Mosquito Control wants to spend $1.2 million for a new poison spray plane

Discussion in 'Local Government and Groups' started by Smiling JOe, May 5, 2007.

  1. mothernature

    mothernature Beach Comber

    Nov 8, 2005
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    OrganicMama: Thanks for the posting!

    Re-read the Adobe pdf on the Dibrom Naled. Under hazards, it mentions acute cholinesterase depression......

    Without the cholinesterase, our nerve impulses have no "shut off". In other words, the transmission is continual. Here's some info on Cholinesterase:
    The transmission of nerve impulses across synapses and the junctions between nerve and an effector organ (gland, muscle, nerve) is accomplished by the release of a chemical agent, acetylcholine. If actions within the central nervous system and at peripheral nerve terminations are to be kept localized and capable of repetition, acetylcholine must be destroyed or inactivated at or near the site of its release, and with great speed. The destruction of acetylcholine at such sites is accomplished by an enzyme, acetylcholinesterase. Present at the neurosynaptic junctions, acetylcholinesterase breaks acetylcholine into acetyl and choline fragments. Acetylcholinesterase functions to increase the precision of nerve firing, enabling some nerve cells to fire as rapidly as 1,000 times per second without overlap of the of the neural impulses

    Cholinesterase InhibitorsThe poisonous effects of organophosphorous and carbamate pesticides come about through the inhibition of cholinesterase, an enzyme produced in the liver. One form, acetylcholinesterase, can be found at the neurosynaptic junctions while another, butyryl cholinesterase, is primarily located in the plasma and pancreas, although small quantities of it exist in all tissues including our blood.

    Organophosphate Insecticides
    Organophosphorus compounds differ from one another in many important respects, although chemically, all can be considered to be derivatives of phosphoric or thiophosphoric acids. They differ widely in inherent toxicity and in their ability to penetrate the skin. However, mevinphos (Phosdrin) is extremely dangerous by both oral and dermal routes.

    Some organophosphates act directly while others require activation by enzymes within the body. Some are destroyed and eliminated more rapidly than others. Also, they differ with respect to the manner of their reaction with the cholinesterase enzyme.

    Organophosphate pesticides inhibit cholinesterase by forming covalent chemical bonds through a process called phosphorylation. Spontaneous enzymatic regeneration half-lifes may take days to months long. As with carbamates, the nature of the organophosphate involved, the dose received and the duration of exposure all affect the period for regeneration to occur. Because of the prolonged regeneration half-lives, (the time required for half of the cholinesterase to reactivate), organophosphate intoxication is usually considered more serious although some exposures to carbamates lead more rapidly to symptomatology and can be just as lethal. Organophosphates affect both red blood cells (RBC) and plasma cholinesterase activity whereas carbamates normally affect only the plasma fraction (Davies and Freed, 1981).

    Carbamate Insecticides
    Carbamate insecticides inhibit cholinesterase activity in reversible fashion and normally affect only the plasma fraction. Because they interact with cholinesterase by weak, ionic chemical bonding, the cholinesterase usually regenerates itself spontaneously. The half-life of this spontaneous regeneration is on the order of minutes to hours and is dependent on the nature of the specific carbamate involved, the dosage received and the length of exposure (Davies and Freed, 1981).

    Like the organophosphorous pesticides, members of the carbamate group vary widely in inherent toxicity and other toxicological properties. Carbaryl (Sevin), for instance, is not highly toxic by the oral route and is not readily absorbed through the skin. Aldicarb (Temik), on the other hand, is extremely toxic by both oral and dermal routes.

    Signs and Symptoms
    The signs and symptoms are similar for carbamates and organophosphate poisonings. These pesticides combine with cholinesterase at nerve endings in the brain and in the tissues of the body, thereby permitting the accumulation of acetylcholine. The occurrence of symptoms is primarily dependent upon the rate of cholinesterase decline. Most differences are due to the fact that cholinesterase reactivation is much more rapid after carbamate exposure than it is after organophosphate exposure. After carbamate exposure, choli- nesterase recovery may take from several hours to several weeks, depending on the degree of exposure. Also, the dose necessary to produce incapacita- ting symptoms is generally far from the lethal dose for carbamates, while the two doses are often quite close for organophosphates. Symptoms include the following:

    Muscarine Effects

    nausea blurring of vision
    vomiting pain in chest
    involuntary defecation and urination salivation
    diarrhea lacrimation
    sweating excessive bronical secretions

    Nicotinic Effects

    flaccid paralysis
    muscle twitching

    Respiratory failure can also occur as a blockage of small bronchi may result.

    No one can tell when symptoms first appear whether the poisoning will be mild or severe. In many instances involving skin contamination, symptoms progress from mild to severe due to continued absorption, even though an attempt has been made to wash the material away. Such progression can be rapid. At the first signs of poisoning, the victim should be transported to the nearest medical facility. For organophosphate poisoning, atropine and pralidoxime (2-PAM, Protopam) chloride may be administered by the physician. Atropine should be given intravenously, but if this is not possible, the intramuscular route will suffice. Pralidoxime provides an important adjunct to atropine when it is administered within 36 hours of the organophosphate poisoning contact. Atropine is the only antidote necessary for the management of cholinesterase depression resulting from carbamate exposure (Davies and Freed, 1981).

    Cholinesterase surveillance
    Workers occupationally exposed to organophosphate pesticides should be offered an initial pre-employment cholinesterase determination (base-line value) followed by subsequent cholinesterase testing on a regular basis (usually monthly). The laboratory method should be one that provides both red blood cell and plasma values. Red blood cell values are more infor- mative of exposure than are plasma and workers should be withdrawn from exposure when exhibiting greater than 50% inhibition (Davies and Freed, 1981).

    An organophosphate cholinesterase inhibitor that is used as an insecticide and as an acaricide.

    There are many articles on the web concerning Organophosphate Pesticides and Parkinson's:
    Study Links Pesticides to Parkinson?s Disease
    (Beyond Pesticides, May 31, 2005)
    New study results from the University of Aberdeen, England Geoparkinson Project, reported in New Scientist Magazine (May 26, 2005 issue 2501), link pesticide exposure to an increased risk of developing Parkinson?s disease. The study followed the behaviors of nearly 3000 European volunteers with and without Parkinson?s disease from Scotland, Italy, Sweden, Romania and Malta from 2000 to 2005. The project, funded by the European Union, aimed to study the genetic, environmental and occupational risk factors for Parkinson's disease. The research project finds that overall the volunteers with Parkinson?s had more exposures to pesticides throughout their lives compared to volunteers without Parkinson?s. Low level pesticide users were 9% more likely to have Parkinson?s, whereas high level users, like farmers, were 43% more likely. People with Parkinson?s in their family face a 350 percent increase in risk.

    Parkinson?s disease causes nerve cells to stop producing the correct levels of the neurological chemicals, dopamine and acetylcholine. The imbalance of these chemicals leads to problems in motor function, which results in tremors, tics, stiffness in muscles and joints, and/or difficulty moving. Other symptoms include depression, anxiety, dementia, constipation, urinary difficulties, and problems sleeping. Drug therapy exists to help patients cope, but currently there is no cure for this degenerative disease. This study concludes that genetics and having been knocked unconscious contribute to an increased risk of getting Parkinson?s disease. Mounting scientific evidence from this and other studies also suggests that environmental factors, specifically pesticide exposure, is a significant risk factor that contributes to this disease.

    This study could not determine what specific pesticides were linked to Parkinsons?s since participants were not able to identify what they had used. However, other studies show that the pesticides permethrin , maneb, rotenone, and paraquat increase risk of developing Parkinson?s. Read more about the evidence for pesticide?s link to Parkinson?s in Beyond Pesticides Daily News archives.

    For additional links: google - Pesticides and Parkinson's :yikes:

    We can have facts without thinking but we cannot have thinking without facts. John Dewey
    US educator, philosopher, & psychologist (1859 - 1952)
  2. organicmama

    organicmama Beach Fanatic

    Jul 31, 2006
    Likes Received:
    back in SRB
    Mother Nature, thanks for the wealth of info, as usual. :D

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