honeybees when diets included the essential oil at 300 and 3000 ppm. Our results show that the ingestion of an essential oil can impact CHC and that the effect is dose-dependent. Changes in CHC could affect the signaling process mediated by these pheromonal compounds. To our knowledge this is the first report of changes in honeybee cuticular hydrocarbons as a result of essential oil ingestion.

Joint effects of cadmium and copper on Apis mellifera forgers and larvae.

Honey bees (Apis mellifera L.) are important ecological and agricultural resources. They are among the most widely available pollinators and provide products as well as services. Unfortunately, honey bee populations are susceptible to several environmental threats, including heavy metal exposure. Honey bees can be exposed to heavy metals when foraging on contaminated honey and pollen resources, and in some cases by airborne exposure. We studied the joint acute and chronic effects of cadmium (Cd) and copper (Cu) on A. mellifera. A 1:1 solution of the two heavy metals increased larval developmental duration and the mortality of both larvae and foragers in a dose-dependent way, decreased forager feeding, increased body metal burdens, and disrupted the sucrose response behavior of foragers. In combination, Cd and Cu demonstrated a weakly synergistic effect on foragers, but for larvae an initially antagonistic effect at low doses changed to strongly synergistic response at higher concentrations. The sucrose response threshold of foragers decreased significantly when they were dosed with increasing concentrations of the metal mixtures. Overall, the fitness of honey bee larvae and foragers is detrimentally affected when these metals co-occur.

Mitochondrial Respiratory Inhibition Promoted by Pyraclostrobin in Fungi is Also Observed in Honey Bees.

There is no use restriction associated with bees for many fungicides used in agriculture; however, this does not always mean that these pesticides are harmless for these nontarget organisms. We investigated whether the fungicide pyraclostrobin, which acts on fungal mitochondria, also negatively affects honey bee mitochondrial bioenergetics. Honey bees were collected from 5 hives and anesthetized at 4 °C. The thoraces were separated, and mitochondria were isolated by grinding, filtering, and differential centrifugation. An aliquot of 0.5 mg of mitochondrial proteins was added to 0.5 mL of a standard reaction medium with 4 mM succinate (complex II substrate) plus 50 nM rotenone (complex I inhibitor), and mitochondrial respiration was measured at 30 °C using a Clark-type oxygen electrode. Mitochondrial membrane potential was determined spectrofluorimetrically using safranin O as a probe, and adenosine triphosphate (ATP) synthesis was determined by chemiluminescence. Pyraclostrobin at 0 to 50 µM was tested on the mitochondrial preparations, with 3 repetitions. Pyraclostrobin inhibited mitochondrial respiration in a dose-dependent manner at concentrations of 10 µM and above, demonstrating typical inhibition of oxidative phosphorylation. Pyraclostrobin also promoted a decline in the mitochondrial membrane potential at doses of 5 µM and above and in ATP synthesis at 15 µM and above. We conclude that pyraclostrobin interferes with honey bee mitochondrial function, which is especially critical for the energy-demanding flight activity of foraging bees. Environ Toxicol Chem 2020;39:1267-1272. © 2020 SETAC.

Modification of the head proteome of nurse honeybees (Apis mellifera) exposed to field-relevant doses of pesticides.

Understanding the effect of pesticides on the survival of honeybee colonies is important because these pollinators are reportedly declining globally. In the present study, we examined the changes in the head proteome of nurse honeybees exposed to individual and combined pesticides (the fungicide pyraclostrobin and the insecticide fipronil) at field-relevant doses (850 and 2.5 ppb, respectively). The head proteomes of bees exposed to pesticides were compared with those of bees that were not exposed, and proteins with differences in expression were identified by mass spectrometry. The exposure of nurse bees to pesticides reduced the expression of four of the major royal jelly proteins (MRJP1, MRJP2, MRJP4, and MRJP5) and also several proteins associated with carbohydrate metabolism and energy synthesis, the antioxidant system, detoxification, biosynthesis, amino acid metabolism, transcription and translation, protein folding and binding, olfaction, and learning and memory. Overall, when pyraclostrobin and fipronil were combined, the changes in protein expression were exacerbated. Our results demonstrate that vital proteins and metabolic processes are impaired in nurse honeybees exposed to pesticides in doses close to those experienced by these insects in the field, increasing their susceptibility to stressors and affecting the nutrition and maintenance of both managed and natural colonies.

Cadmium and Selenate Exposure Affects the Honey Bee Microbiome and Metabolome, and Bee-Associated Bacteria Show Potential for Bioaccumulation.

Honey bees are important insect pollinators used heavily in agriculture and can be found in diverse environments. Bees may encounter toxicants such as cadmium and selenate by foraging on plants growing in contaminated areas, which can result in negative health effects. Honey bees are known to have a simple and consistent microbiome that conveys many benefits to the host, and toxicant exposure may impact this symbiotic microbial community. We used 16S rRNA gene sequencing to assay the effects that sublethal cadmium and selenate treatments had over 7 days and found that both treatments significantly but subtly altered the composition of the bee microbiome. Next, we exposed bees to cadmium and selenate and then used untargeted liquid chromatography-mass spectrometry (LC-MS) metabolomics to show that chemical exposure changed the bees' metabolite profiles and that compounds which may be involved in detoxification, proteolysis, and lipolysis were more abundant in treatments. Finally, we exposed several strains of bee-associated bacteria in liquid culture and found that each strain removed cadmium from its medium but that only Lactobacillus Firm-5 microbes assimilated selenate, indicating the possibility that these microbes may reduce the metal and metalloid burden on their host. Overall, our report shows that metal and metalloid exposure can affect the honey bee microbiome and metabolome and that strains of bee-associated bacteria can bioaccumulate these toxicants.IMPORTANCE Bees are important insect pollinators that may encounter environmental pollution when foraging upon plants grown in contaminated areas. Despite the pervasiveness of pollution, little is known about the effects of these toxicants on honey bee metabolism and their symbiotic microbiomes. Here, we investigated the impact of selenate and cadmium exposure on the gut microbiome and metabolome of honey bees. We found that exposure to these chemicals subtly altered the overall composition of the bees' microbiome and metabolome and that exposure to toxicants may negatively impact both host and microbe. As the microbiome of animals can reduce mortality upon metal or metalloid challenge, we grew bee-associated bacteria in media spiked with selenate or cadmium. We show that some bacteria can remove these toxicants from their media in vitro and suggest that bacteria may reduce metal burden in their hosts.

An assessment of acute insecticide toxicity loading (AITL) of chemical pesticides used on agricultural land in the United States.

We present a method for calculating the Acute Insecticide Toxicity Loading (AITL) on US agricultural lands and surrounding areas and an assessment of the changes in AITL from 1992 through 2014. The AITL method accounts for the total mass of insecticides used in the US, acute toxicity to insects using honey bee contact and oral LD50 as reference values for arthropod toxicity, and the environmental persistence of the pesticides. This screening analysis shows that the types of synthetic insecticides applied to agricultural lands have fundamentally shifted over the last two decades from predominantly organophosphorus and N-methyl carbamate pesticides to a mix dominated by neonicotinoids and pyrethroids. The neonicotinoids are generally applied to US agricultural land at lower application rates per acre; however, they are considerably more toxic to insects and generally persist longer in the environment. We found a 48- and 4-fold increase in AITL from 1992 to 2014 for oral and contact toxicity, respectively. Neonicotinoids are primarily responsible for this increase, representing between 61 to nearly 99 percent of the total toxicity loading in 2014. The crops most responsible for the increase in AITL are corn and soybeans, with particularly large increases in relative soybean contributions to AITL between 2010 and 2014. Oral exposures are of potentially greater concern because of the relatively higher toxicity (low LD50s) and greater likelihood of exposure from residues in pollen, nectar, guttation water, and other environmental media. Using AITL to assess oral toxicity by class of pesticide, the neonicotinoids accounted for nearly 92 percent of total AITL from 1992 to 2014. Chlorpyrifos, the fifth most widely used insecticide during this time contributed just 1.4 percent of total AITL based on oral LD50s. Although we use some simplifying assumptions, our screening analysis demonstrates an increase in pesticide toxicity loading over the past 26 years, which potentially threatens the health of honey bees and other pollinators and may contribute to declines in beneficial insect populations as well as insectivorous birds and other insect consumers.

The Impact of Pesticides on Flower-Visiting Insects: A Review with Regard to European Risk Assessment.

Flower-visiting insects (FVIs) are an ecologically diverse group of mobile, flying species that should be protected from pesticide effects according to European policy. However, there is an ongoing decline of FVI species, partly caused by agricultural pesticide applications. Therefore, the risk assessment framework needs to be improved. We synthesized the peer-reviewed literature on FVI groups and their ecology, habitat, exposure to pesticides, and subsequent effects. The results show that FVIs are far more diverse than previously thought. Their habitat, the entire agricultural landscape, is potentially contaminated with pesticides through multiple pathways. Pesticide exposure of FVIs at environmentally realistic levels can cause population-relevant adverse effects. This knowledge was used to critically evaluate the European regulatory framework of exposure and effect assessment. The current risk assessment should be amended to incorporate specific ecological properties of FVIs, that is, traits. We present data-driven tools to improve future risk assessments by making use of trait information. There are major knowledge gaps concerning the general investigation of groups other than bees, the collection of comprehensive data on FVI groups and their ecology, linking habitat to FVI exposure, and study of previously neglected complex population effects. This is necessary to improve our understanding of FVIs and facilitate the development of a more protective FVI risk assessment. Environ Toxicol Chem 2019;38:2355-2370. © 2019 The Authors. Environmental Toxicology and Chemistry published by Wiley Periodicals, Inc. on behalf of SETAC.