Humans

An Open Letter to Tom Vilsac, USDA and Lisa Jackson, EPA by Anthony Samsel

Dear Tom Vilsac,
I am writing you as a scientist and as an agribusiness-man who has used both aldicarb and neonicotinoid systemic insecticides commercially and who has suffered losses of honey bees foraging on treated crops. I have had personal experience using systemic insecticides on a commercial scale having been the owner of several agricultural businesses in the Northeast USA.

In the 1990's on two separate occasions I witnessed complete colony collapse of my bees. The first incident losing over a half a million bees that foraged on two acres of potted perennials which were treated with Imidacloprid. The second time I lost several hives to a neighbors 'Grubex' 1 control treated clover lawn. After seeing the total collapse of the hives we stopped using Imidacloprid and all other systemic pesticides. I no longer use any pesticides, or biocides and now practice sustainable organic methods of agriculture.

Prenatal exposures to pesticides may increase the risk of neurological disease later in life

Substantial evidence gathered over the past half century has shown that environmental exposures in early life can alter patterns of childhood development, and influence life-long health and risk of disease and dysfunction. Among the chemical exposures identified as potentially harmful to early development are: cigarette smoking during pregnancy, ionizing radiation, and insecticides. Patterns of illness have changed substantially in the past century among children in the United States and other industrial nations. Today the major illnesses confronting children in the United States include a number of psychosocial and behavioral conditions. Neurodevelopmental disorders, including learning disabilities, dyslexia, mental retardation, attention deficit disorder, and autism – occurrence is more prevalent than previously thought, affecting 5 percent to 10 percent of the 4 million children born in the United States annually. Beyond childhood, incidence rates of chronic neurodegenerative diseases of adult life such as Parkinson’s disease and dementia have increased markedly. These trends raise the possibility that exposures in early life act as triggers of later illness, perhaps by reducing the numbers of cells in essential regions of the brain to below the level needed to maintain function in the face of advancing age. Prenatal and childhood exposures to pesticides have emerged as a significant risk factor explaining impacts on brain structure and health that can increase the risk of neurological disease later in life.

The neonicotinoids may adversely affect human health, especially the developing brain

There have been a few studies of neonicotinoid-induced toxicity in the nervous systems of vertebrates, and these studies were conducted with only a few of the neonicotinoids, such as imidacloprid, thiamethoxam, and clothianidin. Imidacloprid has been reported to act as an agonist or an antagonist of nAChRs at 10 microM in rat pheochromocytoma (PC12) cells and to change the membrane properties of neurons at concentrations greater then or equal to 10 microM in the mouse cochlear nucleus. Exposure to imidacloprid in utero causes decreased sensorimotor performance and increased expression of glial fibrillary acidic protein (GFAP) in the motor cortex and hippocampus of neonatal rats. Furthermore, it has been reported that the neonicotinoids thiamethoxam and clothianidin induce dopamine release in the rat striatum via nAChRs and that thiamethoxam alters behavioral and biochemical processes related to the rat cholinergic systems. Recently, imidacloprid and clothianidin have been reported to agonize human alpha4beta2 nAChR subtypes. This study is the first to show that acetamiprid, imidacloprid, and nicotine exert similar excitatory effects on mammalian nAChRs at concentrations greater than 1 microM. In the developing brain, alpha4beta2 and alpha7 subtypes of the nAChR have been implicated in neuronal proliferation, apoptosis, migration, differentiation, synapse formation, and neural-circuit formation. Accordingly, nicotine and neonicotinoids are likely to affect these important processes when it activates nAChRs. Accumulating evidence suggests that chronic exposure to nicotine causes many adverse effects on the normal development of a child. Perinatal exposure to nicotine is a known risk factor for sudden infant death syndrome, low-birth-weight infants, and attention deficit/hyperactivity disorder. Therefore, the neonicotinoids may adversely affect human health, especially the developing brain.

Nicotine exposure together with genes in the dopaminergic system confer risk for ADHD

Attention deficit hyperactivity disorder (ADHD) is a multifactorial disorder and both genetic and environmental factors have been implicated in its etiology. Yet, the interaction between genes and environment is seldom studied directly. This article considers the plausibility of nicotine exposure during prenatal development as well as postnatal factors in the etiology of ADHD. The few existent studies show inconsistent results, but provide preliminary evidence suggesting that nicotine exposure together with genes in the dopaminergic system confer risk for ADHD.

The Dynamic Effects of Nicotine on the Developing Brain

Nicotinic acetylcholine receptors (nAChRs) regulate critical aspects of brain maturation during the prenatal, early postnatal, and adolescent periods. During these developmental windows, nAChRs are often transiently upregulated or change subunit composition in those neural structures that are undergoing major phases of differentiation and synaptogenesis, and are sensitive to environmental stimuli. Nicotine exposure, most often via tobacco smoke, but increasingly via nicotine replacement therapy, has been shown to have unique effects on the developing human brain. Consistent with a dynamic developmental role for acetylcholine, exogenous nicotine produces effects that are unique to the period of exposure and that impact the developing structures regulated by acetylcholine at that time. Here we present a review of the evidence, available from both the clinical literature and preclinical animal models, which suggests that the diverse effects of nicotine exposure are best evaluated in the context of regional and temporal expression patterns of nAChRs during sensitive maturational periods, and disruption of the normal developmental influences of acetylcholine. We present evidence that nicotine interferes with catecholamine and brainstem autonomic nuclei development during the prenatal period of the rodent (equivalent to first and second trimester of the human), alters the neocortex, hippocampus, and cerebellum during the early postnatal period (third trimester of the human), and influences limbic system and late monoamine maturation during adolescence.

Imidacloprid residues in fruits, vegetables and water samples from Palestine

The aim of this work was to report on imidacloprid residues in some vegetables, fruits, and water samples collected from the West Bank, Palestine, in 1998 and 1999. Imidacloprid residues were detected in more than half of the analyzed samples. The highest and lowest imidacloprid concentrations were found in eggplant (0.46 mg/kg) and green beans (0.08 mg/kg), respectively. An increase of 11–120% in imidacloprid concentration in the 1999 samples was observed when compared with those of 1998. This may suggest imidacloprid accumulation in the soil and/or increased use by local farmers. The imidacloprid residue concentrations in several crops were found to exceed the CODEX maximum residue limit.

Monitoring of Imidacloprid Residues in Brinjal in Pakistan

Brinjal (Solanum melongena L.) is a summer vegetable grown over 8670 hectares area throughout Pakistan with the annual production of 91260 tonnes. Samples were collected from different locations of Noshera Virkan District Gujranwala during 2006. Out of 24 samples collected from wholesale market, 6 samples (25%) were free of imidacloprid pesticide residues. Imidacloprid residues were in the range of 0 to 0.028 mg kg-1 in the collected samples. The average concentration of imidacloprid in samples collected from main bazar was 0.013 mg kg-1.

Human Exposure to Imidacloprid from Dogs Topically Treated with Imidacloprid to Control Fleas

Advantage® contains 9.1% imidacloprid, which controls fleas on dogs for up to 30 days. Advantage® (364 mg imidacloprid/dog) was applied topically to six household dogs. The glove and blood samples were collected at 24 h, 72 h, and then on a weekly basis for 5 weeks post-Advantage® application. The glove samples were collected by petting each dog for 5 minutes while wearing a different glove per dog. The blood samples (5 mL from each dog) were collected into EDTA tubes. The imidacloprid residue was determined in the blood extracts and glove samples using RP-HPLC. The highest levels of imidacloprid residues were detected at the 24-h interval in both glove (254.16 ± 25.49 ppm) and blood (54.06 ± 3.00 ppb) samples. The blood imidacloprid residue was reduced by one third at the 72-h interval (18.73 ± 2.00 ppb) and was not detected after 1 week. Imidacloprid residue in the glove samples decreased approximately one third between each collection interval. The residue of imidacloprid in the glove extract by the fourth week was very low (0.08 ± 0.02 ppm) and not detected by the fifth week. The present findings suggest that following topical application of Advantage®, imidacloprid residue can be detected in the dog's blood for up to 72 h, and transferable residue on the dog's coat can be detected for up to 4 weeks. Repeated chronic exposure to imidacloprid may pose possible health risks to veterinarians, veterinary technologists, dog caretakers, and owners.

Jongeren dommer door landbouwgif

Het zenuwgif imidacloprid, dat veel in de land- en tuinbouw wordt gebuikt, tast de ontwikkeling van de hersenen van nog ongeboren kinderen aan. De intelligentie kan daar onder lijden. Wetenschappers leiden dat af uit recent Japans onderzoek. Het gevaar voor het menselijk zenuwstelsel wordt volgens hen ernstig onderschat. De maximale norm moet duizend keer scherper.