Commonality And For Those Using Malathion This Year

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        Subject:    Commonality And For Those Using Malathion This Year
            Date:     Fri, 23 Aug 2002 15:11:11 -400 
           From:     Stephen Tvedten <steve@getipm.com>
Organization:     Get Set Inc. (www.getipm.com)

To:     Paul Helliker <phelliker@cdpr.ca.gov>
          Director, State of California, Department of Pesticide Regulation 

cc:   "Brian J. Foster" <bfoster@swlaw.com>
cc:    Christine Whitman whitman.christine@epa.gov

http://www.txdirect.net/users/jeturner/chm-05.html
Well Digger's Workstation -- www.txdirect.net/users/jeturner/
Copyright © 1997-2000, 2001, Jack E. Turner. All rights reserved

V. Nerve Agents

A. Mechanism of action

1. Inhibits acetylcholinesterase throughout bodytissue, most markedly in the nervous system

a. Acetylcholine is the primary neurotransmitter causing innervation.
b. Acetylcholinesterase is the enzyme which breaks down acetylcholine.
c. This process takes place at the synaptic cleff.

2. Causes increase in secretions (sweating, mucus draining, tearing).
3. Causes continuous muscular stimulation (twitching to convulsions).
4. Depresses cardiopulmonary output.
5. "Aging" occurs at different rates for different agents. (Aging: The  irreversible bonding of the nerve agent to the acetylcholinesterase. This takes as long as 6-8 hours in the case of GB and as little as 2-6 minutes in the case of GD.)

B. Examples

1. GB, Sarin, Isopropyl methyl phosphonofluoridate
2. GD, Soman, Pinacolyl methyl phosphonofluoridate
3. (MY INCLUSION) FyFanon ULV -MALATHION-organophosphate sprayed NY 1999/2000 (Malathion is an organophosphate insecticide, one of a class of pesticides that are highly toxic to vertebrates and are chemically related to nerve gases used during World War II. et al.) sensitizing the entire population

C. The patient may present with:

1. Mild exposure:

a. Anorexia.
b. Headache and dizziness.
c. Weakness and anxiety.
d. Tremors of the tongue and eyelids.
e. Miosis - generally seen only when the eyes are exposed.

2. Moderate exposure: (may also present with any or all of the mild symptoms)

a. Nausea.
b. Salivation and tearing.
c. Abdominal cramps and vomiting.
d. Sweating.
e. Bradycardia.
f. Muscular fasiculations (tremors, trembling).

3. Severe exposure: (may also present with any or all of the moderate symptoms)

a. Diarrhea, loss of anal sphincter control.
b. Pinpointed and non-reactive pupils.
c. Respiratory difficulty.
d. Pulmonary edema.
e. Cyanosis.
f. Convulsions (This alone can lead to rapid death from anoxia and acidosis.)
g. Coma.
h. Cardiac sinus node slowdown.
 i. Atrioventricular node blocked.

D. First Aid Measures (First Echelon)
(NOTE: Prior to arrival in an area of known use of Chemical Agent, or in response to a potential threat of use of Chemical Agent, personnel may be directed to initiate a PRE-TREATMENT regimen with the drug pyridostigmine.)

1. Mask yourself
2. Mask the injured
3. Skin decontamination performed with the M258A1 Skin Decontamination Kit.
4. Auto injections of 2-PAM chloride and atropine.
5. Evacuate the obviously injured immediately.
6. Evacuate others as symptoms manifest themselves.

E. Emergency Medical Protocol

   1. Maintain atropinization

   a. Titrate against the secretions

(1) 12mg IV first 2 hrs, is not unusual.
(2) Excess of 60mg in first 24 hrs has been used on combat casualties (Iranian casualties, 1984).

   b. 2-PAM chloride, 1 g IV STAT, repeated at 30 min.

(1) This dosage may be repeated twice within each 24 hr period.
(2) Repeat dosage only if there is no improvement in patient's respiration.
(3) Should "aging" (relatively permanent inactivation of acetylcholinesterase) have occurred, 2-PAM Chloride should still be given to help prevent inactivation of cholinesterase being given up by pyridostigmine if pretreatment was used.

c. Diazepam (Valium) 2-10mg IV at 1 mg/min, as needed, for convulsions.
d. Pulmonary edema, should it develop is best treated by postural drainage and or catheter suction. AVOID the use of respiratory depressant drugs (morphine, barbiturates).

DISCUSSION
If an individual is in respiratory distress or is not breathing ventilatory assistance is obviously needed. There are several problems, particularly in the field. The intense bronchoconstriction and bronchosecretions make ventilation difficult under the best of circumstances. Pressures of 50-70cm H 2 O are often required and some ventilators cannot overcome this resistance. An equally severe problem is caused by the secretions - good adequate suction is needed. In the past the M17A1 mask had a resuscitube for field ventilation. This is being removed from field issue and at least for the time being there is not provision for resuscitation in the field. The drug therapy of choice is atropine. Atropine is an antichoinergic compound and acts by blocking the effects of acetylcholine at the receptor site. It is effective only at the muscarinic sites. It causes the secretions to dry and relieves the smooth muscle constriction in the lung and gastrointestinal tract. It is relatively ineffective at nicotinic sites - It has little effect on the skeletal muscle fasciculation and twitching. The dose and frequency of administration of atropine depend on the condition of the patient. If a patient has mild dyspnea or is in mild distress from gastrointestinal symptoms, an intramuscular dose of 2mg might be adequate. If the distress is more severe the drug might be given intravenously and probably larger doses (2-8mg) might be given. These doses are high, but they are needed. It is better to give too much atropine than too little. Atropine should be titrated against the patient's condition until he recovers. The guide for giving atropine is to dry up secretions, both in the mouth and in the lungs. Atropine also causes mydriasis and tachycardia, but these are not reliable indications of atropinization in nerve agent intoxication. A second drug that is effective as an adjunct is an oxime. Pralidoxime chloride (2-PAM Cl, Protopam R ) is the oxime marketed for use in the U.S. Toxogonin is used in parts of Europe and P 2 S is used in the U.K. and Canada. Whereas atropine acts by blocking the excess acetylcholine, an oxime acts by removing the organophosphate from the enzyme cholinesterase, thus removing the poisoning. However, there are limitations to the effects of oximes. With time many organophosphate compounds become irreversibly bound to cholinesterase and are then refractory to oxime therapy. This process is called aging, and aging occurs about 5 hours after GB (Sarin) poisoning and about 2 minutes after GD (Soman) poisoning. This means that for practical purposes oximes are ineffective in GD poisoning. The dose of 2-PAM Cl is 1 gram given slowly (20-25 minutes) intravenously.

Hypertension will occur if the drug is administered too rapidly. The dose should be repeated at hourly intervals for 2-3 doses if needed. 2-PAM Cl is being fielded in an injector containing 600mg for intramuscular injection for self or buddy aid. Oximes are not effective if given alone (without atropine). Cardiac arrhythmias are usually not a problem with one exception. It has been shown in experimental animals that the rapid I.V. administration of atropine to an anoxic animal may cause ventricular fibrillation. So it might be best to ventilate the patient first or to give atropine slowly while attempting ventilation. On the other hand, ventilation is much easier after atropine is given as the drug markedly reduces the bronchospasm.  

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