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Barbara Patterson                               [log in to unmask]
HSC 2J22                                        905-525-9140, ext. 22403
                        School of Nursing
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---------- Forwarded message ----------
Date: Wed, 5 Jul 1995 18:15:57 -0400
Date: Wed, 05 Jul 95 15:11:00 PDT
From: Carrie Barrott <[log in to unmask]>
Subject: Re: organophosphates and pd
Wendy,
I have read about half of The Case of the Frozen Addicts by Dr. Langston
which I gave to my dad for Father's Day and I am convinced that we have ALL
been poisoned, either by pesticides, herbicides or other chemicals or by
viruses, some of us more severely than others.  It seems to me that some of
us are more susceptible than others to these neurotoxins.  Maybe this will be
traced someday to a genetic marker.
 
We all played on the lawns that our parents so lovingly cared for.  At our
house, a visit from anything with more than four legs was treated immediately
with Raid or Black Flag.  I never saw any bugs at school or church either,
now that I think about it.  Our bug phobia just may be killing us.  I would
be interested to know when pesticides/herbicides were first widely used and
the correlation between this and the first documented cases of PD by Dr.
Parkinson.  Does anyone know?
 
While we have limited control over many environmental factors, we can start
to clean up our act at home.  Here are some suggestions from me:
 
Avoid using pesticides or herbicides in the house or yard - Bugs and weeds
  are annoying, but I'd rather have them than PD.
 
Avoid using illegal chemicals - You don't know what's REALLY in there.
     (Remember the frozen addicts.)
 
Buy all natural cleaning products - These can be obtained at most health food
     stores.
 
Buy only organic fruits and vegetables - My mom says that they probably spray
     anyway, but I think you have to trust somebody sometime.
 
Stay out of the rain - This may be a bit extreme, but when you stop to think
     about where that rain has been, falling through the poisoned air...
 
I would really like to nail this on someone specific, but I feel that I am
responsible, at least in part.  Go get 'em, Wendy.
 
Carrie Barrott
[log in to unmask]
 
 
 
 
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 seudocholinesterase
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
 
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