Humans

Neurobehavioral effects of long-term exposure to pesticides

The aim of this study was to investigate the role of pesticides on neurobehavioral performances in French vineyard workers. 929 Workers affiliated to the health insurance system for farmers in the Bordeaux area of south-western France were enrolled in the study in 1997–1998. They were contacted for a first follow-up in 2001–2003. Participants completed a questionnaire and nine neurobehavioral tests. They were classified according to their life-long pesticide exposure, as directly exposed, indirectly exposed or non-exposed. Educational level, age, sex, alcohol consumption, smoking, psychotropic drug use and depressive symptoms were taken into account in the analysis. 614 subjects were available for investigation at follow-up. Follow-up analysis confirmed that the risk of obtaining a low performance on the tests was higher in exposed subjects, with ORs ranging from 1.35 to 5.60. Evolution of performances over the follow-up period demonstrated that exposed subjects had the worst decreases in performance. The risk of having a two-point lower score on the Mini-Mental State Examination was 2.15 (95% CI 1.18 to 3.94) in exposed subjects. These results suggest long-term cognitive effects of chronic exposure to pesticides and raise the issue of the risk of evolution towards dementia. The study is the first to provide prospective data on the natural history of neurological disorders associated with pesticide exposure.

Oproep tot onderzoek naar het effect van imidacloprid op het IQ van de mens

Een onderzoek naar het effect van langjarige consumptie van minieme doses imidacloprid op het IQ van de mens is ’wenselijk’. Vijf wetenschappers ondersteunen de oproep van toxicoloog dr. ir. Henk Tennekes. Het gaat om dr. Gert van der Laan (AMC - klinische arbeidskunde in relatie met neuropsychologie), Henk .J. Vlug (insectendeskundige), dr. Paul Harrewijn (wis- en natuurkundige, medicus en ex-onderzoeker Wageningen) en prof.dr. Jeroen van der Sluis (senior-onderzoeker nieuwe risico’s UU en professor in Versailles). Prof.dr. Lucas Reijnders (emeritus milieukunde) wil ook onderzoek, maar dan rechtstreeks met proefdieren.

Imidacloprid and acetamiprid detected at concentration levels up to 3.6 ppm in chestnut, shallot, ginger and tea

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.

RIVM: 'Gehaltes imidacloprid in oppervlaktewater leveren geen gevaar op voor de mens'

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.

Imidacloprid is bij de mens een zwakke agonist met een hoge affiniteit voor neuronale nicotinerge acetylcholine receptoren

Neonicotinoïde insecticiden gaan een binding aan met nicotinerge acetylcholine receptoren (nAChRs) die vrijwel onomkeerbaar is omdat deze stoffen door het enzym acetylcholinesterase niet kunnen worden afgebroken. In het centrale zenuwstelsel van insecten zijn neonicotinoiden sterke agonisten (= signaalstof die de receptor activeert en daarmee een reactie of activiteit in gang zet) met een hoge affiniteit voor nAChRs. Uit een recente studie blijkt dat de neonicotinoide insecticiden imidacloprid en clothianidin zwakke agonisten van neuronale nAChRs bij de mens zijn (zie bijlage). Imidacloprid bleek echter wel een hoge affiniteit voor humane nAChRs te hebben, net zoals dat voor insecten het geval is. Nicotinerge acetylcholine receptoren zijn betrokken bij cognitieve functies zoals concentratie en geheugen en spelen ook een rol in specifieke aandoeningen, zoals epilepsie, schizofrenie, en de ziekte van Alzheimer.

Activation and modulation of human alpha4β2 nicotinic acetylcholine receptors by the neonicotinoids clothianidin and imidacloprid

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.

Insektizide: Niedriger IQ nach pränataler Exposition

Chapel Hill/New York City/Berkeley - Insektizide aus der Gruppe der Organophosphate können möglicherweise die Entwicklung des Gehirns beeinträchtigen. In Environmental Health Perspectives (EHP) bringen gleich mehrere Gruppen die pränatale Exposition mit einer verminderten Intelligenz von Kindern im Grundschulalter in Verbindung.
Organophosphate töten Insekten durch die Hemmung des Enzyms Acetylcholinesterase. Sie unterbrechen die Signalübertragung zwischen Nervenzellen beziehungsweise zwischen Nerven- und Muskelzellen. Es handelt sich folglich um Nervengifte, die auch für den Menschen nicht unbedenklich sind.

'They’ve turned the Environment into the Experiment – and WE are all the experimental SUBJECTS'

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

Fatal Imidacloprid Poisoning in Humans

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.