Here's more presticide info - this one in particular has a specific reference
to ALS.  In this same vein, something that may have a definite link to ALS,
could also be extrapolated to having a possible link to pd - as in the case
of the cycad seed poisonings in Guam, which resulted in ALS, AD, and PD.
 Note also the reference to chelation toward the end.
 
Wendy Tebay
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Confirmation of Poisoning
 
Mercury content of blood and tissue can be measured by atomic absorption
spectrometry. Special procedures are needed for extraction and measurement
of organic mercury compounds specifi-cally. These tests are not generally
available.
 
 
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Methoxyethyl Mercury Compounds
 
Methoxyethyl mercury acetate (MEMA, Panogen, Panogen M).
 
Methoxyethyl mercury chloride (MEMC, Emisan 6, Ceresan).
 
 
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Methyl Mercury Compounds
 
Methyl mercury hydroxide, nitrile, benzoate, acetate, propionate,
pentachlorophenate, quinolinolate.
 
 
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Phenyl Mercuric Acetate
 
Agrosan, Cekusil, Celmer, Hong Nien, Liquiphene, Mersolite, Pamisan, Phix,
PMAS, Seedtox, Shimmer-ex, Tag HL 331, Unisan.
 
Setrete (Gallotox, PMAA) is phenyl mercury ammonium acetate.
 
These fungicides have been formulated as aqueous solutions and dusts. They
have been used chiefly as seed protectants. Use of alkyl mercury fungicides
in the United States has been virtually prohibited for several years.
Phenyl mercuric acetate is still used to control diseases of turf, but
other applications have been sharply restricted.
 
 
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Toxicology and Manifestations of Poisoning
 
The mercurial fungicides are among the most toxic pesticides ever
developed, in terms of chronic as well as acute hazard. Epidem-ics of
severe, often fatal, neurologic disease have occurred when indigent
residents of less developed countries consumed methyl mercury-treated grain
intended for planting of crops. Poisoning has also occurred when meat from
animals fed mercury-treated seed was eaten. Most of what is known of
poisoning by organic mercu-rial fungicides has come from these occurrences.
 
Organic mercury compounds are efficiently absorbed across the gut and
possibly across the skin. Volatile organic mercury is readily taken up
across the pulmonary membrane. Methyl mercury is selectively concentrated
in the tissue of the nervous system, and also in the red blood cells. Other
alkyl mercury compounds are probably distributed similarly. Excretion
occurs almost entirely by way of the bile into the bowel. The residence
half-life of methyl mercury in the human is about 70 days. There is
significant conversion of organic mercury to inorganic mercury in the red
cell.
 
Early symptoms of poisoning are metallic taste in the mouth, numbness and
tingling of digits and face, tremor, headache, fatigue, emotional lability,
and difficulty thinking. Manifesta-tions of more severe poisoning are
incoordination, slurred speech, loss of position sense, hearing loss,
constriction of visual fields, spasticity or rigidity of muscle movements,
and deterioration of mental capacity. Many poisonings caused by ingestion
of organic mercurials have terminated fatally, and a large percentage of
survivors have suffered severe permanent neurologic damage.
 
Phenyl mercuric acetate is apparently not as extremely toxic as the alkyl
mercury compounds. However, exposure to it has preced-ed the appearance of
symptoms and signs of neurologic disease resembling amyotrophic lateral
sclerosis in certain reported instances.
 
 
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Treatment of EXTERNAL Toxicosis
 
Skin and hair contaminated by mercury-containing dust or solution should be
cleansed with soap and water. Eye contamination should be removed by
flushing the eye with clean water. If irritation persists, specialized
medical care should be obtained.
 
Persons experiencing symptoms (metallic taste in mouth) after inhalation of
volatile organic mercury compounds (methyl mercury is the most volatile)
should be removed promptly from the contam-inated environment, and observed
closely for indications of neurologic impairment. Every possible precaution
should be taken to avoid exposure to organic mercury compounds.
 
 
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Treatment of Toxicosis by INGESTION
 
Ingestion of organic mercury compound, even at low dosage, is
life-threatening, and management is difficult. Detailed discus-sions of
contemporary treatment options are offered in modern clinical toxicology
texts. Following are the basic steps in management of poisoning.
 
1. Limit gastrointestinal absorption. If a mercurial fungicide has been
ingested in the past few hours, the stomach must be evacuated by intubation
and lavage, taking all precautions to protect the respiratory tract (see
  Organophosphate Insecticides, Treatment). Repeated administration of
activated charcoal may be beneficial.
 
2. Administer a chelating agent. Dimercaprol (BAL) and EDTA are apparently
of little value in poisonings by organic mercury, but other chelators are
effective:
 
A. D-penicillamine. (This is available in the United States, and has proven
effective in reducing the residence half-life of methyl mercury in poisoned
humans, see Arsenical Pesticides for dosage.)
 
B. 2,3-dimercaptopropane-1-sulfonate, and 2,3-dimercaptosuccinic acid.
(Although effective, these agents are not currently approved for use in the
United State.)
 
C. N-acetyl-D,L-penicillamine. (Effective, but not currently approved for
use in the United States.)
 
3. Extracorporeal hemodialysis and hemoperfusion may be consid-ered,
although experience to date has not been encouraging. Although the
unmodified organic mercurials are not efficiently dialyzable across most
membranes, when used in combination with chelating agents, dialysis may be
of some value in removing organic mercury from the blood (A.H. Al-Abbasi,
et al. J. Pharmacol. Exptl. Therap. 207:249-254, 1978).
 
Very little can be done to mitigate neurologic damage caused by organic
mercurials.
 
 
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