Mensen

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.

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.

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.

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.

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.

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.

The initial residue deposit of imidacloprid on grape berries following treatment of Confidor 200 SL at the recommended and double the recommended dose of 80 and 160 g a.i. ha−1 were 0.74 and 1.26 mg kg−1, respectively. Residues remained in the fruits up to 60 days but at a low level of 0.056 and 0.108 mg kg−1.