Multigeneration toxicity of imidacloprid and thiacloprid to Folsomia candida
Multigeneration toxicity of imidacloprid and thiacloprid to Folsomia candida
Cornelis A.M. van Gestel 0 1
● Claudia de Lima e Silva 0 1
● Thao Lam 0 1
● Jacco C. Koekkoek 0 1
● Marja H. Lamoree 0 1
● Rudo A. Verweij 0 1
0 Department of Environment and Health, Faculty of Earth and Life Sciences, Vrije Universiteit , De Boelelaan 1085, Amsterdam 1081 HV , The Netherlands
1 Department of Ecological Science, Faculty of Earth and Life Sciences, Vrije Universiteit , De Boelelaan 1085, Amsterdam 1081 HV , The Netherlands
In a recent study, we showed that the springtail Folsomia candida was quite sensitive the neonicotinoid insecticides imidacloprid and thiacloprid. This study aimed at determining the toxicity of both compounds to F. candida following exposure over three generations, in natural LUFA 2.2 standard soil. In the first generation, imidacloprid was more toxic than thiacloprid, with LC50s of 0.44 and 9.0 mg/kg dry soil, respectively and EC50s of 0.29 and 1.5 mg/kg dry soil, respectively. The higher LC50/EC50 ratio suggests that thiacloprid has more effects on reproduction, while imidacloprid shows lethal toxicity to the springtails. In the multigeneration tests, using soil spiked at the start of the first generation exposures, imidacloprid had a consistent effect on survival and reproduction in all three generations, with LC50s and EC50s of 0.21-0.44 and 0.12-0.29 mg/kg dry soil, respectively, while thiacloprid-exposed animals showed clear recovery in the second and third generations (LC50 and EC50 > 3.33 mg/kg dry soil). The latter finding is in agreement with the persistence of imidacloprid and the fast degradation of thiacloprid in the test soil.
Neonicotinoid insecticides ● Soil ecotoxicity ●; Reproduction
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Neonicotinoids are widely used to protect crops against
herbivorous insects, with application as seed-dressing
agents (Tomizawa and Casida 2003; Douglas and Tooker
2015), soil treatment and spraying (Goulson 2013; Van der
Sluijs et al. 2015). Neonicotinoids are systemic, being
distributed throughout the plants via the sap stream, in this way
making the entire plant toxic to, i.e., the target insects. They
specifically bind to nicotinergic acetylcholine receptors
(nAChR) on the post-synaptic membrane of the neurons of
insects. They compete with ACh neurotransmitters to bind
to and activate the nAChR, an effect called agonistic
binding. The irreversible binding leads to excessive ion
flows (Na+, K+, Ca2+) through cellular membranes and
prolonged action potentials, causing overexcitement of the
neurons. Exposed animals show signs of disorientation and
paralysis, from which they eventually die (Buckingham
et al. 1997; Goulson 2013; Matsuda et al. 2001; Millar and
Denholm 2007; Sheets 2001; Tomizawa and Casida 2003).
Neonicotinoids are divided into three groups,
N-nitroguanidines, N-cyanoguanidines, and nitromethylenes
(Goulson 2013), which differ in toxicity, with the
N-cyanoguanidines being less toxic than the N-nitroguanidines
(Iwasa et al. 2004). The N-nitroguanidine imidacloprid was
about 800 times more toxic to honeybees upon acute dermal
exposure than the related N-cyanoguanidine thiacloprid
(Iwasa et al. 2004). Shi et al. (2011) showed that one of the
target organisms, the aphid Aphis gossypii, was about 7.5
times more sensitive to imidacloprid than to thiacloprid
when exposed dermally for 48 h. The fact that both
insecticides are usually applied at similar dosages (Pisa et al.
2015), however, suggests they are equally effective against
target organisms. This indicates that the difference in
toxicity in short-term laboratory tests does not translate to
differences in longer-term efficacy in the field. What the
reason is for this discrepancy remains unclear.
Following application more than 90% of the
neonicotinoid dose may stay in the soil or may reach the soil by
washing off the treated crop, where the compounds may
persist and accumulate, potentially threatening non-target
soil organisms (Laurent and Rathahao 2003; Goulson
2013). Persistence in soil may contribute to the exposure to
these compounds, causing potential long-term effects on
soil organisms. Thiacloprid is a factor of 10 less persistent
in soil than imidacloprid, with half-lives of 3.4–74 and
28–1250 days, respectively found in laboratory tests
(Goulson 2013; Bonmatin et al. 2015). EFSA (2008)
concluded that the laboratory half-life for imidacloprid
degradation in soil was 106 to 293 days while (under European
conditions) the field half-lives were 40–288 days.
Imidacloprid may therefore persist in soil and cause adverse
effects on multiple generations of soil organisms, especially
of species with short life cycles. For thiacloprid, long-term
exposure may occur when the compound is sprayed
frequently, like in fruit-growing and horticulture.
Relatively little is known about the effects of
neonicotinoids in the soil (EASAC 2015, Van der Sluijs et al.
2015). Recently, we determined the toxicity of imidacloprid
and thiacloprid t (...truncated)