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Here's some info on more pesticides which can cause twitching.  These
particular ones are grouped under the name "chlorophenoxy herbicides."    In
answer to Pat's question,  I've never been exposed to pesticides, that I know
of, in any sort of single, toxic exposure.  I did, however, have a very bad
drug r eaction to an anti-deprressant/anti-psychotic drug, the whole class of
which is chemically similar to some pesticides.  The link is definitely close
enough to warrant some research.  I ran across one that  stated right out
that it had in a few cases, outright caused Lou Gehrig's disease.  From what
happened on Guam back  around WWII with the cycad seed flour causing AD, PD,
 and/or ALS in a significant number of people, all having eaten this flour,
it lends one to consider that all three diseases may have similar outside
causes and environmental factors, but  which one a particular person gets
probably depends on their susceptibilities, which is driven by their genes.
 That MTPP which caused pd in those young people is chemicallly similar to
paraquat & diquat (info to be posted soon here).  Also, I now live in NJ, and
since (yes it's true!) there are alot of farms, there is also alot of
spraying of pesticides.  All the housing complexes too around here spray ALOT
(and our  dogs still get covered in ticks anyway!) .  There is also alot of
pollution, and I worked in a building recently for about 4 years, which when
 it first opened, the tenants who were originally there eventually  leftt and
it closed down for a  while cause everyone was getting sick (sick building
syndrorme).   When new carpet is installed, tile laid with glue, paint spread
around, etc., all this stuff outgasses for a while and these chemical
released can be somewhat toxic, especially to those who are ultra-sensitive
(MCS??)  I know formaldehyde bothers me (I got a sore throat and headache f
rom it  in high school while dissecting a  frog and formaldehyde is used in
all kinds of stuff that we produce.  I've also heard that the prevalence of
pd and ms, etc., is actually worse out in the  midwest, which one typically
thinks of as cleaner than say, NJ, - but with all the heavy duty pesticides
used in farming, etc., it doesn't seem quite so surprising.  I wonder if
anyone's done any sort of quantitative survey of what diseases farmers are
typically afflicted with.  That should give some clues to the r ole of
pesticides in diseases like pd.  So Pat, I don't know really for sure how
many/much pesticides I've been exposed to, but I have been exposed somewhat,
and I know that the compazine was a big factor.  Here goes the info:
 
Subj:   twitching - chlorophyenoxy herbicides
Date:   95-06-27 18:26:39 EDT
From:   [log in to unmask] (Tebay, Wendy)
To:     [log in to unmask] (athome)
 
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Commercial products
 
Several hundred commercial products contain chlorophenoxy herbicides in
various forms, concentrations, and combinations. Following are names of
widely advertised formulations. In some cases, the same name is used for
products with different ingredients. Exact composition must therefore be
determined from the product label.
 
2,4-D or 2,4-dichlorophenoxyacetic acid (Agrotect, Amoxone, AquaKleen, BH
2,4-D, Chipco Turf Herbicide `D', Chloroxone, Crisalamina, Crisamina, Crop
Rider, D50, Dacamine, Debroussaillant 600, DedWeed SULV, Desormone,
Dinoxol, Emulsamine BK, Emulsamine E-3, Envert DT, Envert 171, Super D
Weedone, Weedone, Estone, Farmco, Fernesta, Fernimine, Fernoxone, Ferxone,
Formula 40, Gordon's Amine 400, Gordon's LV 400 2,4-D, Hedonal, Herbidal,
Lawn-Keep, Macondray, Miracle, Netagrone 600, Pennamine D, Planotox,
Plantgard, Salvo, Spritz-Hormin/2,4-D, Spritz-Hormit/2,4-D, Superormone
Concentre, Transamine, Tributon, Tuban, U 46, U 46 D-Ester, U 46 D-Fluid,
Weed-B-Gon, Weedar, Weedatul, Weed-Rhap, Weed Tox, Weedtrol, Gordon's Dymec
Turf Herbicide Amine 2,4-D, Gordon's Phenaban 801, Acme Amine 4, Acme Butyl
Ester 4, Acme LV 6, Acme LV 4, Gordon's Butyl Ester 600, DMA 4, Dormone).
 
2,4-DP or 2,4-dichlorophenoxypropionic acid (BH 2,4-DP, Desormone, Hedonal,
Hedonal DP, Kildip, Polymone, Seritox 50, U 46, U 46 DP-Fluid, Weedone DP,
Weedone 170).
 
2,4-DB or 2,4-dichlorophenoxybutyric acid (Butoxon, Butoxone, Butyrac,
Embutox).
 
2,4,5-T or 2,4,5-trichlorophenoxyacetic acid (Amine 2,4,5-T for rice,
Dacamine, Ded-Weed, Farmco Fence Rider, Forron, Inverton 245, Line Rider,
Super D Weedone, T-Nox, Trinoxol, U 46, Weedar, Weedone).
 
MCPA (metaxon, Agroxone, Weedone), MCPB (Can-Trol, PDQ, Thistrol), and MCPP
(mecoprop, Methoxone M, Mecopex, Gordon's Mecomec) are 2-methyl,
4-chlorophenoxy aliphatic acids and esters.
 
Dicamba (Banvel) is 2-methyl-3,6 dichlorobenzoic acid.
 
Sodium, potassium, and alkylamine salts are commonly formulated as aqueous
solutions, while the less water soluble esters are applied as emulsions.
Low molecular weight esters are more volatile than the acids, salts, or
long-chain esters.
 
Chlorophenoxy compounds are sometimes mixed into commercial fertilizers to
control growth of broadleaf weeds.
 
 
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Confirmation of poisoning
 
Gas-liquid chromatographic methods are available for detecting and
measuring chlorophenoxy compounds in blood and urine. These analyses are
useful in confirming and assessing the magnitude of chlorophenoxy
absorption. Poisonings characterized by unconsciousness have shown initial
blood chlorophenoxy concentrations ranging from 80 to more than 1000 mg per
liter. Urine samples should be collected as soon as possible after exposure
because the herbicides may be almost completely excreted in 24-72 hours,
depending on the extent of toxicant absorption and urine pH. Analyses can
be performed at special laboratories usually known to local poison control
centers. If circumstances indicate strongly that excessive exposure to
chlorophenoxy compounds has occurred, INITIATE appropriate
  TREATMENT measures immediately, not waiting for chemical confirmation of
toxicant absorption.
 
 
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Symptoms and signs of poisoning
 
Chlorophenoxy compounds are moderately IRRITATING to skin and mucous
membranes. Inhalations of sprays may cause burning sensations in the
nasopharynx and chest and coughing may result. Prolonged inhalation
sometimes causes dizziness. Adjuvant chemicals added to enhance foliage
penetration may account for the irritant effects of some formulations.
 
Manifestations of systemic toxicity of chlorophenoxy compounds are known
mainly from clinical experience with cases of deliberate suicidal ingestion
of large quantities. The agents most often involved in these incidents have
been 2,4-D and mecoprop. The toxic effects of other chlorophenoxy compounds
are probably similar but not identical. Few cases of deliberate ingestion
of chlorophenoxy compounds have terminated fatally.
 
Irritation of the stomach usually leads to VOMITING soon after ingestion.
Pain in the chest and abdomen and diarrhea may ensue. Headache, mental
confusion, and bizarre behavior are early manifestations of severe
poisoning which may progress to UNCONSCIOUSNESS. MYOTONIA (muscular
stiffness on passive movement of the limbs) has occurred in persons
poisoned by 2,4-D. Areflexia is sometimes observed. Muscle twitching may or
may not be evident. Convulsions occur very rarely. Respiratory drive is not
depressed; hyperventilation is sometimes evident. Body temperature may be
moderately elevated, but this is rarely a life-threatening feature of the
poisoning. With effective urinary excretion of the toxicant, consciousness
returns in 48-96 hours.
 
Metabolic acidosis is manifest as a low arterial pH and bicarbonate
content. The urine is usually acid. Skeletal muscle injury, if it occurs,
is reflected in elevated creatine phosphokinase, and sometimes
myoglobinuria. Moderate temporary elevations of blood urea nitrogen and
serum creatinine are commonly found as the toxicant is excreted, but acute
renal failure is uncommon. Mild leukocytosis and biochemical changes
indicative of liver cell injury have been reported. Both tachycardia and
bradycardia have been observed. T-wave flattening and inversion may occur.
 
Myotonia and muscle weakness may persist for months after acute poisoning.
Electromyographic and nerve conduction studies in some recovering patients
have demonstrated a mild proximal neuropathy and myopathy.
 
 
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Toxicology
 
Some of the chlorophenoxy acids, salts, and esters are moderately
irritating to skin, eyes, and respiratory and gastrointestinal linings. In
a few individuals, local depigmentation has apparently resulted from
protracted dermal contact with chlorophenoxy compounds.
 
The chlorophenoxy compounds are absorbed across the gut wall, lung, and
skin. They are not significantly fat storable. Excretion occurs almost
entirely by the way of urine. Apart from some conjugation of the acids,
there is limited biotransformation in the body. The average residence
half-life of 2,4-D in the human is about 18 hours, that of 2,4,5-T about 24
hours. These averages lie within very wide ranges (4-140 hours in the case
of 2,4-D), depending on the urinary pH (alkalinity enhances secretion).
 
Given in large doses to experimental animals, 2,4-D causes vomiting,
diarrhea, anorexia, weight loss, ulcers of the mouth and pharynx, and toxic
injury to the liver, kidneys, and central nervous system. Myotonia
(stiffness and incoordination of hind extremities) develops in some species
and is apparently due to CNS damage: demyelination has been observed in the
dorsal columns of the cord, and EEG changes have indicated functional
disturbances in the brains of heavily dosed experimental animals.
 
Ingestion of large amounts of chlorophenoxy acids has resulted in severe
metabolic acidosis in humans. Such cases have been associated with
electrocardiographic changes, myotonia, muscle weakness, myoglo-binuria,
and elevated serum creatine phosphokinase, all reflecting injury to
striated muscle. Because chlorophenoxy acids are weak uncouplers of
oxidative phosphorylation, extraordinary doses may produce hyperthermia
from increased production of body heat.
 
Chlorinated Dibenzo Dioxin (CDD) and Chlorinated Dibenzo Furan (CDF)
compounds are generated in the manufacture of chlorophenoxy compounds,
particularly at excessive temperatures. The 2,3,7,8-tetra CDD form is
extraordinarily toxic to multiple mammalian tissues; it is formed only in
the synthesis of 2,4,5-T. Hexa-, hepta-, and octa-compounds exhibit less
systemic toxicity, but are the likely cause of chloracne (a chronic,
disfiguring skin condition) seen in workers engaged in the manufacture of
2,4,5-T and certain other chlorinated organic com-pounds. Although toxic
effects, notably chloracne, have been observed in manufacturing plant
workers, these effects have not been observed in formulators or applicators
regularly exposed to 2,4,5-T or other chlorophenoxy compounds.
 
The medical literature contains several reports of peripheral neuropathy
following what seemed to be minor dermal exposures to 2,4-D. It is not
certain that exposures to other neurotoxicants were entirely excluded in
these cases. Single doses of 5 mg/kg body weight of 2,4-D and 2,4,5-T have
been administered to human subjects without adverse effects. One subject
consumed 500 mg of 2,4-D per day for 3 weeks without experiencing symptoms
or signs of illness.
 
 
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Treatment of EXTERNAL Poisoning by Chlorophenoxy Compounds
 
1. BATHE and SHAMPOO with soap and water to remove chemicals from skin and
hair. Obtain medical treatment if irritation persists. Individuals with
chronic skin disease or known sensitivity to these herbicides should either
avoid using them or take strict precautions to avoid contact (respirator,
gloves, etc.).
 
2. FLUSH contaminating chemicals from eyes with copious amounts of clean
water for 10-15 minutes. If irritation persists, obtain medical treatment.
 
3. If symptoms of illness occur during or following inhalation of spray,
REMOVE victim FROM CONTACT with the material for at least 2-3 days. Allow
subsequent contact with chlorophenoxy compounds only if effective
respiratory protection is practiced.
 
 
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Treatment of Poisoning by Chlorophenoxy Compounds by INGESTION
 
1. If substantial amounts of chlorophenoxy compounds have been INGESTED,
spontaneous emesis may occur. If vigorous emesis has not occurred measures
should be taken to empty the stomach and limit gastrointestinal absorption
by GASTRIC INTUBATION, ASPIRATION, and LAVAGE, following placement of a
cuffed endotracheal tube. Lavage procedure is described in
  Organophosphate Insecticides, Treatment, Section 5. Repeated
administration of charcoal at half or more the original dosage every 2-4
hours may be beneficial.
 
If gastric aspiration and lavage is not performed due to delay in
treatment, and if the patient is fully alert, ADMINISTER CHARCOAL AND
LAXATIVE ORALLY, at the dosages indicated in the
  above reference.
 
2. Administer INTRAVENOUS FLUIDS to accelerate excretion of the
chlorophenoxy compound, and to limit concentration of the toxicant in the
kidney. A urine flow of 4-6 ml/minute is desirable. Intravenous
saline/dextrose has sufficed to rescue comatose patients who drank 2,4-D
and mecoprop several hours before hospital admission.
 
CAUTION: Monitor urine protein and cells, BUN, serum creatinine, serum
electrolytes, and fluid intake/output carefully to insure that renal
function remains unimpaired and that fluid overload does not occur.
 
Forced ALKALINE DIURESIS has been used successfully in management of
suicidal ingestions of chlorophenoxy compounds. Alkalinizing the urine by
including sodium bicarbonate (44-88 mEq per liter) in the intravenous
solution apparently accelerates excretion of 2,4-D dramatically and
mecoprop excretion substantially. Urine pH should be maintained in the
7.6-8.8 range. Include potassium chloride as needed to offset increased
potassium losses: add 20-40 mEq of potassium chloride to each liter of
intravenous solution. Monitor serum electrolytes carefully. There may
possibly be some hazard to the kidneys when urine concentrations of
toxicant are very high, so the integrity of renal function and fluid
balance should be monitored carefully as the chlorophenoxy compound is
excreted.
 
3. Hemodialysis is not likely to be of significant benefit in poisonings by
chlorophenoxy compounds because of the extensive protein binding of these
chemicals.
 
4. Follow-up clinical examination should include electromyographic and
nerve conduction studies to detect any neuropathic changes and
neuromuscular junction defects.
 
 
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