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Of all the info I've posted so far on pesticides, this group, organophosphates,seems to me to be a likely culprit in pd. Since there was alot of info to go thru, I thought I'd summarize with some excerpts here: 1) A minimum amount of organophosphate must be absorbed to depress blood cholinesterase activities, but enzyme activities are lowered by dosage considerably less than are required to cause symptomatic poisoning. The enzyme depression is usually apparent within a few minutes or hours of significant absorption of organophosphate. Depression of the plasma enzyme generally persists several days to a few weeks; the RBC enzyme activity may not reach its minimum for several days, and usually remains depressed longer, sometimes 1-3 months, until new enzyme replaces that inactivated by organophosphate. *** It's supposedly an enzyme deficiency which may be the culprit in pd, according to much research, in that it causes the liver/kidneys to be unable to effectively filter toxins out of the body. What if taking that one step further, as is implied here, that the pesticide is also part of the reason for the enzyme deficiency itself? ************ 2) About 3% of individuals have a genetically determined low level of plasma pseudo-cholinesterase. These persons are particularly vulnerable to the action of the muscle-paralyzing drug succinylcholine, often administered to surgical patients. They are usually more sensitive to organophosphate toxicity, although this has not been proven. Patients with advanced liver disease, malnutrition, chronic alcoholism, and dermatomyositis exhibit low plasma cholinesterase activities. A number of toxicants, notably carbon disulfide, benzalkonium salts, organic mercury compounds, ciguatoxins, and solanines may reduce plasma pseudocholinesterase activity. Early pregnancy and birth control pills may also cause some depression. The RBC acetylcholinesterase is less likely than the plasma enzyme to be affected by factors other than organophosphates. It is reduced, however, in certain rare conditions that damage the red cell membrane, such as hemolytic anemias. ************** As far as I know, I'm not sensitive to "muscle-paralyzing drug succinylcholine", but I am to Compazine, known to cause pd-like symptoms in some cases. It mentions here that birth control pills may depress this plasma activity, making one more susceptible. Well, I was given the compazine originally to counteract the nausea I was supposed to have felt due to, I believe, Progesterone (or else it was Estrogen), which I had also been given. Could the hormone have depressed my system and added to my reaction to the compazine? Also, about a year after moving to NJ (which has pesticides EVERYWHERE), I started taking the pill (which I have since stopped). Could taking the pill have made me more susceptible to these pesticides and added to the earlier damage? I was only half-joking when I told my neurologist that the symptoms started after moving to NJ, known for its pollution and after starting the pill.************ 3) Repeated absorption of organophosphate at significant dosage, but in amounts not sufficient to cause acute poisoning, may cause persistent weakness, anorexia, and malaise. ************ Parkies have muscle weakness, are often thin, and of course suffer from general malaise************ 4) Some recently reported cases of organophosphate poisoning, mostly from suicidal ingestion of large quantities, have been characterized by prolonged (1-3 weeks) paralysis of muscles of the head, neck, limbs, and thorax, commencing one to four days following apparent resolution of acute cholinergic manifestations. Continuous medical support of pulmonary ventilation was necessary to sustain life in these cases. **********Hmm, sounds like my reaction to compazine almost**************** 5) Organophosphates poison insects and mammals primarily by phosphorylation of the acetylcholinesterase enzyme (AChE) at nerve endings. The enzyme is critical to normal control of nerve impulse transmission from nerve fibers to muscle and gland cells, and also to other nerve cells in autonomic ganglia and in the brain. Some critical proportion of the tissue enzyme mass must be inactivated by phosphorylation before symptoms and signs of poisoning become manifest. At sufficient dosage, loss of enzyme function allows accumulation of acetylcholine (ACh, the impulse-transmitting substance) at cholinergic neuroeffector junctions (muscarinic effects), at skeletal nerve-muscle junctions and autonomic ganglia (nicotinic effects), and in the brain. At choliner-gic nerve junctions with smooth muscle and gland cells, high ACh concentration causes muscle contraction and secretion, respectively. At skeletal muscle junctions, excess ACh may be excitatory (cause muscle twitching), but may also weaken or paralyze the cell by depo-larizing the end-plate. In the brain, high ACh concentrations cause sensory and behavioral disturbances, incoordination and depressed motor function. Depression of respiration and pulmonary edema are the usual causes of death from organophosphate poisoning. Recovery depends ultimately on generation of new enzyme in all critical issues. ***********Sounds like pd to me - too much acetylcholine, senosry/behavorial disturbances, incoordination and depressed motor function... ad infinitum************** 6) Organophosphates are efficiently absorbed by inhalation, ingestion, and skin penetration. To a degree, the occurrence of poisoning depends on the rate at which the pesticide is absorbed. Breakdown occurs chiefly by hydrolysis in the liver; rates of hydrolysis vary widely from one compound to another. In the case of certain organophosphates whose breakdown is relatively slow, significant temporary storage in body fat may occur. ***********If it's stored in body fat, then it remains there indefinitely, to be released at a later (stressful?) time********* 7) Rarely, certain organophosphates have caused a different kind of neurotoxicity consisting of damage to the axons of peripheral and central nerves and associated with inhibition of "neurotoxic esterase" (NTE). Manifestations have been chiefly weakness or paralysis and paresthesia of the extremities, predominantly the legs, persistent for weeks to years. Most of these rare occurrences have followed (8-21 days) an acute poisoning episode of the anticholinesterase type, but some have not been preceded by acute poisoning. Only a few of the many organophosphates used as pesticides have been implicated as causes of delayed neuropathy in humans. EPA guidelines require that organophosphate and carbamate compounds which are candidate pesticides be tested in susceptible animal species for this neurotoxic property *********** Sound familiar at all to pd? ******************* 8) Other specific properties of individual organophosphates may render them more hazardous than basic toxicity data suggest. By-products can develop in long-stored malathion which strongly inhibit the hepatic enzymes operative in malathion degradation, thus enhancing its toxicity. Certain organophosphates are exceptionally prone to storage in fat tissue, prolonging the need for antidote as stored pesticide is released back into the circulation. Animal studies have demonstrated potentiation of effect when two or more organophosphates are absorbed simultaneously: enzymes critical to the degradation of one are inhibited by the other. Whether this interaction is a significant factor in human poisonings is not known. ******* How encouraging - "more hazardous than basic toxicity data suggests"! Are we getting warm yet? *************** In conclusion, let me pose the question - ARE WE SUFFERING FROM A DISEASE OR HAVE WE BEEN POISONED??!! And if the latter is true then - WHO'S RESPONSIBLE AND WHAT DO WE DO NOW??!! Wendy "Troublemaker" Tebay