We are putting chemicals originally developed as neuro toxins in the second world war on our food and therefore in our food, our rivers, our soil and our oceans. This affects those who apply the chemicals, and those who consume them as well as those who are nearby when the application is happening or afterwards.

The following information is a copy and paste from Medscape, I have highlighted a few sentences

Authors:

Frances M Dyro, MD  Associate Professor of Neurology, New York Medical College; Neuromuscular Section, Department of Neurology, Westchester Medical Center

Organophosphates (OPs) are chemical substances originally produced by the reaction of alcohols and phosphoric acid. In the 1930s, organophosphates were used as insecticides, but the German military developed these substances as neurotoxins in World War II. They function as cholinesterase inhibitors, thereby affecting neuromuscular transmission.

Organophosphate insecticides, such as diazinon, chlorpyrifos, disulfoton, azinphos-methyl, and fonofos, have been used widely in agriculture and in household applications as pesticides. Over 25,000 brands of pesticides are available in the United States, and their use is monitored by the Environmental Protection Agency (EPA).

Diazinon was sold in the United States for 48 years with 14.7 million pounds sold annually. It was the most widely used ingredient in lawn and garden sprays in the United States. Diazinon was found under the brand names Real Kill, Ortho, and Spectracide. In the past decade, the EPA reached an agreement with the pesticide industry to end the production of diazinon by March 2001 for indoor use and June 2003 for lawn and garden use. Chlorpyrifos (Dursban) was involved in a negotiated phaseout in June 2000. These phaseouts resulted from recognition of the special risk that these substances posed for children. Four percent of patients presenting to poison control centers report pesticide exposure. Of those patients, 34% are children younger than 6 years.

Toxic nerve agents used by the military are often of the organophosphate group; an example is sarin, the nerve gas used in a terrorist action in Tokyo in 1995. In anticipation of military use of OP neurotoxins during the Gulf War, the US military was given prophylactic agents which some believe caused some of the symptoms of Gulf War syndrome.

With the emergence of the West Nile virus in the northeastern United States, programs of spraying have been implemented in large urban areas, in particular New York’s Central Park.

Controversy exists regarding the long-term effects of exposure to low levels of potentially neurotoxic substances.

Therapeutic uses of organophosphates

Several organophosphate agents are being tried therapeutically. Cholinesterase inhibition, which in large doses makes these agents effective pesticides, also may be useful in other doses for treating dementia. Metrifonate has been used to treat schistosomiasis and is undergoing trials for the treatment of primary degenerative dementia.

The organophosphates pyridostigmine and physostigmine are carbamate anticholinesterases that have been used for many years for the treatment of myasthenia gravis. Although the short-duration anticholinesterases are generally safe, reports of their abuse are associated with a picture similar to pesticide intoxication.

One of the author’s patients had been diagnosed erroneously as a myasthenic. Long-term “therapeutic” doses of physostigmine chemically altered her neuromuscular junctions to the point where she had to be slowly weaned from the drug.

Sung and others have reported on the ability of these substances to induce nicotinic receptor modulation. This explains the action of these drugs and may result in development of more effective agents.

Historic and new uses of organophosphates

The first organophosphate was synthesized in 1850. Physostigmine was used to treat glaucoma in the 1870s. By the 1930s, synthetic cholinesterase inhibitors were being used for skeletal muscle and autonomic disorders. Some organophosphates were tried in the treatment of parkinsonism.

In 1986, testing began for tacrine, the first cholinesterase inhibitor to be tried for Alzheimer disease; it was released for clinical use in 1993. It is no longer in use. The blood-brain barrier has been the limiting factor in developing a cholinesterase inhibitor for use in dementia. Drugs such as rivastigmine are now widely used. Reported adverse effects are nausea and vomiting, with resultant weight loss because of the increase in cholinergic activity. It has been shown to be useful in mild to moderately severe Alzheimer disease.

Pyridostigmine has been tried for the fatigue of postpolio syndrome but showed no benefit.

 

http://emedicine.medscape.com/article/1175139-overview

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