Insecticiden

Are Bee Diseases Linked to Pesticides? — A Brief Review of Immune Suppression by Neonicotinoid Insecticides

Outbreaks of infectious diseases in honey bees, fish, amphibians, bats and birds in the past two decades have coincided with the increasing use of systemic insecticides, notably the neonicotinoids and fipronil. A link between insecticides and such diseases is hypothesised. Firstly, the disease outbreaks started in countries and regions where systemic insecticides were used for the first time, and later they spread to other countries. Secondly, recent evidence of immune suppression in bees and fish caused by neonicotinoids has provided an important clue to understand the sub-lethal impact of these insecticides not only on these organisms, but probably on other wildlife affected by emerging infectious diseases. The negative impacts of pesticides, in particular insecticides, on bees and other pollinators have never been disputed. Insecticides can directly kill these vital insects, whereas herbicides reduce the diversity of their food resources, thus indirectly affecting their survival and reproduction. At sub-lethal level (bLD50), neurotoxic insecticide molecules are known to influence the cognitive abilities of bees, impairing their performance and ultimately impacting on the viability of the colonies. In addition, widespread systemic insecticides appear to have introduced indirect side effects on both honey bees and wild bumblebees, by deeply affecting their health. Immune suppression of the natural defences by neonicotinoid and phenyl-pyrazole (fipronil) insecticides opens the way to parasite infections and viral diseases, fostering their spread among individuals and among bee colonies at higher rates than under conditions of no exposure to such insecticides. This causal link between diseases and/or parasites in bees and neonicotinoids and other pesticides has eluded researchers for years because both factors are concurrent: while the former are the immediate cause of colony collapses and bee declines, the latter are a key factor contributing to the increasing negative impact of parasitic infections observed in bees in recent decades.

Rückgang der Fledermausarten in NRW

In der Roten Liste der gefährdeten Pflanzen, Pilze und Tiere in Nordrhein-Westfalen (2011) werden für Nordrhein-Westfalen 21 Fledermausarten genannt. Die meisten der genannten Arten sind vom Aussterben bedroht oder stark gefährdet. Eine Fledermausart gilt in NRW bereits als ausgestorben. Lediglich zwei Fledermausarten in NRW werden als ungefährdet eingestuft. Ursache für den Rückgang der Fledermauspopulationen ist insbesondere die Verringerung des Nahrungsangebotes infolge einer intensiver Landnutzung und des Einsatzes von Pflanzenschutzmitteln. Fledermäuse sind besonders im Umkreis von Wochenstuben auf das Vorhandensein geeigneter Jagdgebiete angewiesen. Dort müssen sie Insekten in ausreichender Menge und Qualität erbeuten können. Durch der fortschreitenden Intensivierung der Landnutzung reduziert sich das Nahrungsangebot für Insekten und in der Folge das Nahrungsangebot für die Fledermäuse. Regionale Messungen haben ergeben, dass innerhalb der vergangenen 20 Jahre bis zu 80 Prozent der Biomasse aller Fluginsekten in Nordrhein-Westfalen verschwunden sind.

Beter even nadenken alvorens de kinderen te laten spelen op een vloer waar mierenpoeder gestrooid is

Pesticiden worden doorgaans in verband gebracht met hun gebruik in de landbouw, waar ze ingezet worden voor de bestrijding van allerlei ziekten en plagen om hogere opbrengsten en een hogere voedselkwaliteit te bekomen. Het ontgaat echter velen dat ze ook buiten de landbouw toegepast worden. Dergelijk gebruik van bestrijdingsmiddelen ter verdelging van allerlei schadelijke, vervelende en ongewenste insecten en andere geleedpotigen (spinnen) vindt frequent plaats in onze huishoudelijke omgeving en op het werk. In 2013 kochten Belgen ongeveer 800 ton producten om insecten te bestrijden, zoals spuitbussen, verdampers, strips, cassettes, lokazen en vlooienbanden. Het gaat dan vooral om producten tegen insecten (muggen, vliegen, mieren, enz.), mijten (tapijtmijt, enz.) en andere geleedpotigen (spinnen, enz.). Deze producten bevatten in totaal 75 ton aan werkzame stoffen om binnenshuis insecten te bestrijden, hetgeen een aanzienlijke hoeveelheid is. De particuliere gebruiker is doorgaans niet volledig op de hoogte van de risico’s van deze producten en is, in tegenstelling tot de professionele gebruiker, weinig of niet beschermd tijdens de toepassing. De mate van blootstelling is daarenboven moeilijk in te schatten en afhankelijk van diverse factoren, zoals de frequentie van gebruik, het gebruik van beschermende kledij, de dosering en het type van formulering (aerosol, verdamper,…). In opdracht van de Hoge Gezondheidsraad werd dat onderzocht door professor Pieter Spanoghe (UGent) en andere experten. De blootstelling op deze manier ligt vele malen hoger dan de opname van residuen van gewasbeschermingsmiddelen die kunnen achterblijven op groenten en fruit. Door insecticidensprays of luizenshampoos in huis te gebruiken, krijg je 100 tot 1.000 keer meer van een chemisch bestrijdingsmiddel in je lichaam.

Metabolomics to Explore Imidacloprid-Induced Toxicity in the Central Nervous System of the Freshwater Snail Lymnaea stagnalis

Metabolomics was applied to investigate imidacloprid induced sublethal toxicity in the central nervous system of the freshwater snail Lymnaea stagnalis. The snails (n = 10 snails) were exposed for 10 days to increasing imidacloprid concentrations (0.1, 1, 10, and 100 μg/L). The comparison between control and exposure groups highlighted the involvement and perturbation of many biological pathways. The levels of several metabolites belonging to different metabolite classes were significantly changed by imidacloprid exposure. A change in the amino acids and nucleotide metabolites like tryptophan, proline, phenylalanine, uridine, and guanosine was found. Many fatty acids were down-regulated, and the levels of the polyamines, spermidine and putrescine, were found to be increased which is an indication of neuron cell injury. A turnover increase between choline and acetylcholine led us to hypothesize an increase in cholinergic gene expression to overcome imidacloprid binding to the nicotinic acetylcholine receptors. Metabolomics revealed imidacloprid induced metabolic changes at low and environmentally relevant concentration in a nontarget species and generated a novel mechanistic hypothesis.

Sublethal Effect of Imidacloprid on Solenopsis invicta (Hymenoptera: Formicidae) Feeding, Digging, and Foraging Behavior

In this study, we exposed red imported fire ants, Solenopsis invicta Buren, to sublethal dosages of dietary imidacloprid and investigated its effect on ant feeding, digging, and foraging behavior. S. invicta consumed significantly more sugar water containing 0.01 microgram/ml imidacloprid than untreated sugar water. Ants fed with 0.01 microgram/ml imidacloprid also showed significantly increased digging activity than ants fed with untreated sugar water. However, imidacloprid at 0.25 microgram/ml significantly suppressed sugar water consumption, digging, and foraging behavior. These results indicate that imidacloprid at sublethal concentrations may have a significant and complicated effect on S. invicta.

Systemic Imidacloprid Affects Intraguild Parasitoids Differently

Toxoneuron nigriceps (Viereck) (Hymenoptera, Braconidae) and Campoletis sonorensis (Cameron) (Hymenoptera, Ichneumonidae) are solitary endoparasitoids of the tobacco budworm, Heliothis virescens (Fabricius) (Lepidoptera, Noctuidae). They provide biological control of H. virescens populations in Southeastern US agricultural production systems. Field and greenhouse experiments conducted from 2011–2014 compared parasitism rates of parasitoids that developed inside H. virescens larvae fed on tobacco plants treated with and without imidacloprid. The parasitoids in our study did not have a similar response. Toxoneuron nigriceps had reduced parasitism rates, but parasitism rates of C. sonorensis were unaffected. Preliminary data indicate that adult female lifespans of T. nigriceps are also reduced. ELISA was used to measure concentrations of neonicotinoids, imidacloprid and imidacloprid metabolites in H. virescens larvae that fed on imidacloprid-treated plants and in the parasitoids that fed on these larvae. Concentrations were detectable in the whole bodies of parasitized H. virescens larvae, T. nigriceps larvae and T. nigriceps adults, but not in C. sonorensis larvae and adults. These findings suggest that there are effects of imidacloprid on multiple trophic levels, and that insecticide use may differentially affect natural enemies with similar feeding niches.

Relationship between Urinary N-Desmethyl-Acetamiprid and Typical Symptoms including Neurological Findings: A Prevalence Case-Control Study

We previously determined a metabolite of acetamiprid, N-desmethyl-acetamiprid in the urine of a patient, who exhibited some typical symptoms including neurological findings. We sought to investigate the association between urinary N-desmethyl-acetamiprid and the symptoms by a prevalence case-control study. Spot urine samples were collected from 35 symptomatic patients of unknown origin and 50 non-symptomatic volunteers (non-symptomatic group, NSG, 4–87 year-old). Patients with recent memory loss, finger tremor, and more than five of six symptoms (headache, general fatigue, palpitation/chest pain, abdominal pain, muscle pain/weakness/spasm, and cough) were in the typical symptomatic group (TSG, n = 19, 5–69 year-old); the rest were in the atypical symptomatic group (ASG, n = 16, 5–78 year-old). N-desmethyl-acetamiprid and six neonicotinoids in the urine were quantified by liquid chromatography-tandem mass spectrometry. The detection of N-desmethyl-acetamiprid was the most frequent and highest in TSG (47.4%, 6.0 ppb (frequency, maximum)), followed by in ASG (12.5%, 4.4 ppb) and in NSG (6.0%, 2.2 ppb), however acetamiprid was not detected. Thiamethoxam was detected in TSG (31.6%, 1.4 ppb), in ASG (6.3%, 1.9 ppb), but not in NSG. Nitenpyram was detected in TSG (10.5%, 1.2 ppb), in ASG (6.3%, not quantified) and in NSG (2.0%, not quantified). Clothianidin was only detected in ASG (6.3%, not quantified), and in NSG (2.0%, 1.6 ppb). Thiacloprid was detected in ASG (6.3%, 0.1 ppb). The cases in TSG with detection of N-desmethyl-acetamiprid and thiamethoxam were aged 5 to 62 years and 13 to 62 years, respectively. Detection of N-desmethyl-acetamiprid was associated with increased prevalence of the symptoms (odds ratio: 14, 95% confidence interval: 3.5–57). Urinary N-desmethyl-acetamiprid can be used as a biomarker for environmental exposure to acetamiprid. Further multi-centered clinical research in larger patients groups with more metabolites analysis is needed

The number of insecticide spray applications on oilseed rape/canola continued to increase after introduction neonicotinoid insecticide seed treatments in 2000

Although pesticide treatment for oilseed rape (OSR) will vary from place to place and year to year, depending upon local conditions and needs, this review of pesticide usage on OSR between 1988 and 2014 has identified a long-term upward trend. Overall, the average number of pesticide treatments on OSR has more than doubled since 1994, accompanied by an increase in weight of pesticide active substances, from 2.1 kg/ha in 1994 to 3.3 kg/ha in 2014. The combined number of pesticide active substances has more than doubled during the same period. In respect of insecticides, the weight of insecticide active substances per hectare increased from 32 g/ha in 2002 to 50 g/ha in 2014. The number of insecticide spray rounds, products and active substances has also increased since 2002. Although Budge et al (2015) established that neonicotinoid seed coatings enabled farmers to reduce the number of insecticide sprays on OSR, this is not evident from the survey data after 2000 when neonicotinoid seed treatments were introduced. The weight of insecticide active substance per hectare and the number of insecticide spray applications has continued to increase after the introduction of neonicotinoid insecticide seed treatments in 2000.

Pathology reports on the first cows fed with Bt176 maize (1997–2002)

On an independent modern farm followed by certified veterinarians, dairy cows (mean of 62 per year) were maintained in optimized milk production for 3 years each. From 1997 to 2002, just after the commercial release of the first GMO (genetically modified organism) in Europe, genetically modified (GM) Bt176 maize grown on the farm was progressively introduced in controlled diets. The results are described in the following account, which has an historical value as it is the longest and first on-farm observation of mammals, performed by an experienced farmer and veterinarians, during a period of unusual pathological problems in cows receiving a GMO-rich diet. Thus it was not designed as a scientific experiment. Over the years, and coinciding with regular increases in GMO content of the diet (0–40%), the proportion of healthy cows with high milk yield diminished from 70% (normal rate) to only 40%. At the peak of mortalities in 2002, 10% of the cows died, preceded by a long-lasting paresis syndrome without hypocalcemia or fever, but with kidney biochemical failure and mucosa or epithelial problems. No microbial origin was identified, though intensively investigated. The GM maize, subsequently withdrawn from the market, was at the time the only intended managerial change for the cows. It is proposed that it provoked long-term toxic effects on mammals, which are not observable in most common conditions of intensive farming with high and rapid animal turnover and with no specific labels on GM feed (identifying amount and precise identity of GMO content). More long-term assessments during GMO feeding trials should be performed.

US EPA Codifies New Changes to FIFRA Minimum Risk Pesticide Requirements

On December 28, 2015, the U.S. Environmental Protection Agency (EPA) finalized important changes to the “minimum risk” pesticide exemption under the Federal Insecticide, Fungicide, and Rodenticide Act (FIFRA). See EPA, “Pesticides; Revisions to Minimum Risk Exemption,” 80 Fed. Reg. 80653 (Dec. 28, 2015). EPA’s new rule goes into effect February 26, 2016, with the exception of the deadline for compliance with new labeling requirements for minimum risk products, which is February 26, 2019. EPA’s action follows changes proposed in December 2012 and marks the first set of revisions to EPA’s minimum risk pesticide regulations since the Agency originally promulgated them in 1996. As briefly summarized below, the changes include more detailed EPA listings of the active and inert ingredients that may be used in minimum risk pesticides. Although EPA has not added or subtracted any ingredients from its lists of eligible minimum risk product ingredients, in its survey of personal insect repellent products currently distributed as minimum risk pesticides, it found that nearly half contain ingredients not permitted by its regulations. Based on this analysis, EPA suggests that the more detailed listings included in its newly codified provisions may require manufacturers who currently distribute pesticides under the minimum risk exemption to reformulate their products to achieve compliance.