Interaction of acetamiprid, Varroa destructor, and Nosema ceranae in honey bees.

Health of honey bees is threatened by a variety of stressors, including pesticides and parasites. Here, we investigated effects of acetamiprid, Varroa destructor, and Nosema ceranae, which act either alone or in combination. Our results suggested that interaction between the three factors was additive, with survival risk increasing as the number of stressors increased. Although exposure to 150 µg/L acetamiprid alone did not negatively impact honey bee survival, it caused severe damage to midgut tissue. Among the three stressors, V. destructor posed the greatest threat to honey bee survival, and N. ceranae exacerbated intestinal damage and increased thickness of the midgut wall. Transcriptomic analysis indicated that different combinations of stressors elicited specific gene expression responses in honey bees, and genes involved in energy metabolism, immunity, and detoxification were altered in response to multiple stressor combinations. Additionally, genes associated with Toll and Imd signalling, tyrosine metabolism, and phototransduction pathway were significantly suppressed in response to different combinations of multiple stressors. This study enhances our understanding of the adaptation mechanisms to multiple stressors and aids in development of suitable protective measures for honey bees. ENVIRONMENTAL IMPLICATION: We believe our study is environmentally relevant for the following reasons: This study investigates combined effects of pesticide, Varroa destructor, and Nosema ceranae. These stressors are known to pose a threat to long-term survival of honey bees (Apis mellifera) and stability of the ecosystems. The research provides valuable insights into the adaptive mechanisms of honey bees in response to multiple stressors and developing effective conservation strategies. Further research can identify traits that promote honey bee survival in the face of future challenges from multiple stressors to maintain the overall stability of environment.

Effects of biochar and compost on microbial community assembly and metabolic processes in glyphosate, imidacloprid and pyraclostrobin polluted soil under freezethaw cycles.

Biochar and organic compost are widely used in agricultural soil remediation as soil immobilization agents. However, the effects of biochar and compost on microbial community assembly processes in polluted soil under freezingthawing need to be further clarified. Therefore, a freezethaw cycle experiment was conducted with glyphosate (herbicide), imidacloprid (insecticide) and pyraclostrobin (fungicide) polluted to understand the effect of biochar and compost on microbial community assembly and metabolic behavior. We found that biochar and compost could significantly promote the degradation of glyphosate, imidacloprid and pyraclostrobin in freezethaw soil decrease the half-life of the three pesticides. The addition of immobilization agents improved soil bacterial and fungal communities and promoted the transformation from homogeneous dispersal to homogeneous selection. For soil metabolism, the combined addition of biochar and compost alleviated the pollution of glyphosate, imidacloprid and imidacloprid to soil through up-regulation of metabolites (DEMs) in amino acid metabolism pathway and down-regulation of DEMs in fatty acid metabolism pathway. The structural equation modeling (SEM) results showed that soil pH and DOC were the main driving factors affecting microbial community assembly and metabolites. In summary, the combined addition of biochar and compost reduced the adverse effects of pesticides residues.

Integration of transcriptome, gut microbiota, and physiology reveals toxic responses of the red claw crayfish (Cherax quadricarinatus) to imidacloprid.

Imidacloprid enters the water environment through rainfall and causes harm to aquatic crustaceans. However, the potential chronic toxicity mechanism of imidacloprid in crayfish has not been comprehensively studied. In this study, red claw crayfish (Cherax quadricarinatus) were exposed to 11.76, 35.27, or 88.17 µg/L imidacloprid for 30 days, and changes in the physiology and biochemistry, gut microbiota, and transcriptome of C. quadricarinatus and the interaction between imidacloprid, gut microbiota, and genes were studied. Imidacloprid induced oxidative stress and decreased growth performance in crayfish. Imidacloprid exposure caused hepatopancreas damage and decreased serum immune enzyme activity. Hepatopancreatic and plasma acetylcholine decreased significantly in the 88.17 µg/L group. Imidacloprid reduced the diversity of the intestinal flora, increased the abundance of harmful flora, and disrupted the microbiota function. Transcriptomic analysis showed that the number of up-and-down-regulated differentially expressed genes (DEGs) increased significantly with increasing concentrations of imidacloprid. DEG enrichment analyses indicated that imidacloprid inhibits neurotransmitter transduction and immune responses and disrupts energy metabolic processes. Crayfish could alleviate imidacloprid stress by regulating antioxidant and detoxification-related genes. A high correlation was revealed between GST, HSPA1s, and HSP90 and the composition of gut microorganisms in crayfish under imidacloprid stress. This study highlights the negative effects and provides detailed sequencing data from transcriptome and gut microbiota to enhance our understanding of the molecular toxicity of imidacloprid in crustaceans.

Effects of imidacloprid on the survival and biomarker responses of Eristalis tenax larvae (Diptera: Syrphidae): a comparative study between indoor and outdoor exposures.

Imidacloprid is a widely used pesticide in agriculture. It is being found in aquatic ecosystems in agricultural regions. This study aimed to evaluate its effects on the survival rates, acetylcholinesterase (AChE) and catalase (CAT) responses of larval Eristalis tenax hoverflies. The larvae were exposed for 3, 7 and 14 days to increasing concentrations of imidacloprid (0, 0.1, 0.5 and 2 mg L-1) both indoors at a constant temperature of 20 °C and outdoors under varying environmental conditions. The results revealed that indoors and outdoors, the mortality of E. tenax significantly increased with increasing imidacloprid concentration and duration of exposure. Median lethal concentrations (LC50) varied from 0.03 to 0.17 mg L-1 depending on the duration and conditions of exposure. Indoors, AChE activity decreased in all the treatments for all three exposure durations, whereas outdoors the decrease was observed after the short (3-day) and long (14-day) exposure durations. AChE inhibition ranged from 6% to 62% (indoors) and 12% to 62% (outdoors). Variations in CAT activity were observed for both experimental setups, with a decrease outdoors in larvae exposed to 0.5 mg L-1 for 7 days and a gradual dose-dependent increase indoors for exposure lasting 3 and 7 days. This study sheds light on the potential ecological implications of imidacloprid contamination which may cause the decline of aquatic insect populations and pollination rates, leading to disruptions of the food chain and the overall decline of aquatic and terrestrial ecosystem health.

Comparative evaluation of neonicotinoids and their metabolites-induced oxidative stress in carp primary leukocytes and CLC cells.

Neonicotinoids (NEOs) have been designed to act selectively on insect nicotinic acetylcholine receptors (nAChRs). However, nAChRs are also expressed in vertebrate immune cells, so NEOs may interfere with the immune system in exposed non-target animals. The present study shows that NEOs: imidacloprid and thiacloprid, and their main metabolites: desnitro-imidacloprid and thiacloprid amide, at sub-micromolar concentrations ranging from 2.25 to 20 µM, affect the immune cells of fish. This was found both in primary cultures of leukocytes isolated from the carp head kidney and in the continuous adherent carp monocyte/macrophage cell line. Moreover, the results revealed that the studied pesticides and metabolites generate oxidative stress in carp immune cells and that this is one of the most important mechanisms of neonicotinoid immunotoxicity. Significant increases were observed in the formation of ROS and malondialdehyde (MDA). The antioxidant status alteration was linked with decrease in antioxidant enzyme activity: superoxide dismutase (SOD), catalase (CAT), and non-enzymatic antioxidant glutathione (GSH). Importantly, the metabolites: desnitro-imidacloprid and thiacloprid amide showed significantly higher cytotoxicity towards fish leukocytes than their parent compounds, imidacloprid and thiacloprid, which emphasizes the importance of including intermediate metabolites in toxicology studies.

Assessment of toxic effects of imidacloprid on freshwater zooplankton: An experimental test for 27 species.

The neonicotinoid pesticide imidacloprid has been used worldwide since 1992. As one of the most important chemicals used in pest control, there have been concerns that its run-off into rivers and lakes could adversely affect aquatic ecosystems, where zooplankton play a central role in the energy flow from primary to higher trophic levels. However, studies assessing the effects of pesticides at the species level have relied on a Daphnia-centric approach, and no studies have been conducted using species-level assessments on a broad range of zooplankton taxa. In the present study, we therefore investigated the acute toxicity of imidacloprid on 27 freshwater crustacean zooplankton (18 cladocerans, 3 calanoid copepods and 6 cyclopoid copepods). The experiment showed that a majority of calanoid copepods and cladocerans were not affected at all by imidacloprid, with the exception of one species each of Ceriodaphnia and Diaphasoma, while all six cyclopoid copepods showed high mortality rates, even at concentrations of imidacloprid typically found in nature. In addition, we found a remarkable intra-taxonomic variation in susceptibility to this chemical. As many cyclopoid copepods are omnivorous, they act as predators as well as competitors with other zooplankton. Accordingly, their susceptibility to imidacloprid is likely to cause different responses at the community level through changes in predation pressure as well as changes in competitive interactions. The present results demonstrate the need for species-level assessments of various zooplankton taxa to understand the complex responses of aquatic communities to pesticide disturbance.

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.

Imidacloprid reduces the mating success of males in bumblebees.

Bumblebees play a vital role in both natural and agricultural environments, but there has been a noticeable decline in their populations. Pesticides, particularly neonicotinoids, are widely regarded as a substantial contributing factor to the decline in bumblebee populations, as evidenced by the detrimental impacts documented across many stages of their life cycle. Mating is vital for the population maintenance of bumblebees. Nevertheless, there is a scarcity of research conducted on the effects of pesticides on the mating process. In this study, we individually examined the impact of imidacloprid on the mating behavior of bumblebee males and queens. A competitive mating experiment was conducted to evaluate the effect on the competitive prowess of male individuals and the mate selection behavior of female individuals. The study revealed that the mating rate of bumblebees exposed to a concentration of 10 ppb of imidacloprid was 3 %. This finding demonstrated a statistically significant impact when compared to the control group, which exhibited a mating rate of 58 % in the normal mating experiment. Furthermore, in the competitive mating experiment, we found that the competitive mating success rate of treated males (1 %) was significantly lower than that of untreated males (35 %). Hence, it provides evidence that neonicotinoid imidacloprid negatively affects bumblebee mating success and cautions us to protect bumblebees from pesticide exposure to prevent a severe impact on their populations.

Rifampicin synergizes the toxicity of insecticides against the green peach aphid, Myzus persicae.

Myzus persicae is an important pest that has developed resistance to nearly all currently used insecticidal products. The employment of insecticide synergists is one of the effective strategies that need to be developed for the management of this resistance. Our study showed that treatment with a combination of the antibiotic, rifampicin, with imidacloprid, cyantraniliprole, or clothianidin significantly increased their toxicities against M. persicae, by 2.72, 3.59, and 2.41 folds, respectively. Rifampicin treatment led to a noteworthy reduction in the activities of multifunctional oxidases (by 32.64%) and esterases (by 23.80%), along with a decrease in the expression of the CYP6CY3 gene (by 58.57%) in M. persicae. It also negatively impacted the fitness of the aphids, including weight, life span, number of offspring, and elongation of developmental duration. In addition, bioassays showed that the combination of rifampicin and a detoxification enzyme inhibitor, piperonyl butoxide, or dsRNA of CYP6CY3 further significantly improved the toxicity of imidacloprid against M. persicae, by 6.19- and 7.55-fold, respectively. The present study suggests that development of active ingredients such as rifampicin as candidate synergists, show promise to overcome metabolic resistance to insecticides in aphids.

Interactive effects of dinotefuran and Nosema ceranae on the survival status and gut microbial community of honey bees.

Growing evidences have shown that the decline in honey bee populations is mainly caused by the combination of multiple stressors. However, the impacts of parasitic Nosema ceranae to host fitness during long-term pesticide exposure-induced stress is largely unknown. In this study, the effects of chronic exposure to a sublethal dose of dinotefuran, in the presence or absence of N. ceranae, was examined in terms of survival, food consumption, detoxification enzyme activities and gut microbial community. The interaction between dinotefuran and Nosema ceranae on the survival of honey bee was synergistic. Co-exposure to dinotefuran and N. ceranae led to less food consumption and greater changes of enzyme activities involved in defenses against oxidative stress. Particularly, N. ceranae and dinotefuran-N. ceranae co-exposure significantly impacted the gut microbiota structure and richness in adult honey bees, while dinotefuran alone did not show significant alternation of core gut microbiota compared to the control group. We herein demonstrated that chronical exposure to dinotefuran decreases honey bee's survival but is not steadily associated with the gut microbiota dysbiosis; by contrast, N. ceranae parasitism plays a dominant role in the combination in influencing the gut microbial community of the host honey bee. Our findings provide a comprehensive understanding of combinatorial effects between biotic and abiotic stressors on one of the most important pollinators, honey bees.

Modeling temperature-dependent life-cycle toxicity of thiamethoxam in Chironomus riparius using a DEB-TKTD model.

The neonicotinoid insecticide thiamethoxam (TMX) is widely used to protect crops against insect pests. Despite some desirable properties such as its low toxicity to birds and mammals, concerns have been raised about its toxicity to non-target arthropods, including freshwater insects like chironomids. Whereas multiple studies have investigated chronic effects of neonicotinoids in chironomid larvae at standardized laboratory conditions, a better understanding of their chronic toxicity under variable temperatures and exposure is needed for coherent extrapolation from the laboratory to the field. Here, we developed a quantitative mechanistic effect model for Chironomus riparius, to simulate the species' life history under dynamic temperatures and exposure concentrations of TMX. Laboratory experiments at four different temperatures (12, 15, 20, 23 °C) and TMX concentrations between 4 and 51 µg/L were used to calibrate the model. Observed concentration-dependent effects of TMX in C. riparius included slower growth, later emergence, and higher mortality rates with increasing concentrations. Furthermore, besides a typical accelerating effect on the organisms' growth and development, higher temperatures further increased the effects associated with TMX. With some data-informed modeling decisions, most prominently the inclusion of a size dependence that makes larger animals more sensitive to TMX, the model was parametrized to convincingly reproduce the data. Experiments at both a constant (20 °C) and a dynamically increasing temperature (15-23 °C) with pulsed exposure were used to validate the model. Finally, the model was used to simulate realistic exposure conditions using two reference exposure scenarios measured in Missouri and Nebraska, utilizing a moving time window (MTW) and either a constant temperature (20 °C) or the measured temperature profiles belonging to each respective scenario. Minimum exposure multiplication factors leading to a 10% effect (EP10) in the survival at pupation, i.e., the most sensitive endpoint found in this study, were 25.67 and 21.87 for the Missouri scenario and 38.58 and 44.64 for the Nebraska scenario, when using the respective temperature assumptions. While the results illustrate that the use of real temperature scenarios does not systematically modify the EPx in the same direction (making it either more or less conservative when used as a risk indicator), the advantage of this approach is that it increases the realism and thus reduces the uncertainty associated with the model predictions.

Imidacloprid effects on acetylcholinesterase and nicotinic acetylcholine receptor in Apis mellifera. Experimental and molecular modeling approaches.

Although the neonicotinoid insecticides have good selectivity towards insects rather than vertebrates, they have severe effects on honeybee production and pollination activities. Therefore, the effects of imidacloprid (IMI), the most used neonicotinoid, on the two main bioreceptors, acetylcholinesterase (AChE) and nicotinic acetylcholine receptor alpha subunit (nAChRα1) of honeybees were examined to identify their roles in honeybee toxicity and possible binding sites which assist in selecting and designing neonicotinoids. In vivo, IMI showed a high inhibitory effect on AChE (IC50 5.63 mg/L); however, the effect was much lower in vitro experiment (IC50 719 mg/L). This result induced us to examine the IMI effect on AChE gene expression which revealed that the AChE-2 gene expression was severely affected by IMI explaining the observed high enzyme inhibition. In addition, although toxicity increased by increasing exposure to IMI (LC50 2.9 mg/L after 4h and 0.75 mg/L after 48h), AChE was not elevated (IC50 5.63 and 5.52 mg/L respectively). Besides, Despite resuming most enzyme activity (77% during 2 h and 84.14% after 4 h), a high mortality level was observed with LC50 2.9 mg/L. These results reinforced that the observed high toxicity is a multifactor process. Accordingly, Molecular modeling and docking of IMI into honeybee AChE and nAChRα1were also performed to examine their possible interactions and identify the important binding sites. Results models indicated that the first two binding sites in AChE were found in the esteratic subunit in the active site explaining the observed in vitro inhibition. In nAChRα1, four of the highest five free energy binding sites are located in the large TM3-TM4 loop and one in the extracellular loops. Consequently, the present work revealed that IMI toxicity is attributed to various factors including direct interaction with both AChE and nAChRα1 as well as downregulating AChE-2 gene expression.

Evaluation of imidacloprid (Confidor OD®) genotoxicity in Chrysoperla externa eggs (Neuroptera: Chrysopidae) through comet assay.

The comet assay allows the analysis of DNA damage caused by different genotoxins. This assay has recently gained interest because of its ease of studying the interactions of xenobiotics with different organisms. Chrysoperla externa (Hagen, 1861) is a species of great economic relevance because it is a predator of major agricultural pests during its larval stage. Neonicotinoids are the most important chemical class of insecticides introduced into markets. A previous imidacloprid toxicity assessment on C. externa showed that this neonicotinoid insecticide reduced the egg viability. The objective of this study was to analyze the genotoxicity of Confidor OD® (imidacloprid 20% a.i., LS, Bayer CropScience) on the biological control agent C. externa at DNA level using the comet assay as an ecotoxicological biomarker. A comet assay protocol has been developed for this species at first time. For the bioassays, the commercial product formulated Confidor OD® was used at two concentrations: 100 and 180 mg/l of the active ingredient. Selected eggs were dipped in a Confidor OD® solution for 15 s. Descriptors evaluated in the comet assay were damage index, % DNA damage, and tail length. The damage index did not show any significant differences between the different concentrations evaluated, but differences were observed for tail length, because at higher concentrations of Confidor OD®, there were greater DNA breaks. The DNA of the cells from treated eggs analyzed at 48 h and 96 h of development showed the same % DNA damage; that is, they had no recovery capacity. Application of Confidor OD® to C. externa eggs produced irreparable breaks at the DNA level. The technique adjusted for C. externa can be used in other beneficial insects to study pesticide genotoxicity using a comet assay.

Mixture of pesticides based on dimethylamine and imidacloprid affects locomotion of adult zebrafish.

Numerous chemical compounds are found in aquatic environments; among them are pesticides. Pesticides are widely used worldwide, and this use has progressively increased in recent decades, resulting in the accumulation of potentially toxic compounds in surface waters. Dimethylamine-based herbicides (DBH) and imidacloprid-based insecticides (IBI) have low soil absorption and high water solubility, facilitating the arrival of these compounds in aquatic environments. In this study, our objective was to analyze whether two pesticides, DBH and IBI at environmentally relevant concentrations of 320 µg/L for each compound, and their mixtures impact the behavioral and endocrine parameters of adult zebrafish, verifying the effect of pesticides on exploratory behavior and social and analyzing hormonal parameters related to stress. Acute exposure to the mixture of pesticides reduced fish locomotion. Pesticides alone and in combination did not affect cortisol levels in exposed animals. Pesticides, when tested together, can cause different effects on non-target organisms, and the evaluation of mixtures of these compounds is extremely important.

Sub-lethal effects of the insecticide, imidacloprid, on the responses of damselfly larvae to chemosensory cues indicating predation risk.

Insecticides, including the widely used neonicotinoids, can affect both pest and non-target species. In addition to lethal effects, these insecticides at sub-lethal levels may cause disruption to sensory perception and processing leading to behavioural impairments. In this laboratory experiment, we investigated the effects of a 10-day exposure to the neonicotinoid insecticide, imidacloprid, on the behaviour of larvae of the damselfly, Lestes congener. In tests of baseline activity, imidacloprid concentrations of 1.0 and 10.0 µg/L caused significant reductions in foraging behaviour. Moreover, in response to chemical cues that indicate a potential risk to the larvae, imidacloprid caused the loss of an appropriate antipredator response (reduced foraging) depending on the concentration and duration of exposure. Imidacloprid at 0.1 µg/L caused the loss of responses toward the odour of a beetle (Dytiscus spp.) predator after 10 days of exposure, whereas 1.0 µg/L caused lost responses toward both the predator odour and injured conspecific cues (i.e., alarm cues) and after only 2 days of exposure. However, at 10.0 µg/L, larvae responded appropriately to both cues throughout the duration of the study, suggesting compensatory responses to imidacloprid at higher concentrations. Hence, the lack of appropriate responses at 1.0 µg/L likely resulted from a cognitive impairment rather than chemical alteration of these important chemosensory cues. In the natural environment, such effects will likely cause decreased survivorship in predator encounters. Hence, imidacloprid exposure, even at low concentrations, could have adverse consequences for chemosensory ecology of this damselfly species.

Single and combined exposure to 'bee safe' pesticides alter behaviour and offspring production in a ground-nesting solitary bee (Xenoglossa pruinosa).

Mounting evidence supporting the negative impacts of exposure to neonicotinoids on bees has prompted the registration of novel 'bee-friendly' insecticides for agricultural use. Flupyradifurone (FPF) is a butenolide insecticide that shares the same mode of action as neonicotinoids and has been assessed to be 'practically non-toxic to adult honeybees' using current risk assessment procedures. However, these assessments overlook some routes of exposure specific to wild bees, such as contact with residues in soil for ground-nesters. Co-exposure with other pesticides may also lead to detrimental synergistic effects. In a fully crossed experiment, we assessed the possible lethal and sublethal effects of chronic exposure to two pesticides used on Cucurbita crops, the insecticide Sivanto Prime (FPF) and the fungicide Quadris Top (azoxystrobin and difenoconazole), alone or combined, on solitary ground-nesting squash bees (Xenoglossa pruinosa). Squash bees exposed to Quadris Top collected less pollen per flower visit, while Sivanto-exposed bees produced larger offspring. Pesticide co-exposure induced hyperactivity in female squash bees relative to both the control and single pesticide exposure, and reduced the number of emerging offspring per nest compared to individual pesticide treatments. This study demonstrates that 'low-toxicity' pesticides can adversely affect squash bees under field-realistic exposure, alone or in combination.

Non-acute exposure of neonicotinoids, health risk assessment, and evidence integration: a systematic review.

Neonicotinoid pesticides are utilized against an extensive range of insects. A growing body of evidence supports that these neuro-active insecticides are classified as toxicants in invertebrates. However, there is limited published data regarding their toxicity in vertebrates and mammals. the current systematic review is focused on the up-to-date knowledge available for several neonicotinoid pesticides and their non-acute toxicity on rodents and human physiology. Oral lethal dose 50 (LD50) of seven neonicotinoids (i.e. imidacloprid, acetamiprid, clothianidin, dinotefuran, thiamethoxam, thiacloprid, and nitenpyram) was initially identified. Subsequently, a screening of the literature was conducted to collect information about non-acute exposure to these insecticides. 99 studies were included and assessed for their risk of bias and level of evidence according to the Office of Health and Translation (OHAT) framework. All the 99 included papers indicate evidence of reproductive toxicity, hepatotoxicity, nephrotoxicity, neurotoxicity, immunotoxicity, and oxidative stress induction with a high level of evidence in the health effect of rodents and a moderate level of evidence for human health. The most studied type of these insecticides among 99 papers was imidacloprid (55 papers), followed by acetamiprid (22 papers), clothianidin (21 papers), and thiacloprid (11 papers). While 10 of 99 papers assessed the relationship between clothianidin, thiamethoxam, dinotefuran, and nitenpyram, showing evidence of liver injury, dysfunctions of oxidative stress markers in the reproductive system, and intestinal toxicity. This systematic review provides a comprehensive overview of the potential risks caused by neonicotinoid insecticides to humans and rodents with salient health effects. However, further research is needed to better emphasize and understand the patho-physiological mechanisms of these insecticides, taking into account various factors that can influence their toxicity.

Inhalation bioaccessibility of imidacloprid in particulate matter: Implications for risk assessment during spraying.

Adverse health outcomes due to the inhalation of pesticide residues in atmospheric particulate matter (PM) are gaining global attention. Quantitative health risk assessments of pesticide inhalation exposure highlight the need to understand the bioaccessibility of pesticide residues. Herein, the inhalation bioaccessibility of imidacloprid in PM was determined using three commonly used in vitro lung modeling methods (Artificial Lysosomal Fluid, Gamble Solution, and Simulated Lung Fluid). To validate its feasibility and effectiveness, we evaluated the bioavailability of imidacloprid using a mouse nasal instillation assay. The in vitro inhalation bioaccessibility of imidacloprid was extracted using Gamble Solution with a solid-liquid ratio of 1/1000, an oscillation rate of 150 r/min, and an extraction time of 24 h, showed a strong linear correlation with its in vivo liver-based bioavailability (R2 =0.8928). Moreover, the margin of exposure was incorporated into the inhalation exposure risk assessment, considering both formulations and nozzles. The inhalation unit exposure of imidacloprid for residents was 0.95-4.09 ng/m3. The margin of exposure for imidacloprid was determined to be acceptable when considering inhalation bioaccessibility. Taken together, these results indicate that the inhalation bioaccessibility of pesticides should be incorporated into assessments of human health risks posed by PM particles.

Exploring the neurotoxicity of chiral dinotefuran towards nicotinic acetylcholine receptors: Enantioselective insights into species selectivity.

Dinotefuran is a chiral neonicotinoid that is widely distributed in environmental matrices, but its health risks to different organisms are poorly understood. This study investigated the neurotoxic responses of honeybee/cotton aphid nicotinic acetylcholine receptors (nAChRs) to chiral dinotefuran at the enantiomeric scale and demonstrated the microscopic mechanism of species selectivity in nAChR-mediated enantioselective neurotoxicity. The findings indicated that (S)-dinotefuran had a higher affinity for honeybee nAChR than (R)-dinotefuran whereas both enantiomers exhibited similar bioactivity toward cotton aphid nAChR. The results of dynamic neurotoxic processes indicated the association of conformational changes induced by chiral dinotefuran with its macroscopic neurotoxicity, and (R)-dinotefuran, which exhibit low toxicity to honeybee, was found to induce significant conformational changes in the enantioselective neurotoxic reaction, as supported by the average root-mean-square fluctuation (0.35 nm). Energy decomposition results indicated that electrostatic contribution (ΔGele) is the critical energy term that leads to substantial enantioselectivity, and both Trp-51 (－2.57 kcal mol-1) and Arg-75 (－4.86 kcal mol-1), which form a hydrogen-bond network, are crucial residues in mediating the species selectivity for enantioselective neurotoxic responses. Clearly, this study provides experimental evidence for a comprehensive assessment of the health hazards of chiral dinotefuran.

An integrated approach to assess human health risk of neonicotinoid insecticides in surface water of the Yangtze River Basin, China.

Neonicotinoids are widely used insecticides that have raised considerable concerns for both environmental and human health. However, there lack of comprehensive evaluation of their accumulation in surface water ecosystems and exposure to various human groups. Additionally, there's a distinct lack of scientific evidence describing the carcinogenic and non-carcinogenic impacts of neonicotinoids from surface water. Using an integrated approach employing the Relative Potency Factor (RPF), Hazard Index (HI), and Monte Carlo Simulation (MCS), the study assessed neonicotinoid exposure and risk to four demographic groups via dermal contact and mistaken oral intake pathways in the Yangtze River Basin (YRB), China. Neonicotinoid concentrations range from 0.1 to 408.12 ng/L, indicating potential risk (10-3 to 10-1) across the studied demographic groups. The Incremental Lifetime Cancer Risk (ILCR) for dermal contact was within a moderate range of 2.00 × 10-3 to 1.67 × 10-2, while the mistaken oral intake was also within a moderate range of 3.07 × 10-3 to 7.05 × 10-3. The Hazard Index (HI) for dermal exposure ranged from 1.49 × 10-2 to 0.125, while for mistaken oral intake, it varied between 2.69 × 10-2 and 0.14. The findings highlight the importance of implementing specific interventions to address neonicotinoid exposure, especially among demographic groups that are more susceptible. This research underscores the urgent need for targeted strategies to address neonicotinoid risks to vulnerable populations within the YRB while contributing to insights for effective policies to mitigate neonicotinoid exposure in surface water ecosystems globally.