Humans

This work reports a new sensitive multi-residue liquid chromatography–tandem mass spectrometry (LC–MS/MS) method for detection, confirmation and quantification of six neonicotinoid pesticides (dinotefuran, thiamethoxam, clothiandin, imidacloprid, acetamiprid and thiacloprid) in agricultural samples (chestnut, shallot, ginger and tea). Limits of quantification (LOQs) were 0.01 mg kg−1 for chestnut, shallot, ginger sample and 0.02 mg kg−1 for tea sample. The method was satisfactorily validated for the analysis of 150 agricultural samples (chestnut, shallot, ginger and tea). Imidacloprid and acetamiprid were detected at concentration levels ranging from 0.05 to 3.6 mg kg−1.

Het RIVM heeft de risico's voor de mens beoordeeld als gevolg van de aanwezigheid van imidacloprid in oppervlaktewater. Mensen kunnen met imidacloprid in contact komen via het drinken van water dat uit oppervlaktewater wordt gemaakt, via het eten van vis waarin de stof zich heeft opgehoopt en via zwemmen. Voor elk van deze drie blootstellingsroutes is een risicoschatting gemaakt. De gemeten concentraties Imidacloprid zijn echter volgens het RIVM in alle gevallen lager dan de gehaltes die een gevaar op kunnen leveren voor de mens. In een reactie schrijft toxicoloog Henk Tennekes dat belangwekkende recente studies (zie bijlage) niet zijn meegenomen in de analyse en dat op basis van nieuwe inzichten lange termijn effecten bij de mens niet meer kunnen worden uitgesloten.

Neonicotinoids are synthetic, nicotine-derived insecticides used for agricultural and household pest control. Though highly effective at activating insect nicotinic receptors, many neonicotinoids are also capable of directly activating and/or modulating the activation of vertebrate nicotinic receptors. In this study, we have investigated the actions of the neonicotinoids clothianidin (CTD) and imidacloprid (IMI) on human neuronal alpha4β2 nicotinic acetylcholine receptors.

The data demonstrate that the compounds are weak agonists of the human receptors with relative peak currents of 1–4% of the response to 1 mM acetylcholine (ACh). Coapplication of IMI strongly inhibited currents elicited by ACh. From Schild plot analysis, we estimate that the affinity of IMI for the human alpha4β2 receptor is 18 μM. The application of low concentrations of CTD potentiated responses to low concentrations of ACh, suggesting that receptors occupied by one ACh and one CTD molecule have a higher gating efficacy than receptors with one ACh bound. Interestingly, subunit stoichiometry affected inhibition by CTD, with alpha(4)2(β2)3 receptors significantly more strongly inhibited than the alpha(4)3(β2)2 receptors.

Phil Chandler's audio-interview with Tom Theobald - the Colorado bee-farmer who uncovered the duplicity of the American EPA - in licensing Clothianidin against the official judgement of their own scientific officers. The scientists noted that as a nicotinoid, Clothianidin was 'highly toxic to bees by contact and oral exposure' and that is was 'highly mobile' in soil and groundwater - very likely to migrate into streams, ponds and other fields, where it would be absorbed by wildflowers - and go on to kill more bees and non-target insects like butterflies and bumblebees (attached). They judged it to be many times more toxic than its sister nicotinoid Imidacloprid, which is "7,000 times more toxic to bees than DDT". Despite the strong advice of their own scientists, the American EPA gave Clothianidin a conditional license in 2003 and it was planted on 88 million acres of American maize (corn, sweetcorn). Since 2004 - over a million beehives have died across America - and many science studies point the finger at Clothianidin (and Imidacloprid) , because in the vast monocultural maize prairies of America - bees rely heavily on maize pollen for the protein to feed their young.

The full audio interview can be listened to as a Podcast online at:

http://biobees.libsyn.com

Neonicotinoids, agonists at the nicotinic acetylcholine receptors (nAChRs), induce neuromuscular paralysis. The high selectivity for nAChRs (particularly the a4b2 subtype) in insects compared with mammals results in their favorable toxicological profile. We describe fatal toxicity with one such insecticide, imidacloprid, considered relatively safe. This patient manifested neurological dysfunction and rhabdomyolysis. The initial neurological dysfunction, probably due to central nicotinic stimulation, was compounded by ischemic and metabolic encephalopathy. This report of imidacloprid toxicity sensitizes clinicians to an emerging cause of poisoning and highlights the need for a careful review of its toxicity profile.