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79 results for “pesticide exposure”
Exposure to sublethal concentrations of a pesticide or predator cues induces changes in brain architecture in larval amphibians, 2013.
Naturally occurring environmental factors shape developmental trajectories to produce variable phenotypes. Such developmental phenotypic plasticity can have important effects on fitness, and has been demonstrated for numerous behavioral and morphological traits. However, surprisingly few studies have examined developmental plasticity of the nervous system in response to naturally occurring environmental variation, despite accumulating evidence for neuroplasticity in a variety of organisms. Here, we asked whether the brain is developmentally plastic by exposing larval amphibians to natural and anthropogenic factors. Leopard frog tadpoles were exposed to predator cues, reduced food availability, or sublethal concentrations of the pesticide chlorpyrifos in semi-natural enclosures. Mass, growth, survival, activity, larval period, external morphology, brain mass, and brain morphology were measured in tadpoles and after metamorphosis. Tadpoles in the experimental treatments had lower masses than controls, although developmental rates and survival were similar. Tadpoles exposed to predator cues or a high dose of chlorpyrifos had altered body shapes compared to controls. In addition, brains from tadpoles exposed to predator cues or a low dose of chlorpyrifos were narrower and shorter in several dimensions compared to control tadpoles and tadpoles with low food availability. Interestingly, the changes in brain morphology present at the tadpole stage did not persist in the metamorphs. Our results show that brain morphology is a developmentally plastic trait that is responsive to ecologically relevant natural and anthropogenic factors. Whether these effects on brain morphology are linked to performance or fitness is unknown.
Exposure to pesticides data for residents and bystanders, and for environmental risk assessment
<p>In 2014, EFSA has commissioned a study to review and evaluate all published data related to the exposure to pesticides for residents and bystanders and for environmental risk assessment. The aim was to conduct a literature review and to produce a database containing all published data (predominately peer-reviewed publications supplemented by grey-literature) for the last 25-years, which will support the non-dietary exposure assessment to pesticides for bystanders and residents, as well as daily air concentration (vapours and aerosols) of pesticides, drift values from spray, seed and granular applications, and dislodgeable foliar residues.</p> <p>The data has been collated via a systematic and extensive literature review defined and managed according to a pre-defined 'review protocol'. The data was also exported in a format that meets the requirements of the EFSA Data Collection Framework (DCF).</p> <p>Based on quality and relevance criteria, articles and related studies have been selected. For dislodgeable foliar residues the assessment includes 27 articles (containing 49 discrete studies); for air concentrations, 26 articles (containing 84 discrete studies); for resident and bystander exposure, 5 articles (containing 8 discrete studies); and for drift values 55 articles (containing 275 discrete studies). </p> <p>For dislodgeable foliar residues the data retained covered 17 crops (including grass, glasshouse crops, lucerne, and citrus) and 29 pesticides; for air concentrations the data retained covered 21 crops (including fruit, glasshouse crops, ornamentals, grass, vegetables and cereals) and 39 pesticides. For drift values, the data covers a range of crops and landscapes from cereals, grass and turf, orchards, vineyards and regenerated forestry. The vast majority of the data retrieved applies to field studies for liquid spray drift, measured either as ground deposits or collected at various heights and were conducted using fluorescent tracers rather than pesticides. No data was found for microbials (biopesticides). For resident and bystander exposure, many articles were rejected due to the applied inclusion/exclusion criteria.</p>
C2D2: An Open-Source, Pan-European, Harmonised Crop Development Database for Use in Regulatory Pesticide Exposure Modelling and Risk Assessment.
<p>There is a regulatory need for crop development dates to assess current default values used within chemical exposure assessments as well as to justify refinements within risk assessments. However, a readily available pan-European crop phenology database covering key FOCUS (FOrum for the Co-ordination of pesticide fate models and their USe) crops and scenarios to meet this need is not currently available. Therefore, we describe the development of a harmonised, pan-European, CropLife Europe Crop Development Database, C2D2, that is fully aligned with this regulatory requirement utilising efficacy trials data generated for regulatory submissions when registering plant protection products under Regulation (EU) 1107/2009. Evaluation of C2D2 against an independent dataset showed good agreement for equivalent time periods, crop growth stages and geographical regions. We illustrate how this database can be used to evaluate existing default crop development dates mandated by regulatory agencies for use within exposure assessments. Despite the large dataset compiled and the geographical coverage of C2D2, not all FOCUSsw/gw scenarios have sufficient data to facilitate comparison, with less significant scenarios, like FOCUSgw Porto, being under-represented. For those scenarios with sufficient data, clear differences between C2D2 and crop development dates assumed in the FOCUS modelling framework (using the AppDate tool) are often indicated over some/many growth stages suggesting that amendment of the existing representation of crop development within the risk assessment process may be required. C2D2 is freely available under a Creative Commons licence to facilitate innovation in exposure science to allow for more accurate and realistic risk assessment leading to enhanced crop and environmental protection.</p>
Pesticide exposure triggers sex-specific inter- and trans-generational effects conditioned by past sexual selection
<p>Environmental variation often induces plastic responses in organisms that can trigger changes in subsequent generations through non-genetic inheritance mechanisms. Such transgenerational plasticity thus consists of environmentally-induced non-random phenotypic modifications that are transmitted through generations. Transgenerational effects may vary according to the sex of the organism experiencing the environmental perturbation, the sex of their descendants, or both, but whether they are affected by past sexual selection is unknown. Here we use experimental evolution on an insect model system to conduct a first test of the involvement of sexual selection history in shaping transgenerational plasticity in the face of rapid environmental change (exposure to pesticides). We manipulated evolutionary history in terms of the intensity of sexual selection for over 80 generations before exposing individuals to the toxicant. We found that sexual selection history constrained adaptation under rapid environmental change. We also detected intergenerational and transgenerational effects of pesticide exposure in the form of increased fitness and longevity. These cross-generational influences of toxicants were sex-dependent (they affected only male descendants), and intergenerational, but not transgenerational, plasticity was modulated by sexual selection history. Our results highlight the complexity of intragenerational, intergenerational, and transgenerational influences of past selection and environmental stress on phenotypic expression.</p>
Annexes to the external scientific report on the cumulative dietary exposure assessment of pesticides that have acute effects on the nervous system using MCRA software - Input and output data sets
<p>Retrospective dietary exposure assessments were conducted for two groups of pesticides that have acute effects on the nervous system: </p> <ol> <li>brain and/or erythrocyte acetylcholinesterase inhibition (CAG-NAN);</li> <li>functional alterations of the motor division (CAG-NAM).</li> </ol> <p>The pesticides considered in this assessment were identified and characterised in the scientific report on the establishment of cumulative assessment groups of pesticides for their effects on the nervous system (<a href="https://doi.org/10.2903/j.efsa.2019.5800">here</a>).</p> <p>The exposure calculations used monitoring data collected by Member States under their official pesticide monitoring programmes in 2014, 2015 and 2016 and individual food consumption data from ten populations of consumers from different countries and from different age groups. Regarding the selection of relevant food commodities, the assessment included water, foods for infants and young children and 30 raw primary commodities of plant origin that are widely consumed within Europe.</p> <p>Exposure estimates were obtained with Monte Carlo Risk Assessment (MCRA) software using a 2-dimensional Monte Carlo simulation, which is composed of an inner-loop execution and an outer-loop execution. Variability within the population is modelled through the inner-loop execution and is expressed as a percentile of the exposure distribution. The outer-loop execution is used to derive 95% confidence intervals around those percentiles (reflecting the sampling uncertainty of the input data).</p> <p>Furthermore, calculations were carried out according to a tiered approach. While the first-tier calculations (Tier I) use very conservative assumptions for an efficient screening of the exposure with low risk for underestimation, the second-tier assessment (Tier II) includes assumptions that are more refined but still conservative. For each scenario, exposure estimates were obtained for different percentiles of the exposure distribution and the total margin of exposure (MOET, i.e. the ratio of the toxicological reference dose to the estimated exposure) was calculated at each percentile.</p> <p>The input and output data for the exposure assessment are reported in the following annexes:</p> <ul> <li>Annex A.1 – Input data for the exposure assessment of CAG-NAN</li> <li>Annex A.2 – Input data for the exposure assessment of CAG-NAM</li> <li>Annex B.1 – Output data from the Tier II exposure assessment of CAG-NAN</li> <li>Annex B.2 – Output data from the Tier II exposure assessment of CAG-NAM</li> </ul> <p>Further information on the data, methodologies and interpretation of the results are provided in the external scientific report on the cumulative dietary exposure assessment of pesticides that have acute effects on the nervous system using MCRA software (<a href="https://doi.org/10.2903/sp.efsa.2019.en-1708">here</a>).</p> <p>The results reported in this assessment only refer to the exposure and are not an estimation of the actual risks. These exposure estimates should therefore be considered as documentation for the final scientific report on the cumulative risk assessment of dietary exposure to pesticides for their effects on the nervous system (<a href="https://www.efsa.europa.eu/en/consultations/call/public-consultation-scientific-report-cumulative">here</a>). The latter combines the hazard assessment and exposure assessment into a consolidated risk characterisation, including all related uncertainties.</p>
Annexes to the external scientific report on the cumulative dietary exposure assessment of pesticides that have chronic effects on the thyroid using MCRA software - Input and output data sets
<p>Retrospective dietary exposure assessments were conducted for two groups of pesticides that have chronic effects on the thyroid: </p> <ol> <li>hypertrophy, hyperplasia and neoplasia of C-cells, i.e. affecting the parafollicular cells or the calcitonin system of the thyroid (CAG-TCP);</li> <li>hypothyroidism, i.e. affecting the follicular cells and/or the hormone system of the thyroid (CAG-TCF).</li> </ol> <p>The pesticides considered in this assessment were identified and characterised in the scientific report on the establishment of cumulative assessment groups of pesticides for their effects on the thyroid (<a href="https://doi.org/10.2903/j.efsa.2019.5801">here</a>).</p> <p>The exposure calculations used monitoring data collected by Member States under their official pesticide monitoring programmes in 2014, 2015 and 2016 and individual food consumption data from ten populations of consumers from different countries and from different age groups. Regarding the selection of relevant food commodities, the assessment included water, foods for infants and young children and 30 raw primary commodities of plant origin that are widely consumed within Europe.</p> <p>Exposure estimates were obtained with Monte Carlo Risk Assessment (MCRA) software using a 2-dimensional probabilistic method, which is composed of an inner-loop execution and an outer-loop execution. Variability within the population is modelled through the inner-loop execution and is expressed as a percentile of the exposure distribution. The outer-loop execution is used to derive 95% confidence intervals around those percentiles (reflecting the sampling uncertainty of the input data).</p> <p>Furthermore, calculations were carried out according to a tiered approach. While the first-tier calculations (Tier I) use very conservative assumptions for an efficient screening of the exposure with low risk for underestimation, the second-tier assessment (Tier II) includes assumptions that are more refined but still conservative. For each scenario, exposure estimates were obtained for different percentiles of the exposure distribution and the total margin of exposure (MOET, i.e. the ratio of the toxicological reference dose to the estimated exposure) was calculated at each percentile.</p> <p>The input and output data for the exposure assessment are reported in the following annexes:</p> <ul> <li>Annex A.1 – Input data for the exposure assessment of CAG-TCP</li> <li>Annex A.2 – Input data for the exposure assessment of CAG-TCF</li> <li>Annex B.1 – Output data from the Tier II exposure assessment of CAG-TCP</li> <li>Annex B.2 – Output data from the Tier II exposure assessment of CAG-TCF</li> </ul> <p>Further information on the data, methodologies and interpretation of the results are provided in the external scientific report on the cumulative dietary exposure assessment of pesticides that have chronic effects on the thyroid using MCRA software (<a href="https://doi.org/10.2903/sp.efsa.2019.en-1707">here</a>).</p> <p>The results reported in this assessment only refer to the exposure and are not an estimation of the actual risks. These exposure estimates should therefore be considered as documentation for the final scientific report on the cumulative risk assessment of dietary exposure to pesticides for their effects on the thyroid (<a href="https://www.efsa.europa.eu/en/consultations/call/public-consultation-scientific-report-cumulative">here</a>). The latter combines the hazard assessment and exposure assessment into a consolidated risk characterisation, including all related uncertainties.</p>
Annexes to the scientific report on the cumulative dietary exposure assessment of pesticides that have chronic effects on the thyroid using SAS® software - Input and output data sets
<p>Retrospective dietary exposure assessments were conducted for two groups of pesticides that have chronic effects on the thyroid: </p> <ol> <li>hypertrophy, hyperplasia and neoplasia of C-cells, i.e. affecting the parafollicular cells or the calcitonin system of the thyroid (CAG-TCP);</li> <li>hypothyroidism, i.e. affecting the follicular cells and/or the hormone system of the thyroid (CAG-TCF).</li> </ol> <p>The pesticides considered in this assessment were identified and characterised in the scientific report on the establishment of cumulative assessment groups of pesticides for their effects on the thyroid (<a href="https://doi.org/10.2903/j.efsa.2019.5801">here</a>).</p> <p>The exposure calculations used monitoring data collected by Member States under their official pesticide monitoring programmes in 2014, 2015 and 2016 and individual food consumption data from ten populations of consumers from different countries and from different age groups. Regarding the selection of relevant food commodities, the assessment included water, foods for infants and young children and 30 raw primary commodities of plant origin that are widely consumed within Europe.</p> <p>Exposure estimates were obtained with SAS<sup>®</sup> software using a 2-dimensional probabilistic method, which is composed of an inner-loop execution and an outer-loop execution. Variability within the population is modelled through the inner-loop execution and is expressed as a percentile of the exposure distribution. The outer-loop execution is used to derive 95% confidence intervals around those percentiles (reflecting the sampling uncertainty of the input data).</p> <p>Furthermore, calculations were carried out according to a tiered approach. While the first-tier calculations (Tier I) use very conservative assumptions for an efficient screening of the exposure with low risk for underestimation, the second-tier assessment (Tier II) includes assumptions that are more refined but still conservative. For each scenario, exposure estimates were obtained for different percentiles of the exposure distribution and the total margin of exposure (MOET, i.e. the ratio of the toxicological reference dose to the estimated exposure) was calculated at each percentile.</p> <p>The input and output data for the exposure assessment are reported in the following annexes:</p> <ul> <li>Annex A.1 – Input data for the exposure assessment of CAG-TCP</li> <li>Annex A.2 – Input data for the exposure assessment of CAG-TCF</li> <li>Annex B.1 – Output data from the Tier I exposure assessment of CAG-TCP</li> <li>Annex B.2 – Output data from the Tier I exposure assessment of CAG-TCF</li> <li>Annex C.1 – Output data from the Tier II exposure assessment of CAG-TCP</li> <li>Annex C.2 – Output data from the Tier II exposure assessment of CAG-TCF</li> </ul> <p>Further information on the data, methodologies and interpretation of the results are provided in the scientific report on the cumulative dietary exposure assessment of pesticides that have chronic effects on the thyroid using SAS<sup>®</sup> software (<a href="https://doi.org/10.2903/j.efsa.2019.5763">here</a>).</p> <p>The results reported in this assessment only refer to the exposure and are not an estimation of the actual risks. These exposure estimates should therefore be considered as documentation for the final scientific report on the cumulative risk assessment of dietary exposure to pesticides for their effects on the thyroid (<a href="https://www.efsa.europa.eu/en/consultations/call/public-consultation-scientific-report-cumulative">here</a>). The latter combines the hazard assessment and exposure assessment into a consolidated risk characterisation, including all related uncertainties.</p>
Annexes to the scientific report on the cumulative dietary exposure assessment of pesticides that have acute effects on the nervous system using SAS® software - Input and output data sets
<p>Retrospective dietary exposure assessments were conducted for two groups of pesticides that have acute effects on the nervous system: </p> <ol> <li>brain and/or erythrocyte acetylcholinesterase inhibition (CAG-NAN);</li> <li>functional alterations of the motor division (CAG-NAM).</li> </ol> <p>The pesticides considered in this assessment were identified and characterised in the scientific report on the establishment of cumulative assessment groups of pesticides for their effects on the nervous system (<a href="https://doi.org/10.2903/j.efsa.2019.5800">here</a>).</p> <p>The exposure calculations used monitoring data collected by Member States under their official pesticide monitoring programmes in 2014, 2015 and 2016 and individual food consumption data from ten populations of consumers from different countries and from different age groups. Regarding the selection of relevant food commodities, the assessment included water, foods for infants and young children and 30 raw primary commodities of plant origin that are widely consumed within Europe.</p> <p>Exposure estimates were obtained with SAS<sup>®</sup> software using a 2-dimensional Monte Carlo simulation, which is composed of an inner-loop execution and an outer-loop execution. Variability within the population is modelled through the inner-loop execution and is expressed as a percentile of the exposure distribution. The outer-loop execution is used to derive 95% confidence intervals around those percentiles (reflecting the sampling uncertainty of the input data).</p> <p>Furthermore, calculations were carried out according to a tiered approach. While the first-tier calculations (Tier I) use very conservative assumptions for an efficient screening of the exposure with low risk for underestimation, the second-tier assessment (Tier II) includes assumptions that are more refined but still conservative. For each scenario, exposure estimates were obtained for different percentiles of the exposure distribution and the total margin of exposure (MOET, i.e. the ratio of the toxicological reference dose to the estimated exposure) was calculated at each percentile.</p> <p>The input and output data for the exposure assessment are reported in the following annexes:</p> <ul> <li>Annex A.1 – Input data for the exposure assessment of CAG-NAN</li> <li>Annex A.2 – Input data for the exposure assessment of CAG-NAM</li> <li>Annex B.1 – Output data from the Tier I exposure assessment of CAG-NAN</li> <li>Annex B.2 – Output data from the Tier I exposure assessment of CAG-NAM</li> <li>Annex C.1 – Output data from the Tier II exposure assessment of CAG-NAN</li> <li>Annex C.2 – Output data from the Tier II exposure assessment of CAG-NAM</li> </ul> <p>Further information on the data, methodologies and interpretation of the results are provided in the scientific report on the cumulative dietary exposure assessment of pesticides that have acute effects on the nervous system using SAS<sup>®</sup> software (<a href="https://doi.org/10.2903/j.efsa.2019.5764">here</a>).</p> <p>The results reported in this assessment only refer to the exposure and are not an estimation of the actual risks. These exposure estimates should therefore be considered as documentation for the final scientific report on the cumulative risk assessment of dietary exposure to pesticides for their effects on the nervous system (<a href="https://www.efsa.europa.eu/en/consultations/call/public-consultation-scientific-report-cumulative">here</a>). The latter combines the hazard assessment and exposure assessment into a consolidated risk characterisation, including all related uncertainties.</p>
Fig. 3 in The threat of pesticide and disease co-exposure to managed and wild bee larvae
Fig. 3. Pesticide research bias across bee genera depending on pesticide type based on Web of Science searches. The number of studies per search term is indicated for each genus with at least 10 studies across search terms; Understudied is a cumulative group including genera which contain less than 10 studies; Unexplored is a cumulative group including genera which have no published papers for any pesticide exposure category. Warmer colours are used to indicate a higher number of studies related to a genus for the corresponding pesticide search term, while colder colours indicate a lower number of studies found. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)
Fig. 4 in The threat of pesticide and disease co-exposure to managed and wild bee larvae
Fig. 4. Brood pathogens studies per bee genera found from Web of Science searches using search terms "brood disease", "brood pathogen", "brood virus", "larvae disease", "larvae pathogen" and "larvae virus" across bee genera. Red squares indicate that a pathogen on the x-axis has been found to infect at least one species in the bee genus corresponding to its position in the phylogeny shown on the y-axis; yellow squares indicate that the pathogen on the x-axis has been found in individuals from at least one species in the genus on the y-axis but no symptoms were reported in the studies; dark grey squares indicate that the pathogen on the x-axis has been tested for in at least one species in the genus corresponding on the yaxis, however has not been found; white squares indicate that the searches found no studies where any bee species of the genus on the y-axis were tested for in the corresponding pathogens on the x-axis. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)
Fig. 2 in The threat of pesticide and disease co-exposure to managed and wild bee larvae
Fig. 2. Proportion of results per search term across bee genera on the Web of Science search engine (n = the total number of studies corresponding to each search term). Search terms related to brood disease (A) and pesticide exposure (B) are both compared to species diversity at the genus level. Genera with less than 5 studies in any brood disease search term (A) and less than 10 studies across any pesticide exposure search term (B) have been classified as 'Understudied' (brown) and grouped. Genera with no studies related to any brood disease search term (A) and no studies related to any pesticide exposure search term (B) have been classified as 'Unexplored' (grey) and grouped. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)
Fig. 1 in The threat of pesticide and disease co-exposure to managed and wild bee larvae
Fig. 1. Flowers contaminated with brood pathogens and pesticides can lead to simultaneous exposure to pesticides and brood pathogens from flowers in adult foraging bees (A). This leads to brood being co-exposed to the stressors via food provisioning (B). Pesticides may increase larval mortality from brood infections directly through compromised immunocompetence (C), and/or indirectly through manipulating microbial communities and compromising food provisions from adult bees (D) (Icons8, 2022).
Supplementary Material: Assessment of Environmental Pollution and Human Exposure to Pesticides by Wastewater Analysis in a Seven-Year Study in Athens, Greece
<p>Supplementary Material</p>
Pesticide exposure triggers sex-specific inter- and trans-generational effects conditioned by past sexual selection
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Data for: Developmental origins of Parkinson’s disease risk: perinatal exposure to the organochlorine pesticide dieldrin leads to sex-specific DNA modifications in critical neurodevelopmental pathways in the mouse midbrain
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Data from: Pesticide and pathogen exposure causes idiosyncratic gene expression responses across four diverse North American bumble bee species
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Flower plantings support wild bee reproduction and may also mitigate pesticide exposure effects
<p>1. Sustainable agriculture relies on pollinators, and wild bees benefit yield of multiple crops. However, the combined exposure to pesticides and loss of flower resources, driven by agricultural intensification, contribute to declining diversity and abundance of many bee taxa. Flower plantings along the margins of agricultural fields offer diverse food resources not directly treated with pesticides.</p> <p>2. To investigate the potential of flower plantings to mitigate bee pesticide exposure effects and support bee reproduction, we selected replicated sites in intensively farmed landscapes where half contained flower plantings. We assessed solitary bee <em>Osmia lignaria</em> and bumble bee <em>Bombus vosnesenskii</em> nesting and reproduction throughout the season in these landscapes. We also quantified local and landscape flower resources and used bee-collected pollen to determine forage resource use and pesticide exposure and risk.</p> <p>3. Flower plantings, and their local flower resources, increased <em>O. lignaria</em> nesting probability. <em>Bombus vosnesenskii</em> reproduction was more strongly related to landscape than local flower resources.</p> <p>4. Bees at sites with and without flower plantings experienced similar pesticide risk, and the local flowers, alongside flowers in the landscape, were sources of pesticide exposure particularly for <em>O. lignaria</em>. However, local flower resources mitigated negative pesticide effects on <em>B. vosnesenskii</em> reproduction.</p> <p>5. <em>Synthesis and applications</em>. Bees in agricultural landscapes are threatened by pesticide exposure and loss of flower resources through agricultural intensification. Therefore, finding solutions to mitigate negative effects of pesticide use and flower deficiency is urgent. Our findings point towards flower plantings as a potential solution to support bee populations by mitigating pesticide exposure effects and providing key forage. Further investigation of the balance between forage benefits and added pesticide risk is needed to reveal contexts where net benefits occur.</p>
Evolutionary consequences of pesticide exposure include transgenerational plasticity and potential terminal investment transgenerational effects
<p>Transgenerational plasticity, the influence of the environment experienced by parents on the phenotype and fitness of subsequent generations, is being increasingly recognised. Human-altered environments, such as those resulting from the increasing use of pesticides, may be major drivers of such cross-generational influences, which in turn may have profound evolutionary and ecological repercussions. Most of these consequences are, however, unknown. Whether transgenerational plasticity elicited by pesticide exposure is common, and the consequences of its potential carry-over effects on fitness and population dynamics remains to be determined. Here we investigate whether exposure of parents to a common pesticide elicits intra-, inter- and transgenerational responses (in F0, F1 and F2 generations) in life-history (fecundity, longevity, and lifetime reproductive success-LRS-), in an insect model system, the seed beetle <em>Callosobruchus</em> <em>maculatus</em>. We also assessed sex-specificity of the effects. We found sex-specific and hormetic intergenerational and transgenerational effects on longevity and lifetime reproductive success, manifested both in the form of maternal and paternal effects. In addition, the transgenerational effects via mothers detected in this study are consistent with a new concept: terminal investment transgenerational effects. Such effects could underlie cross-generational responses to environmental perturbation. Our results indicate that pesticide exposure leads to unanticipated effects on population dynamics and have far-reaching ecological and evolutionary implications.</p>
Parameters for the modelization of operator, worker, and bystander exposure to pesticides in market gardening areas in Burkina Faso using three international exposure assessment models.
<p>Parameters used for the modelization of operator, worker, and bystander exposure to pesticides in market gardening areas in Burkina Faso using the following exposure assessment models:</p> <p>EFSA 2014: EFSA, 2014. Guidance on the assessment of exposure of operators, workers, residents and bystanders in risk assessment for plant protection products. EFSA J. 12, 3874. doi:10.2903/j.efsa.2014.3874</p> <p>HAIR2010: Kruijne, R., Deneer, J.W., Lahr, J., Vlaming, J., 2011. HAIR2010 Documentation: calculating risk indicators related to agricultural use of pesticides within the EU 205.</p> <p>WHO 2011: WHO, 2011. Generic risk assessment model for indoor and outdoor space spraying - WHO Pesticide Evaluation Scheme 1–72.</p> <p><br> This work was realized in the framework of the research component "Pesticides" (1.2.4) of the 3E program funded by the Swiss Agency for Development and Cooperation (SDC).</p> <p><br> Details on algorithm adaptations, scenario definitions and model outputs are available in the PhD thesis of Dr. Edouard Lehmann available from 2018 at https://infoscience.epfl.ch/</p>
Data from: Influence of agricultural intensification on pollinator pesticide exposure, food acquisition and diversity
<p>Pollinators are essential for maintaining sustainable crop production, while the decline of pollinators is a widespread concern. Agricultural intensification is one of the primary drivers of the decline of insect pollinators. Agricultural intensification usually involves a decreasing of non-crop semi-natural habitat and an increasing of pesticide exposure for pollinators. However, causal links between agricultural intensification, increased pesticide exposure, and reduced pollinator's food sources and pollinator diversity remain underexplored.</p> <p>We assessed pollinator diversity across a landscape gradient where the proportion of rice ranged from 11% to 85% in South China. We placed honeybee (<em>Apis mellifera</em>) and mason bee (<em>Osmia excavata</em>) in these landscapes and investigated pesticide exposure in honeybee foragers and pollen, and in mason bee pollen and nesting materials. We also assessed the acquisition of food by mason bees.</p> <p>We found a higher frequency of pesticide detection in honeybee foragers and honeybee pollen samples in areas with a higher proportion of rice fields. There was a strong positive relationship between mason bee food acquisition and the proportion of semi-natural habitats, while no significant effects of pesticide exposure on pollinator diversity were found in addition to the effect of semi-natural habitat.</p> <p><em>Synthesis and applications</em>: Our results suggest that pollinator communities could be at an increased risk of pesticide exposure due to intensified agriculture, while the negative impact on pollinator diversity mainly results from the loss of habitat and/or reduced food sources. This study highlights the importance of conserving semi-natural habitat to mitigate the causes of decline in pollinator diversity. We also recommend long-term, multi-year studies to further understand the mechanisms behind the loss of pollinators in farming landscapes.</p>
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.