Environmental occurrence, toxicity concerns, and biodegradation of neonicotinoid insecticides.

Neonicotinoids (NEOs) are fourth generation pesticides, which emerged after organophosphates, pyrethroids, and carbamates and they are widely used in vegetables, fruits, cotton, rice, and other industrial crops to control insect pests. NEOs are considered ideal substitutes for highly toxic pesticides. Multiple studies have reported NEOs have harmful impacts on non-target biological targets, such as bees, aquatic animals, birds, and mammals. Thus, the remediation of neonicotinoid-sullied environments has gradually become a concern. Microbial degradation is a key natural method for eliminating neonicotinoid insecticides, as biodegradation is an effective, practical, and environmentally friendly strategy for the removal of pesticide residues. To date, several neonicotinoid-degrading strains have been isolated from the environment, including Stenotrophomonas maltophilia, Bacillus thuringiensis, Ensifer meliloti, Pseudomonas stutzeri, Variovorax boronicumulans, and Fusarium sp., and their degradation properties have been investigated. Furthermore, the metabolism and degradation pathways of neonicotinoids have been broadly detailed. Imidacloprid can form 6-chloronicotinic acid via the oxidative cleavage of guanidine residues, and it is then finally converted to non-toxic carbon dioxide. Acetamiprid can also be demethylated to remove cyanoimine (=N-CN) to form a less toxic intermediate metabolite. A few studies have discussed the neonicotinoid toxicity and microbial degradation in contaminated environments. This review is focused on providing an in-depth understanding of neonicotinoid toxicity, microbial degradation, catabolic pathways, and information related to the remediation process of NEOs. Future research directions are also proposed to provide a scientific basis for the risk assessment and removal of these pesticides.

Zebrafish embryo neonicotinoid developmental neurotoxicity in the FET test and behavioral assays.

The need for reliable, sensitive (developmental) neurotoxicity testing of chemicals has steadily increased. Given the limited capacities for routine testing according to accepted regulatory guidelines, there is potential risk to human health and the environment. Most toxicity studies are based on mammalian test systems, which have been questioned for low sensitivity, limited relevance for humans, and animal welfare considerations. This increased the need for alternative models, one of which is the zebrafish (Danio rerio) embryo. This study assessed selected neonicotinoids at sub-lethal concentrations for their effects on embryonic development and behavior. The fish embryo acute toxicity test (OECD TG 236) determined the lowest observable effective concentrations, which were used as the highest test concentrations in subsequent behavioral assays. In the FET test, no severe compound-induced sublethal effects were seen at < 100 µM. In the coiling assay, exposure to ≥ 1.25 µM nicotine (positive control) affected both the burst duration and burst count per minute, whereas ≥ 50 µM thiacloprid affected the mean burst duration. Exposure to ≥ 50 µM acetamiprid and imidacloprid induced significant alterations in both mean burst duration and burst count per minute. In the swimming assay, 100 µM acetamiprid induced alterations in the frequency and extent of movements, whilst nicotine exposure only induced non-significant changes. All behavioral changes could be correlated to findings in mammalian studies. Given the quest for alternative test methods of (developmental) neurotoxicity, zebrafish embryo behavior testing could be integrated into a future tiered testing scheme.