Abstract

Various environmental and ecotoxicological aspects related to applications of neonicotinoid insecticides are assessed. Dosages of neonicotinoids applied in seed coating materials were determined and are compared to other applications (spray and granule). Environmental levels in soils and affecting factors in translocation are discussed. Excretion of neonicotinoids via guttation from coated maize seeds up to two months upon emergence, as well as cross-contamination of plants emerged from non-coated seeds or weeds nearby have been demonstrated. Contamination of surface waters is discussed in scope of a worldwide review and the environmental fate of the neonicotinoid active ingredients and the formulating surfactant appeared to be mutually affected by each other. Toxicity of neonicotinoid active ingredients and formulations on Daphnia magna completed with some investigations of activity of the detoxifying glutathione S-transferase enzyme demonstrated the modified toxicity due to the formulating agents. Electrophysiological results on identified central neurons of the terrestrial snail Helix pomatia showed acetylcholine antagonist (inhibitory) effects of neonicotinoid insecticide products, but no agonist (ACh-like) effects were recorded. These data also suggested different molecular targets (nicotinergic acetylcholine receptors and acetylcholine esterase enzyme) of neonicotinoids in the snail central nervous system.

Highlights

  • The first neonicotinoid insecticide, imidacloprid (IMI) was introduced in 1991 as a result of Japanese and European research activities, followed by nitenpyram and acetamiprid (ACE) in1995, thiamethoxam (TMX) in 1997, thiacloprid (TCL) in 1999 and clothianidin (CLO) in 2002 [1].Other active ingredients (AIs) were commercialized and a research program for the discovery of new neonicotinoid type insecticides was established in China [2]

  • Translocation via soil was observed for both weeds, but the levels were substantially lower in the guttation liquid of the weeds than in that of maize plants that emerged from coated seeds

  • ACh-evoked membrane currents can be resulted by inhibiting the acetylcholine esterase enzyme (AChE), observed in L. sativum, but 22.0% inhibition of plant growth was detected in the groups exposed to which contributes in breakdown synaptically released ACh in the synaptic cleft

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Summary

Introduction

The first neonicotinoid insecticide, imidacloprid (IMI) was introduced in 1991 as a result of Japanese and European research activities, followed by nitenpyram and acetamiprid (ACE) in. Other active ingredients (AIs) were commercialized and a research program for the discovery of new neonicotinoid type insecticides was established in China [2] Their large-scale deployment in seed treatments [3] as preventive pest management in field crops (e.g., maize, sunflower, cotton) has driven their rapid increase in worldwide use. Due to their broad-spectrum activity on a range of insects, the introduction of neonicotinoids was initially regarded as a substantial improvement in insect control, and their use was considered to exert only a minimal impact on wildlife and the environment. Considerably soil surface exposure as well, in-furrow and surface applications, but contamination cases were detected for the use of seed coating asRecommended well [21]

18.6 Number
Thestandard
Excretion via Guttation
Concentration
The Presence of Neonicotinoids in Surface Waters
Neuronal
Dose of ACh-evoked inward currents the presence of MOSPILAN
Toxicity
Conclusions
Findings
Toxicity Tests of Neonicotinoids on other Indicator Organisms
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