Sulfoxaflor is a systemic insecticide which acts as an insect neurotoxin.
It is a derivative of Nicotine, which is highly poisonous:
"Nicotine
From Wikipedia, the free encyclopedia
This article is about the chemical. For other uses, see Nicotine (disambiguation).
Toxicology
See also: Nicotine poisoning
Historically, nicotine has not been regarded as a carcinogen and the IARC has not evaluated nicotine in its standalone form or assigned it to an official carcinogen group. While no epidemiological evidence supports that nicotine alone acts as a carcinogen in the formation of human cancer, research over the last decade has identified nicotine's carcinogenic potential in animal models and cell culture.[64][65] Nicotine has been noted to directly cause cancer through a number of different mechanisms such as the activation of MAP Kinases.[66] Indirectly, nicotine increases cholinergic signalling (and adrenergic signalling in the case of colon cancer[67]), thereby impeding apoptosis (programmed cell death), promoting tumor growth, and activating growth factors and cellular mitogenic factors such as 5-LOX, and EGF. Nicotine also promotes cancer growth by stimulating angiogenesis and neovascularization.[68][69] In one study, nicotine administered to mice with tumors caused increases in tumor size (twofold increase), metastasis (nine-fold increase), and tumor recurrence (threefold increase).[70] N-Nitrosonornicotine (NNN), classified by the IARC as a Group 1 carcinogen, is produced endogenously from nitrite in saliva and nicotine. The teratogenic properties of nicotine has been investigated. According to a study of ca. 77,000 pregnant women in Denmark,[citation needed] women who used nicotine gum and patches during the early stages of pregnancy were found to face an increased risk of having babies with birth defects. The study showed that women who used nicotine-replacement therapy in the first 12 weeks of pregnancy had a 60% greater risk of having babies with birth defects compared to women who were non-smokers.[citation needed] Tobacco use among pregnant women has also been correlated to increased frequency of ADHD. Children born to mothers who used tobacco were two and a half times more likely to be diagnosed with ADHD.[71] Froelich estimated that "exposure to higher levels of lead and prenatal tobacco each accounted for 500,000 additional cases of ADHD in U.S. children".[72] Effective April 1, 1990, the Office of Environmental Health Hazard Assessment (OEHHA) of the California Environmental Protection Agency added nicotine to the list of chemicals known to cause developmental toxicity.[73] In the Central Nervous SystemBy binding to nicotinic acetylcholine receptors, nicotine increases the levels of several neurotransmitters – acting as a sort of "volume control". It is thought that increased levels of dopamine in the reward circuits of the brain one of the major contributors of the apparent euphoria and relaxation, and addiction caused by nicotine consumption. This release of Dopamine induced by Nicotine is thought to occur via a cholinergic–dopaminergic link, mediated by a neuropeptide, ghrelin, in the ventral tegmentum.[88] Nicotine has a higher affinity for acetylcholine receptors in the brain than those in skeletal muscle, though at toxic doses it can induce contractions and respiratory paralysis.[89] Nicotine's selectivity is thought to be due to a particular amino acid difference on these receptor subtypes.[90]Tobacco smoke contains anabasine, anatabine, and nornicotine. It also contains the monoamine oxidase inhibitors harman and norharman.[91] These beta-carboline compounds significantly decrease MAO activity in smokers.[91][92] MAO enzymes break down monoaminergic neurotransmitters such as dopamine, norepinephrine, and serotonin. It is thought that the powerful interaction between the MAOIs and the nicotine is responsible for most of the addictive properties of tobacco smoking.[93] The addition of five minor tobacco alkaloids increases nicotine-induced hyperactivity, sensitization and intravenous self-administration in rats.[94] Chronic nicotine exposure via tobacco smoking up-regulates alpha4beta2* nAChR in cerebellum and brainstem regions[95][96] but not habenulopeduncular structures.[97] Alpha4beta2 and alpha6beta2 receptors, present in the ventral tegmental area, play a crucial role in mediating the reinforcement effects of nicotine.[98] In the sympathetic nervous systemNicotine also activates the sympathetic nervous system,[99] acting via splanchnic nerves to the adrenal medulla, stimulates the release of epinephrine. Acetylcholine released by preganglionic sympathetic fibers of these nerves acts on nicotinic acetylcholine receptors, causing the release of epinephrine (and noradrenaline) into the bloodstream. Nicotine also has an affinity for melanin-containing tissues due to its precursor function in melanin synthesis or due to the irreversible binding of melanin and nicotine. This has been suggested to underlie the increased nicotine dependence and lower smoking cessation rates in darker pigmented individuals. However, further research is warranted before a definite conclusive link can be inferred.[100]In adrenal medullaChemical IdentificationNicotine was first isolated from the tobacco plant in 1828 by physician Wilhelm Heinrich Posselt and chemist Karl Ludwig Reimann of Germany, who considered it a poison.[103][104] Its chemical empirical formula was described by Melsens in 1843,[105] its structure was discovered by Adolf Pinner and Richard Wolffenstein in 1893,[106][107][108][clarification needed] and it was first synthesized by Amé Pictet and A. Rotschy in 1904.[109]As an InsecticideTobacco was introduced to Europe in 1559, and by the late 17th century, it was used not only for smoking but also as an insecticide. After World War II, over 2,500 tons of nicotine insecticide (waste from the tobacco industry) were used worldwide, but by the 1980s the use of nicotine insecticide had declined below 200 tons. This was due to the availability of other insecticides that are cheaper and less harmful to mammals.[4]Currently, nicotine, even in the form of tobacco dust, is prohibited as a pesticide for organic farming.[110][111] In 2008, the EPA received a request, from the registrant, to cancel the registration of the last nicotine pesticide registered in the United States.[112] This request was granted, and after 1 January 2014, this pesticide will not be available for sale." Read the Eentire article at: http://en.wikipedia.org/wiki/Nicotine | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||


This week marked a grim anniversary: It's been a year since BP's oil rig exploded in the Gulf of Mexico, eventually leaking more than 200 million gallons of oil and unleashing the worst environmental disaster in U.S. history. Thousands of birds, sea turtles and dolphins died -- and some are still washing up. Yet there have been no meaningful reforms to guarantee a similar spill will never happen again.
A year after the ocean was polluted with more than 2 million gallons of toxic oil dispersants to break up oil from BP's devastating Deepwater Horizon spill, the Center for Biological Diversity on Monday filed a notice of intent to sue the Environmental Protection Agency for authorizing the use of dispersants without analyzing their effects on endangered species and habitat. In fact, the dispersant most used by BP to combat the catastrophic Gulf spill is actually banned in England and much of Europe, but was used liberally in our waters without environmental analysis.
As we've been telling you over the past couple months, the Center for Biological Diversity is in an all-out fight against oil companies' attack on our hard-won legal victory to protect 120 million acres of "critical habitat" for the polar bear. Thanks to the generous support of more than 2,200 members, we were able to raise the funds to take the next critical step and keep the momentum going to protect these majestic animals and their habitat.
To help save one of the most magnificent sea turtles on Earth, the Center for Biological Diversity and allies this week sued the feds for failing to protect "critical habitat" for the Pacific leatherback. In response to a legal petition by the Center and partners, last year the National Marine Fisheries Service proposed to protect about 70,000 square miles (45 million acres) of ocean off California, Oregon and Washington for the sea turtle -- but missed its deadline to finalize the proposal. Meanwhile, leatherbacks continue to die on their epic 12,000-mile journey from Indonesia to the West Coast -- tangled in commercial fishing gear, poisoned by pollution, killed by poaching and facing many other threats.
Florida is on the verge of losing its last large, wild feline and the Southeast's only remaining large, wild cat: the stealthy, majestic Florida panther. To make sure this powerful hunter gets the roaming room it needs to survive, the Center for Biological Diversity this Wednesday appealed a court decision denying federal protections for the species' habitat. The cat's habitat has been under assault for decades, shrinking rapidly in the face of growing human population and sprawling development in South Florida.
In defense of one of North America's most iconic animals, last Wednesday the Center for Biological Diversity and Western Watersheds Project filed a notice of intent to sue the feds for not protecting the imperiled plains bison. This species once roamed a wide swath of the continent by the millions, but slaughter, disease, habitat loss and other threats have reduced it to a fraction of what it once was. Today just a few conservation herds remain. Despite that, the U.S. Fish and Wildlife Service, in deciding whether the plains bison needs federal protection, is only considering the species' current range -- and not the fact that it's gone from most of its historic range. That's not good enough and won't give this shaggy beast the help it desperately needs to survive and recover.
The Miami blue butterfly has waited 27 years for Endangered Species Act protection. That's far too long. So last week the Center for Biological Diversity filed a notice of intent to sue to help this fast-declining insect. Though the species is on the brink of extinction due to urban sprawl, fire suppression, pesticides, severe weather and other threats, the U.S. Fish and Wildlife Service denied it a place on the endangered species list when the Center petitioned for emergency protection after it disappeared from Florida's Bahia State Park in January. Instead of protection, the feds granted the bright blue, inch-long butterfly a place on the "candidate list," which now includes 260 imperiled species whose protections have been put off indefinitely.
There was more troubling news this week about hydraulic fracturing, or "fracking," which is a process where chemicals, water and sand are blasted into the earth to pry natural gas and oil from rock. On Tuesday night, a natural-gas well blew out in Bradford County, Penn., leaking thousands and thousands of gallons of fracking fluid through fields and farms and into a stream.
Would you laze in the shade of a black elm tree? Eat black lettuce in your salad or play soccer on black grass? New astrobiological research suggests that on a different world, green plants might not exist at all. They might even be black.
































