Negative impact on brain and nervous system.
Metabolic Interference or Disruption
Interferes with human metabolism. This can be a very serious thing. Some of these interference mechanics are well established. However, often long term effects and health consequences remain largely unknown. Additionally an emerging area of concern and one that is not currently studied, is the combined synergistic effects these metabolically disrupting chemicals have on human health.
Metabolic interference happens when the substance produces highly reactive and often damaging intermediates during detoxification or when the substance binds to specific enzymes, important structural groups on molecules, receptors and membranes or targets DNA or mimics key nutrients.
Exposure Produces Health Symptoms
Symptoms maybe short term or long term depending on the exposure duration and intensity and effects areas like Cardiovascular, Gastrointestinal, Cognition, Fatigue. A substance with this attribute may cause an allergic skin reaction, serious eye irritation, allergy or asthma symptoms or breathing difficulties if inhaled.
Toxic to Bees
Bees pollinate plants. No pollination no plants. No plants no food. We go hungry or starve.
These attributes are ONLY based on peer-reviewed evidence. See link to Data Sources below. Everyone benefits from knowing this stuff. Please Share.
- CATEGORIES: Pesticide | Household Toxin | Food Toxin | Synthetic Toxin | PESTICIDE active ingredient | organic | insecticide | Pesticide or Plant Growth Regulator Approved in Australia | Pesticide approved in USA (California) | Pesticide approved or pending approval in EU | Highly Toxic and Dangerous to bees. Currently used in USA | Australia as a pesticide | NEONICOTINOID Pesticide
- SUBSTANCE LINEAGE: Organic Compounds | Organonitrogen Compounds | Amines | Aralkylamines | Pyridines and Derivatives
- SYNONYMS: (e)-Imidacloprid | (z)-Imidacloprid | 1-((6-Chloro-3-pyridyl)methyl)-N-nitro-2-imidazolidinimine | 1-(2-Chloro-5-pyridylmethyl)-2-(nitroimino)imidazolidine | 1-[(6-Chloro-3-pyridinyl)methyl]-4,5-dihydro-N-nitro-1H-imidazol-2-amine | Admire | Advantage | Confidor | Confidor 200 SL | Confidor SL | Gaucho | Imazethapyr | Imidacloprid (old RN) | Merit | Premise 75 | Provado
- DESCRIPTION: Imidacloprid is a neonicotinoid insecticide, which is a class of neuro-active insecticides modeled after nicotine. Nicotine was identified and used as an insecticide and rat poison as early as the 1600’s. Its effectiveness as an insecticide spurred a search for insecticidal compounds that have selectively less effect on mammals, which led to the discovery of neonicotinoids. Neonicotinoids, like nicotine, bind to nicotinic acetylcholine receptors of a cell. In mammals, nicotinic acetylcholine receptors are located in cells of both the central and peripheral nervous systems. In insects these receptors are limited to the CNS. While low to moderate activation of these receptors causes nervous stimulation, high levels overstimulate and block the receptors causing paralysis and death. Nicotinic acetylcholine receptors are activated by the neurotransmitter acetylcholine. Acetylcholine is broken down by acetylcholinesterase to terminate signals from these receptors. However, acetylcholinesterase cannot break down neonicotinoids and the binding is irreversible. Because most neonicotinoids bind much more strongly to insect neuron receptors than to mammal neuron receptors, these insecticides are selectively more toxic to insects than mammals. The low mammalian toxicity of neonicotinoids can be explained in large part by their lack of a charged nitrogen atom at physiological pH. The uncharged molecule can penetrate the insect blood–brain barrier, while the mammalian blood–brain barrier filters it. However, Some neonicotinoid breakdown products are toxic to humans, especially if they have become charged. Because of their low toxicity and other favorable features, neonicotinoids are among the most widely used insecticides in the world. Most neonicotinoids are water-soluble and break down slowly in the environment, so they can be taken up by the plant and provide protection from insects as the plant grows. Neonicotinoids are currently used on corn, canola, cotton, sorghum, sugar beets and soybeans. They are also used on the vast majority of fruit and vegetable crops, including apples, cherries, peaches, oranges, berries, leafy greens, tomatoes, and potatoes. The use of neonicotinoids has been linked in a range of studies to adverse ecological effects, including honey-bee colony collapse disorder (CCD) and loss of birds due to a reduction in insect populations. This has led to moratoriums and bans on their use in Europe.
- COMMENTS: Residues of this pesticide are tested for on Australian Foods | Pesticide approved in Australia Dangerous to bees. DO NOT spray any plants in flower where bees are foraging. In January 2013, the European Food Safety Authority determined that the neonicotinoids imidacloprid, clothianidin, and thiamethoxam pose unacceptable risks to bees, prompting an EU-wide ban. A 2013 study published in the Journal of Experimental Biology revealed that honey bees exposed to imidacloprid were less likely to form long-term memory required for remembering food locations. Imidacloprid is one of the most widely used insecticide in the world> annual turnover of sales in 2009 was over 1 billion Us dollars.
- FORMULA: C9H10ClN5O2
- DATA SOURCES: DATA SOURCES: T3DB | PubChem | Consolidated Pesticide Information Dataset (CPI) from the USA EPA | Compendium of Pesticide Common Names | APVMA | DPR | EU Pesticides | Rural Industries Research and Development Corporation; Honeybee pesticide poisoning: a risk management tool for Australian farmers and beekeepers 2012 | Beekeeping -Department of Entomology - PROTECTING HONEY BEES FROM PESTICIDES, Christian H. Krupke et al.; www.extension.purdue.edu
- LAST UPDATE: 28/04/2018
Mostly focused on Health Implications of Long Term Exposure to this substance
- SYMPTOMS: Fatigue, twitching, cramps, and weakness leading to asphyxia (L1130).
- POSSIBLE HEALTH CONSEQUENCES: Hypotension, fatal ventricular dysrhythmias, tremors, impaired pupillary function, and hypothermia may result from Imidacloprid poisoning (T36). | Two main routes of metabolism responsible for the degradation of imidacloprid were identified. The first is oxidative cleavage, yielding 6-chloronicotinic acid, which is conjugated with glycine to form a hippuric acid-type conjugate. These two metabolites together represented most of the identified metabolites, or about 30% of the recovered radiolabel. Of minor importance in terms of quantity is dechlorination of the pyridinyl moiety, producing the 6-hydroxy nicotinic acid and its methylmercapturic acid derivative, probably as a degradation product of a glutathione conjugate. The 6-methylmercapto nicotinic acid conjugated with glycine, and the glycine conjugate constituted 5.6% of the recovered radiolabel. The second important biodegradation step starts with hydroxylation of the imidazolidine ring at the 4 or 5 position, and about 16% of the recovered radiolabel was identified as the sum of 4- and 5-hydroxy imidacloprid. The loss of water yields the olefinic compound. These biotransformation products and the unchanged parent compound were excreted in urine and feces, while the guanidine compound was a less important metabolite and was eliminated only in feces (A623).
- ACTION OF TOXIN: Imidacloprid acts on the nicotinic acetylcholine receptor; the chlorination inhibits degradation by acetylcholine-esterase (L1130). | Imidacloprid binds specifically to nicotinic acetylcholine receptors in various nervous systems and acts as a partial agonist. (T10)
- TOXIN SITES OF ACTION IN CELL: "Cytoplasm", "Extracellular"
- Additional Exposure Routes: The most widely used applications for Imidacloprid in California are pest control in structures, turf pest control, grape growing, and head and leaf lettuce growing. Other widespread crop uses are rice, grains/cereals (L1130).
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