Partition coefficients between n-octanol and water (Kow) indicate bioaccumulation potential when Log Kow > 4. \*The Groundwater Ubiquity Score (GUS) is calculated using soil half-life (DT50) and organic-carbon sorption constant (Koc) as follows: GUS = log(DT50) x (4-log Koc). A compound is likely to leach if GUS > 2.8 and unlikely to leach when

regulator; N = neonicotinoid; OP = organophosphate; PP = phenylpyrazole

GUS < 1.8; other values in between indicate that leaching potential is marginal.

**Solubilityin water (mg/L)**

hexaflumuron IGR 0.059 0.027 **5.68** -0.03 unlikely to leach

**Log Kow# GUS**

**index\***

**Leaching potential**


**Table 2.** Degradation of systemic insecticides expressed as half-lives in days. Compounds with half-lives longer than 100 days are considered persistent (Sources: Footprint database & [284]. a for pH 9C = carbamates; D = dithiol; IGR = Insect growth regulator; N = neonicotinoid; OP = organophosphate; PP = phenylpyrazole

Aquatic organisms take up easily whatever residues reach the waterbodies, through runoff from treated fields or contaminated groundwater. Some 20% systemic insecticides are prone to leaching, and 45% are mobile in wet soils (Table 1). For example, acephate leaches more easily than methamidophos [305], and so acephate should be restricted or avoided in tropi‐ cal areas and rice crops [46]. Residues of aldicarb and methomyl in groundwater can have sublethal effects in mammals [215]. Even if residue levels of systemic insecticides in rivers and lakes are usually at ppb levels (µg/L), persistent compounds such as fipronil, neonicoti‐ noids and growth regulators can have chronic effects due to their constant presence throughout several months in the agricultural season [123]. For example, about 1-2% of imi‐ dacloprid in treated soil moves into runoff after rainfall events, with the highest concentra‐ tions recorded at 0.49 mg/L [12]. Systemic carbamates and OPs do not last long in water because they breakdown through photolysis or hydrolysis in a few days, or are taken up and degraded by aquatic plants [100]. In any case, their presence and frequency of detection in water depends on local usage patterns [39, 171]. The acute toxicity of most systemic com‐ pounds is enhanced in aquatic insects and shrimp under saline stress [22, 253].

**Figure 1.** Increasing toxicity of several systemic insecticides with time of exposure. LD50 for acephate to *Episyrphus bateatus* and for methomyl to *Bombus terrestris* [75]; LC50 for imidacloprid to *Cypridopsis vidua* [234] and thiacloprid

Impact of Systemic Insecticides on Organisms and Ecosystems

http://dx.doi.org/10.5772/52831

371

Before describing their impacts on organisms and ecosystems, a description of the mecha‐

Carbamates and organophosphorus compounds are inhibitors of the acetylcholinesterase enzyme (AChE), thus blocking the transmission of the nervous impulse through the neuro‐ nal synapses. The binding of carbamates to the enzyme is slowly reversible and temporary, i.e. < 24 h [197], whereas that of alkyl OPs is irreversible. The binding of methyl-OPs does not last as long as that of alkyl-OPs, and this feature is compound specific [182]. Given their mode of action, all these compounds are broad-spectrum insecticides, extremely toxic to most animal taxa, from worms to mammalian vertebrates. Avian species are often more sus‐ ceptible to these compounds due to relatively low levels of detoxifying enzymes in birds [207, 297]. Thus, recovery of ducklings exposed to a range of carbamate and OP insecticides

Neonicotinoids are derived from nicotine, which is found in the nightshade family of plants (Solanaceae), and particularly in tobacco (*Nicotiana tabacum*). They all are agonists of the nic‐ otinic acetylcholinesterase receptor (nAChR), which mediate fast cholinergic synaptic trans‐ mission and play roles in many sensory and cognitive processes in invertebrates. Binding of neonicotinoids to these receptors is irreversible in arthropods [40, 307]. Given that nAChRs are embedded in the membrane at the neuronal synapses, their regeneration seems unlikely

occurred within eight days after being depressed 25-58% following dosing [91].

**3.2. Insecticides acting on nicotinic acetylcholine receptors (nAChR)**

to *Sympetrum striolatum* [28].

**3.1. Acetylcholinesterase inhibitors**

**3. Modes of action of systemic insecticides**

nisms of toxicity of systemic insecticides is briefly outlined.

A characteristic feature of most systemic insecticides –except carbamates– is their increased toxicity with exposure time, which results from a constant or chronic uptake through either feeding or aquatic exposure (Figure 1). Effects are more pronounced some time after the ini‐ tial application [16], and could last up to eight months [286]. Also, as a result of chronic in‐ toxication, there may not be limiting toxic concentrations (e.g. NOEC or NOEL) in compounds that have irreversible mechanism of toxicity, since any concentration will pro‐ duce an effect as long as there is sufficient exposure during the life of the organism [274]. This is precisely their main advantage for pest control: any concentration of imidacloprid in the range 0.2-1.6 ml/L can reduce the population of mango hoppers (*Idioscopus* spp.) to zero within three weeks [291]. However, it is also the greatest danger for all non-target species affected, e.g. predators, pollinators and parasitoids. By contrast, contact insecticides act usu‐ ally in single exposures (e.g. spray droplets, pulse contamination after spraying, etc.) and have the highest effects immediately after application.

**Figure 1.** Increasing toxicity of several systemic insecticides with time of exposure. LD50 for acephate to *Episyrphus bateatus* and for methomyl to *Bombus terrestris* [75]; LC50 for imidacloprid to *Cypridopsis vidua* [234] and thiacloprid to *Sympetrum striolatum* [28].
