Bees: Sulfoxaflor: Nicotine

 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).

Nicotine

Toxicology See also: Nicotine poisoning NFPA 704 1 4 0 The LD50 of nicotine is 50 mg/kg for rats and 3 mg/kg for mice. 30–60 mg (0.5–1.0 mg/kg) can be a lethal dosage for adult humans.[5][62] However the widely used human LD50 estimate of 0.5–1.0 mg/kg was questioned in a 2013 review, in light of several documented cases of humans surviving much higher doses; the 2013 review suggests that the lower limit causing fatal out-comes is 500–1000 mg of ingested nicotine, corresponding to an oral lD50 of 6.5–13 mg/kg .[7] Nevertheless nicotine has a relatively high toxicity in comparison to many other alkaloids such as cocaine, which has an LD50of 95.1 mg/kg when administered to mice. It is unlikely that a person would overdose on nicotine through smoking alone, although overdose can occur through combined use of nicotine patches or nicotine gum and cigarettes at the same time.[6][unreliable source?] Spilling a high concentration of nicotine onto the skin can cause intoxication or even death, since nicotine readily passes into the bloodstream following dermal contact.[63] 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 System Effect of nicotine on dopaminergic neurons. By 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 system Nicotine 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 medulla Chemical Identification Nicotine 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 Insecticide Tobacco 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

Bees vs. Bayer

Bayer is suing Europe to overturn the landmark ban on bee-killing pesticides -- and we're excited to announce we're joining the legal battle to make sure Bayer fails.

 

Europe's bee-saving ban has only just gone into force, but Bayer is fighting in the courts to overturn it. If Bayer wins, it will be a huge setback for the bees -- and so we're asking the European Court of Justice to let us join in the case and defend the ban.

The first hearings could happen in just a few weeks, and we've only got a few days to finalize our case. If the court accepts our application, we'll represent the interests of hundreds of thousands of SumOfUs members who have already spoken up -- and make sure the court has real evidence to counter Bayer's propaganda. 

It's crucial we make our voices heard in the court and on the streets. We’ve already made a downpayment to hire European legal specialists to help us fight the case, but we know Bayer and Syngenta are going to throw everything they’ve got at defeating the bee-saving ban. That's why we need to stand ready to fight Bayer every step of the way -- no matter how long it takes.

We've already asked for a lot, so understand if you can't give now. But if you can, can you help us fight Bayer and Syngenta inside and outside the European Court by making a $1 donation to our ‘Save the Bees’ fund?

The upcoming court case is more than just a European battle -- this will be seen as a test case around the world. That’s why hiring a crack team of EU hotshot lawyers is so  important. Winning at the European court could mean helping to save our bees around the world. But if Bayer and Syngenta manage to overturn the EU’s ban, then there’s a good chance that we might fail to get neonics banned elsewhere.

And we're not stopping with the EU court battle. Just last week, we worked together with partners leading the fight in the US to sign on to a major advertisment in the New York Times calling on the US to act, we've taken out ads in commercial garden magazines, and taken the fight to the world's largest commercial gardening convention -- putting more and more pressure on Bayer to stop killing the bees. And we've got much, much more planned.

Right around the world, bees are dying off and the situation seems to be getting worse. In China, people are having to resort to hand pollinating. In the USA, hive after hive is collapsing. In Europe too, bees are dying off with whole hives dying in places like the UK, Poland, Switzerland and Spain. Our fight to save the bees is global but the first battle will be in Europe at the European Court. 

It will be the people vs multinational corporations, the little guy versus the big guy, David vs Goliath. Bayer and Syngenta will dig deep and spend whatever is necessary to win. That’s why it’s so important we can build up a fighting fund so we can take on these corporate big boys -- and win.

Bayer and Syngenta are hiring the very best lawyers that money can buy. Can you help us fight back against them around the world by making a donation of just $1 today?

Court documents show how Bayer and Syngenta are going to try and get the ban scrapped. They will argue that there isn’t enough science to support a temporary ban. They are also going to argue that the European Commission doesn’t have the power to ban neonics. But we know on both of these counts they are wrong, but if we don’t stand up in court and say so, then there’s a real risk the court will only get one side of the argument. We can’t let that happen.

So we need to stand ready in case the court costs start to mount. Bayer and Syngenta have very deep pockets and will see the European ban on neonics as a huge threat to their profits and so will throw everything they’ve got at the upcoming court case. We need to make sure we’ve got enough firepower to fight back. 

We know the fight to protect our bees from neonics is going to be more of a marathon than a sprint. Already, together we’ve achieved a lot. We came together to fight to stop Bayer pushing their disingenuous ‘we love the bees’ marketing campaign at a Chicago garden center show. Hundred of thousands of us have signed petition demanding big retailers remove neonics from their shelves. And most impressive of all together we chipped in to be able to participate in the European test case. While we can never match their near unlimited resources, being sure of our financial firepower will help us take the fight back to Bayer and Syngenta.

Can you help us with $1 to keep on fighting to save the world’s bees?

Thanks for all you do,
Martin, Paul, Johnny and the rest of us.

The Importance of Bees

This is a Bee.... A Bee w/ a Very Important Job......

This Bee and all the other Bees keep us Alive... Oh yes they do!  Bees are responsible for pollinating not just flowers, but the fruits, vegetables, & herbs we eat as well.  If not for the Bees & the job of Pollination, we'd have nothing to eat except for GMO food-like-products.

So here's the problem:
Earthjustice
GENUINE CRISIS: Have you heard of colony collapse disorder (CCD)? Honeybees have been suffering from CCD as a result of the widespread use of neonicotinoid pesticides. This type of pesticide is used on 140 different crops, and very harmful to our primary pollinators. LISTEN TO THE PODCAST to learn how Earthjustice is using the power of the law to stop the EPA from approving more bee-killing pesticides. 

In this interview, Earthjustice attorney Greg Loarie discusses his efforts to get the toxic pesticide, sulfoxaflor, off of the market due to the threat it poses to honeybees.

https://soundcloud.com/earthjustice-down2earth/feeling-the-sting-toxic-pesticide-threatens-honeybees

Pesticide News Story: The EPA’s Final Decision on the New Active Ingredient: Sulfoxaflor

For Release: May 6, 2013

The EPA has granted unconditional registrations for the new active ingredient sulfoxaflor, formulated as a manufacturing use product and two end-use products for use in production agriculture. The EPA is granting the use of sulfoxaflor on barley, bulb vegetables, canola, citrus, cotton, cucurbit vegetables, fruiting vegetables, leafy vegetables, low-growing berries, okra, ornamentals (herbaceous and woody), pistachio, pome fruits, root and tuber vegetables, small vine climbing fruit (except fuzzy kiwifruit), soybean, stone fruit, succulent, edible podded and dry beans, tree nuts, triticale, turfgrass, watercress and wheat.

Occupational worker and food safety data confirm these uses are safe when sulfoxaflor is used in accordance with the labeling terms and restrictions. Also, the ecological effects profile for sulfoxaflor supports the registration finding. One area of focus in the review involved pollinator health, and the final label includes robust terms for protecting pollinators. The EPA performed its data evaluation and assessments in collaboration with its counterpart agencies in Canada and Australia. Scientists from the three authorities reviewed over 400 studies and peer reviewed each other’s work.


The registration will provide growers with a new pest management tool for use on piercing/sucking insects. Sulfoxaflor has been used under an emergency clearance on cotton in Arkansas, Mississippi, Tennessee and Louisiana to control the tarnished plant bug, an insect that has developed resistance to alternative registered pesticides. Sulfoxaflor belongs to its own new insecticide subclass in terms of its mode of action, so it is expected to be used by producers faced with pests that have developed resistance to other alternatives.

For additional information please refer to the docket EPA-HQ-OPP-2010-0889 at the Federal e-Rulemaking Portal: http://www.regulations.gov.

Sulfoxaflor 
http://en.wikipedia.org/wiki/Sulfoxaflor

From Wikipedia, the free encyclopedia

Jump to: navigation, search

Sulfoxaflor
IUPAC name[hide] [Methyl(oxo){1-[6-(trifluoromethyl)-3-pyridyl]ethyl}-λ6-sulfanylidene]cyanamide
Identifiers
CAS number	946578-00-3
InChI [show]
Properties
Molecular formula	C10H10F3N3OS
Molar mass	277.27 g mol−1
Except where noted otherwise, data are given for materials in their standard state (at 25 °C (77 °F), 100 kPa)
Infobox references

Sulfoxaflor is a systemic insecticide which acts as an insect neurotoxin and is the only member a class of chemicals called the sulfoximines which act on the central nervous system of insects with much lower toxicity to mammals very similarly to neonicotinoids. The chemical works by interfering with the transmission of stimuli in the insect nervous system. Specifically, it causes a blockage in the nicotinergic neuronal pathway.^[1] This blockage leads to the accumulation of acetylcholine, an important neurotransmitter, resulting in the insect's paralysis, and eventually death. It is effective on contact and via stomach action. Because sulfoxaflor binds much more strongly to insect neuron receptors than to mammal neuron receptors, this insecticide is selectively more toxic to insects than mammals.^[2]
On May 6, 2013, the United States Environmental Protection Agency approved the first two commercial pesticide products that contain sulfoxaflor, marketed under the brand names "Transform" and "Closer", to the Dow Chemical Corporation. This pesticide has been registered to South Korea, Panama, Vietnam, Indonesia, and Guatemala and additional global registrations are expected in the near future.

 See also

• Imidacloprid effects on bees
• Insecticide
• Neonicotinoid
• Pesticide toxicity to bees

References

1. Jump up ^ Cutler, P.; Slater, R.; Edmunds, A. J.; Maienfisch, P.; Hall, R. G.; Earley, F. G.; Pitterna, T.; Pal, S.; Paul, V. L.; Goodchild, J.; Blacker, M.; Hagmann, L.; Crossthwaite, A. J. (2013). "Investigating the mode of action of sulfoxaflor: A fourth-generation neonicotinoid". Pest Management Science 69 (5): 607–619. doi:10.1002/ps.3413. PMID 23112103. edit
2. Jump up ^ "sulfoxaflor". ChemSpider. Royal Society of Chemistry. Retrieved 19 August 2013.

External links

• The EPA’s Final Decision on the New Active Ingredient Sulfoxaflor
• [1]
• [Dow AgroSciences Receives U.S. EPA Registration for Sulfoxaflor]

http://www.croplife.com/crop-inputs/insecticides/beekeeping-industry-files-appeal-against-epa-for-full-registration-of-sulfoxaflor/ 

http://www.govexec.com/management/2013/12/new-suspect-bee-deaths-us-government/76004/?oref=dropdown 

Wilshire (Blvd) United Methodist Church

Home from the Hayride reunion.... Much too short of sharing time at the event itself.

So, then, I had to park a block away (and I didn't) understand (as I usually get a spot right in front).... Okay, so I have to walk a block & it's gonna be good exercise.

I'm walking in front the Wilshire United Methodist Church (Wilshire Blvd & Plymouth)..... And I stop to talk w/ a homeless woman. No big deal until, this crazy Bitch comes running out from the church and tells this homeless woman to go away..... No shit, and it gets better......

Then she starts yelling at me (SUCH A VERY WRONG THING TO DO) that I shouldn't talk to the woman, that I "shouldn't Help her" (I FCKING KID YOU NOT)....

So, I get pissed and I ask her: "Are You 'Christian'?". To which she has no answer.... and I ask two more times: "Answer me.... Are you 'christian'?" And she has the Audacity to tell me: "Yes, I Am!"

WRONG FKING Answer!

Because she then she goes on a Rant about this woman that I'm about to give my last 65 cents to.... "You shouldn't be helping her. She's homeless because she chooses to be. They all choose to be. They are lazy and just don't want to work. They only want to work the system...... Blah, blah, blah, blah...."

And then I tell her: "You know what, I'll NEVER Come to Your Church Now!" So I further get right in her face and ask her: "Well you tell me then... What Would Jesus Do?" "Jesus would feed her!" "Jesus would help her!" "Huh, tell me, what would he do?"

And she gets upset & runs away, and I keep on, "You better get prayin' now, because when you meet Jesus, he isn't gonna be happy!"

And this homeless woman is just shocked.... she hasn't said a word..... And so she thanks me.... And I say to her: "This is one of the reasons I'm not no 'christian'!" And she Hugs me!

Sheesh! All that fuking hatred & greedy bull shit from a woman who works for the Wilshire United Methodist Church!

What the Hell was that all about?

But let me tell you, this is going to go much further than this page.......

 So Reverend, who-ever-you-are......   You have just received a Wake-Up Call from someone who just happened to pass in front of your church this afternoon after she had been at a 25 year Memorial Reunion for people w/ hiv.....

What a strong impression one of your congregation members has made on me.......   This incident of outright hatred & UN-Jesus-like-conduct from a proclaimed 'christian' member of your church speaks volumes about your church's teachings.......

May Creator help you all......

And Now For Some GOOD NEWS!

Frances Beinecke’s Blog

Biggest and Smartest Corporations Already Accounting for Carbon Pollution in Business Plans

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Posted December 5, 2013 in Solving Global Warming

Tags:

carbonpollution, carbonstandards, extremeweather, exxonmobil, microsoft, oilindustry

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Twenty-nine corporations, including five major oil companies, are starting to account for coming carbon limits in their business plans, according to a new report by CDP. These companies recognize the era of unlimited pollution will soon end, and it’s time to rein in their share of global warming emissions.
Right now, companies are free to release as much carbon as they want. This fuels climate change and contributes to the deadly storms, costly droughts, and destructive floods like the ones that have swept through our communities.

We all pay a steep price for unchecked climate change—even if our families haven’t lost a home to a storm surge yet or gone out of business after a prolonged drought. It touches us no matter where we live. The government spent nearly $100 billion to respond to extreme weather events in 2012. That’s more than $1,100 per average US taxpayer.

We can help protect our communities by limiting how much carbon pollution companies release. America has already set limits for arsenic, lead, and mercury, and other pollutants that endanger our health and well-being. Now we must do the same for carbon.



According to the new CDP report, more and more companies know that time has come, and many have already demonstrated what’s possible by reducing their own carbon pollution. Microsoft, for instance, has committed to becoming carbon neutral across all its data centers, labs, offices, and travel. Even fossil fuel giants like ExxonMobil, ConocoPhillips, Chevron, BP, and Shell told CDP researchers they are planning for a carbon-constrained world, because the nation will soon take firm climate action.

President Obama has already begun. In June he released a robust Climate Action Plan and directed the Environmental Protection Agency to establish carbon limits for new and existing power plants. His plan will also target other potent global warming pollutants, including methane from oil and gas production and HFCs. And last year, the president raised fuel economy standards to 54.5 miles per gallon, which will cut carbon pollution from new cars in half and save consumers $1.7 trillion at the pump by 2025.
The clean car standards have unleashed a wave of innovation in the auto sector, contributed to Detroit’s recovery, and helped spur the boom in car sales. The power plants standards will likewise inspire advances in clean energy technologies. They will also level the playing field and allow all sources of energy to compete for low-carbon markets.

The CDP report confirms that many of our smartest and biggest companies are already planning for the low-carbon future. We can usher that future in today by setting strong limits on carbon.  We can hold polluters accountable and leave our children with cleaner air and a more stable climate.














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