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In this paper, we review the effects of large-scale neonicotinoid contaminations in the aquatic environment on non-target aquatic invertebrate and vertebrate species. These aquatic species are the fauna widely exposed to environmental changes and chemical accumulation in bodies of water. Neonicotinoids are insecticides that target the nicotinic type acetylcholine receptors (nAChRs) in the central nervous systems (CNS) and are considered selective neurotoxins for insects. However, studies on their physiologic impacts and interactions with non-target species are limited. In researches dedicated to exploring physiologic and toxic outcomes of neonicotinoids, studies relating to the effects on vertebrate species represent a minority case compared to invertebrate species. For aquatic species, the known effects of neonicotinoids are described in the level of organismal, behavioral, genetic and physiologic toxicities. Toxicological studies were reported based on the environment of bodies of water, temperature, salinity and several other factors. There exists a knowledge gap on the relationship between toxicity outcomes to regulatory risk valuation. It has been a general observation among studies that neonicotinoid insecticides demonstrate significant toxicity to an extensive variety of invertebrates. Comprehensive analysis of data points to a generalization that field-realistic and laboratory exposures could result in different or non-comparable results in some cases. Aquatic invertebrates perform important roles in balancing a healthy ecosystem, thus rapid screening strategies are necessary to verify physiologic and toxicological impacts. So far, much of the studies describing field tests on non-target species are inadequate and in many cases, obsolete. Considering the current literature, this review addresses important information gaps relating to the impacts of neonicotinoids on the environment and spring forward policies, avoiding adverse biological and ecological effects on a range of non-target aquatic species which might further impair the whole of the aquatic ecological web.

The honey bee is a major pollinator whose health is of global concern. Declines in bee health are related to multiple factors, including resource quality and pesticide contamination. Intensive agricultural areas with crop monocultures potentially reduce the quality and quantity of available nutrients and expose bee foragers to pesticides. However, there is, to date, no evidence for synergistic effects between pesticides and nutritional stress in animals. The neonicotinoids clothianidin (CLO) and thiamethoxam (TMX) are common systemic pesticides that are used worldwide and found in nectar and pollen. We therefore tested if nutritional stress (limited access to nectar and access to nectar with low-sugar concentrations) and sublethal, field-realistic acute exposures to two neonicotinoids (CLO and TMX at 1/5 and 1/25 of LD50) could alter bee survival, food consumption and haemolymph sugar levels. Bee survival was synergistically reduced by the combination of poor nutrition and pesticide exposure (−50%). Nutritional and pesticide stressors reduced also food consumption (−48%) and haemolymph levels of glucose (−60%) and trehalose (−27%). Our results provide the first demonstration that field-realistic nutritional stress and pesticide exposure can synergistically interact and cause significant harm to animal survival. These findings have implications for current pesticide risk assessment and pollinator protection.

Pollinators in agroecosystems are often exposed to pesticide mixtures. Even at low concentrations, the effects of these mixtures on bee populations are difficult to predict due to potential synergistic interactions. In this paper, we orally exposed newly emerged females of the solitary bee Osmia bicornis to environmentally realistic levels of clothianidin (neonicotinoid insecticide) and propiconazole (fungicide), singly and in combination. The amount of feeding solution consumed was highest in bees exposed to the neonicotinoid, and lowest in bees exposed to the pesticide mixture. Ovary maturation and longevity of bees of the neonicotinoid and the fungicide treatments did not differ from those of control bees. By contrast, bees exposed to the pesticide mixture showed slow ovary maturation and decreased longevity. We found a synergistic interaction between the neonicotinoid and the fungicide on survival probability. We also found an interaction between treatment and emergence time (an indicator of physiological condition) on longevity. Longevity was negatively correlated to physiological condition only in the fungicide and the mixture treatments. Delayed ovary maturation and premature death imply a shortened nesting period (highly correlated to fecundity in Osmia ). Our findings provide a mechanism to explain the observed dynamics of solitary bee populations exposed to multiple chemical residues in agricultural environments.

Bumblebees are essential pollinators of crops and wild plants, but are in decline across the globe. Neonicotinoid pesticides have been implicated as a potential driver of these declines, but most of our evidence base comes from studies of a single species. There is an urgent need to understand whether such results can be generalized across a range of species. Here, we present results of a laboratory experiment testing the impacts of field-relevant doses (1.87–5.32 ppb) of the neonicotinoid thiamethoxam on spring-caught wild queens of four bumblebee species: Bombus terrestris, B. lucorum, B. pratorum and B. pascuorum. Two weeks of exposure to the higher concentration of thiamethoxam caused a reduction in feeding in two out of four species, suggesting species-specific anti-feedant, repellency or toxicity effects. The higher level of thiamethoxam exposure resulted in a reduction in the average length of terminal oocytes in queens of all four species. In addition to providing the first evidence for general effects of neonicotinoids on ovary development in multiple species of wild bumblebee queens, the discovery of species-specific effects on feeding has significant implications for current practices and policy for pesticide risk assessment and use.

Fil: Clark, E. Ann. University of Guelph; Canadá

Birds that travel long distances between their wintering and breeding grounds may be particularly susceptible to neurotoxic insecticides, but the influence of insecticides on migration ability is poorly understood. Following acute exposure to two widely used agricultural insecticides, imidacloprid (neonicotinoid) and chlorpyrifos (organophosphate), we compared effects on body mass, migratory activity and orientation in a seed-eating bird, the white-crowned sparrow ( Zonotrichia leucophrys ). During spring migration, sparrows were captured, held and dosed by gavage daily for 3 days with either the vehicle control, low (10% LD50) or high (25% LD50) doses of imidacloprid or chlorpyrifos and tested in migratory orientation trials pre-exposure, post-exposure and during recovery. Control birds maintained body mass and a seasonally appropriate northward orientation throughout the experiment. Imidacloprid dosed birds exhibited significant declines in fat stores and body mass (mean loss: −17% low, −25% high dose) and failed to orient correctly. Chlorpyrifos had no overt effects on mass but significantly impaired orientation. These results suggest that wild songbirds consuming the equivalent of just four imidacloprid-treated canola seeds or eight chlorpyrifos granules per day over 3 days could suffer impaired condition, migration delays and improper migratory direction, which could lead to increased risk of mortality or lost breeding opportunity.

Pesticide use is one of the main causes of pollinator declines in agricultural ecosystems. Traditionally, most laboratory studies on bee ecotoxicology test acute exposure to single compounds. However, under field conditions, bees are often chronically exposed to a variety of chemicals, with potential synergistic effects. We studied the effects of field-realistic concentrations of three pesticides measured in pollen and nectar of commercial melon fields on the solitary bee Osmia bicornis L. We orally exposed females of this species throughout their life span to 8 treatments combining two neonicotinoid insecticides (acetamiprid, imidacloprid) and a triazole fungicide (myclobutanil) via pollen and sugar syrup. We measured pollen and syrup consumption, longevity, ovary maturation and thermogenesis. Although bees consumed larger amounts of syrup than pollen, pesticide intake via syrup and pollen were similar. At the tested concentrations, no synergistic effects emerged, and we found no effects on longevity and ovary maturation. However, all treatments containing imidacloprid resulted in suppressed syrup consumption and drastic decreases in thoracic temperature and bee activity. Our results have important implications for pesticide regulation. If we had measured only lethal effects we would have wrongly concluded that the pesticide combinations containing imidacloprid were safe to O. bicornis . The incorporation of tests specifically intended to detect sublethal effects in bee risk assessment schemes should be an urgent priority. In this way, the effects of pesticide exposure on the dynamics of bee populations in agroecosystems will be better assessed.

Widespread use of neonicotinoid insecticides, such as imidacloprid, is often associated with diminishing populations of bees; this loss of pollinators presents a concern for food security and may cause unpredictable changes in ecological networks. However, little is known about the potential behavioural mechanisms behind the neonicotinoid-associated pollinator decline. We quantified the effects of low-dose (1 ppb) imidacloprid exposure on the foraging behaviour of bumblebees (Bombus terrestris). Individual bumblebees were released into a flight arena containing three patches of robotic flowers whose colour (yellow, orange, blue) indicated whether the flower delivered a reward (sugar solution). Exposure to imidacloprid had no significant effect on measures of bumblebee physical performance (such as flight speed) or learning (identifying rewarding flowers). However, pesticide-treated bumblebees had reduced foraging motivation compared with the control bumblebees, as they visited fewer robotic flowers, were slower to start foraging and did not visit all three flower colours as often. Neonicotinoid concentrations of 1 ppb, often reported in plant nectar near agricultural lands, can thus affect the foraging behaviour of bumblebees. Even without a notable impact on flight performance and learning, a reduction in foraging motivation could explain the poor performance of colonies of bumblebees exposed to neonicotinoids.

Bumblebees are among the world's most important groups of pollinating insects in natural and agricultural ecosystems. Each spring, queen bumblebees emerge from overwintering and initiate new nests, which ultimately give rise to workers and new reproductives later in the season. Nest initiation and survival are thus key drivers of both bumblebee pollination services and population dynamics. We performed the first laboratory experiment with the model bumblebee species Bombus impatiens that explores how early nesting success is impacted by the effects of temporary or more sustained exposure to sublethal levels of a neonicotinoid-type insecticide (imidacloprid at 5 ppb in nectar) and by reliance on a monofloral pollen diet, two factors that have been previously implicated in bumblebee decline. We found that queens exhibited increased mortality and dramatically reduced activity levels when exposed to imidacloprid, as well as delayed nest initiation and lower brood numbers in the nest, but partially recovered from these effects when they only received early, temporary exposure. The effects of pollen diet on individual queen- and colony-level responses were overshadowed by effects of the insecticide, although a monofloral pollen diet alone was sufficient to negatively impact brood production. These findings speak to the sensitivity of queen bumblebees during the nest initiation phase of the colony cycle, with implications for how queens and their young nests are uniquely impacted by exposure to threats such as pesticide exposure and foraging habitat unsuitability.

Honey bees are critical pollinators in ecosystems and agriculture, but their numbers have significantly declined. Declines in pollinator populations are thought to be due to multiple factors including habitat loss, climate change, increased vulnerability to disease and parasites, and pesticide use. Neonicotinoid pesticides are agonists of insect nicotinic cholinergic receptors, and sub-lethal exposures are linked to reduced honey bee hive survival. Honey bees are highly dependent on circadian clocks to regulate critical behaviors, such as foraging orientation and navigation, time-memory for food sources, sleep, and learning/memory processes. Because circadian clock neurons in insects receive light input through cholinergic signaling we tested for effects of neonicotinoids on honey bee circadian rhythms and sleep. Neonicotinoid ingestion by feeding over several days results in neonicotinoid accumulation in the bee brain, disrupts circadian rhythmicity in many individual bees, shifts the timing of behavioral circadian rhythms in bees that remain rhythmic, and impairs sleep. Neonicotinoids and light input act synergistically to disrupt bee circadian behavior, and neonicotinoids directly stimulate wake-promoting clock neurons in the fruit fly brain. Neonicotinoids disrupt honey bee circadian rhythms and sleep, likely by aberrant stimulation of clock neurons, to potentially impair honey bee navigation, time-memory, and social communication.