SUBJECT:  CHEMICAL WARFARE EXPERIENCE IN IRAN/IRAQ WAR





IRANIAN EXPERIENCE



Introduction:



Iraq is known to have employed nerve agents, Tabun (GA) and Sarin (GB), a blood

agent, hydrogen cyanide gas (HCN), and blister agents, Mustard Gas, "Dusty"

Mustard and probably Lewisite against Iranian soldiers, civilians, and Iraqi

Kurdish civilians.  Early in the conflict Iraq used GB, then switched primarily

to mustard.  The vast majority of the casualties resulted from the use of the

mustard agents, and most of the medical data and casualty treatment obtained from

the conflict pertains to mustard agents.



Mustard Injuries:



Sulfur mustard is a contact vesicant or blister agent with profound systemic

effects on proliferating tissues.  It is a yellow oil liquid that can persist for

2 to 7 days under warm conditions (15C) and 2 to 8 weeks under cold conditions

(-10C).  The primary toxic effects are observed in the skin, eyes, respiratory

tract and systemically on the hematopoietic tissues.  With dusty mustard, finely

ground (0.1 -10.0 microns) silicate (35%) is coated with mustard agent (65%),

producing more pronounced injuries to the respiratory system and a shortened

latent period compared with the neat mustard agent.  Lewisite is an arsenical war

gas, initially a colorless liquid, becoming violet-black or green with time, and

has an odor resembling geraniums.  Toxic effects are similar to mustard, but

Lewisite is immediately painful on contact (no latent period), penetrates skin

more rapidly, and uninfected blisters heal more rapidly. Lewisite blisters are

sharply defined, occupy the entire area of erythema and are filled with an opaque

or opalescent fluid containing trace amounts of arsenic and many leukocytes,

while the typical mustard blister is encompassed by an inflamed area of erythema

filled with a clear, transparent, lemon colored serum containing no trace of any

mustard.  Currently, there is no antidote available to counter mustard or

Lewisite effects once they have reached the cells; therefore, treatment of

vesicant casualties is symptomatic and supportive.  



The minimum contact time for mustard agent to elicit an effect on the skin is 30

seconds to 2 minutes.  If mustard is removed immediately, there is no injury. 

After mustard agent contacts the skin, there is a latent period of 4 to 6 hours

for neat mustard, 15 minutes to 1 hour for dusty mustard, before any symptoms

occur.  This latent period may cause problems of diagnosis, triage and initial

treatment; however the latent period decreases with increasing concentration of

mustard exposure.



Skin absorption and effects of mustard are enhanced with warmth and moisture

making area so the skin such as the groin and armpits exceptionally sensitive to

the effects of mustard.  Of the mustard that contacts the skin, approximately 80%

will evaporate and 20% will penetrate the skin, of which about 18% will be

absorbed into the circulation producing systemic effects and 2% becomes fixed in

the skin.  Exposure to minute quantities (0.001 ug/liter) will produce effects

with only a short contact time if decontamination is not immediate.  Dusty

mustard initially produces small rash like red dots on the skin,  while neat

mustard produces a general reddening and itching in the area of contact, both

types of lesions progressing to exudative blister formation.  Exfoliative

pigmentation was observed in the Iranian casualties, with the skin blackening and

then peeling off the epidermis several days later.  This condition was thought

to be an effect of the dusty mustard.  An intermediate stage in the healing of

mustard lesions involves the formation of a friable granulation tissue which

bleeds with minimal trauma and is easily infected, delaying return to duty. 

These lesions are usually handled as a second degree and third degree burns.



The eyes are especially sensitive to mustard causing immediate lacrimation, pain

and severe photophobia on contact, progressing to conjunctivitis, blisters, and

corneal lesions.  Blindness can occur, but is not common.  Contact lenses will

exacerbate vesicant eye injuries by trapping agent and prolonging contact of

mustard with the cornea if left in place; however, they may offer some limited

physical protection during initial exposure.   



Injury to the respiratory tract begins with irritation of the mucous membranes

with coughing and dyspnea, exudative pulmonary effusions, and frequently

progresses to bronchopneumonia.  Dusty mustard causes much more severe lung

damage, probably resulting form additional physical trauma from the silicate

spicules.  Battlefield deaths resulted from acute respiratory injury in about 2%

of Iranian troops exposed to mustard.



The alkylating effects of mustard result in bone marrow depression with

leukopenia occurring within the first 2 weeks and anemia occurring weeks to

months later.  Liver and kidney damage was also common.



Casualty Care, Mustard:



At the beginning of the Iraqi chemical attacks, the treatment varied greatly. 

Medical personnel eventuially developed a standard treatment protocol for mustard

casualtir=es which can be summarized as follows: (1) Eyes (Corneal injuries):

Rinsed with Ringers' solution, 1% cycloplegic eye drops and 20% sulfacetamide eye

drops were applied.  Eyes were bandaged for 24 to 48 hours for irritation and

photophobia.  In addition to sulfacetamide, other topical; antibiotics

(gentamicin, chloramphenicol, or tetyracycline) and steroidal agents

(betamethasone, hydrocortisone, or dexamethason) were used to treat serious

conreal injuries.  Because of the danger of infection, the antibiotics were used

in conjunction with the steroidal agents.  (2) Skin: Decontamination by thorough

washing, 2% sodium thiosulfate topical solution was applied and 20 grtams of

sodium thiosulfate solution was administered IV.  (The sodium thiosulfate

solution was reported to be effective only if initiated within 3 hours of

exposure.  This was not an accepted therapy, but was used empirically.  A more

recent study reported that mustard is degraded through oxidation when it comes

in contact with sodium thiosulfate.)  Injured areas were bathed daily with tap

water and rinsed with physiological saline.  Blisters were drained in a sterile

manner and treated with silver sulfadiazine.  Hydrocortisone was used in cases

of severe inflammation and antibiotic creams and ointments containing gentamicin,

chloramphenicol, tetracycline, and nitrofurantion were applied as needed.  (3) 

Lungs:  Mustard causes the breakdown of the alveolar membranes reluting in

exudative effusion.  Vaporizers were used along with the administration of

expectorants (frequently Benilyn) and cough suppressants (syrups containing

codine were used only when other syrups were ineffective.)  Oxygen,

bronchodilators, and antibiotics were administered as needed when

bronchopneumonia developed (about 80% were administered parenterally becuase oral

administration was considered less safe).  Severe respiratory injury with

congestion, infiltration and dyspnea was treated with endotrachial intubation and

artificial respiration as needed.  (4)  Bone marrow suppression:  When leukocyte

counts dropped below 1200, leukocyte transfusions were administered.  If isolated

leukocytes were not available, whole blood transfusions were administered. 

Additionally, these patients were isolated and given broad spectrum antibiotics. 

(5)  General measures: Intravenous (IV) crystalloid fluid replacement in addition

to IV glucose and sometimes IV hyperalimentation therapy were usually required

as a resultt of persistent nausea, vomiting and diarrhea that usually began

within hours of exposure (by any method) and continued for days.  Parenteral

antibiotic threatments used for septic shock included ampicillin (6 to 10

grams/24 hours), gentamicin (80 mg/3 times/day), chloramphenical (4 to 6 grams/

24 hours), or carbencillin (25 to 30 mg/24 hours).  The use of steroid therapy

in the treatment of septic shock was highly controversial because of the risk of

adverse effects.  European health care professionals  indicated that this

treatment protocol was relatively effective. 



Nerve and Blood Agents:



The blood agent, HCN gas, blocks tissue oxygen utilization, causing death within

minutes.  Iranian troops carried and self-administered amyl nitrite capsules, the

initial antidote and first line of treatment following exposure to cyanide

poisoning, but was also used for mustard casualties and was thought to be

effective for mustard patients even though the protocol was never evaluated.)



The nerve agents, tabun (GA) and sarin (GB), are colorless, odorless,

organophosphate (OP) that disrupt neurotransmission.  These are the deadliest of

the CW poisons which can kill within minutes when inhaled or absorbed through the

skin.  The Iranian troops carried atropine autoinjectors, an immediate self-

administering OP antidote.  As previously stated, because of the hot dry climate,

the limited chemical protective equipment that was available was not usually

worn, and soldiers with beards could not get a tight seal on their masks.  As a

result, unprotected soldiers exposed to the nerve and blood gases usually died

in forward areas and were thus self-triaging.  Additionally, the autoinjectors

frequently malfunctioned or were ineffective, presumably due to their high

temperatures and aging of the injectors and chemicals.  Pyridostigmine

(carbamate) pretreatment was not used by Iranian troops. Soldiers with mild nerve

agent exposure were returned to their units.  Many casualties seen at the aid

stations were suffering from the effects of excessive atropine self-

administration to include atropinism due to inappropriate use.



Casualty Care, Nerve Agents:



The initial victims brought to the mobile treatment points in the first hour

following nerve agent use were usually the most severe cases.  These averaged

from 10 to 15, most being unconscious, with many in respirator arrest.  Over the

next 1 to 3 hours, about 100 patients would be received who had suffered

significant nerve agent intoxication.  This massive parasympathetic stimulation

resulted in symptoms that included dizziness, disorientation, anxiety, salivation

and respirator difficulty from excess secretions.  From about 3 to 6 hours

following agent use, another 400 troops would be received who had experienced

minor exposures to nerve agent.  Although their symptoms were relatively mild

(salivation, diarrhea, miosis, minor respiratory problems and general

discomfort), they were often disoriented and hyperactive, rocking incessantly and

physically difficult to manage.  Troops overdosed on atropine would continue to

arrive up to a day following each incident.  



Severe nerve agent casualties with respirator problems only were saved with the

available therapy.  Comatose casualties who did not evidence cardiovascular

problems were treated with very large doses of atropine (50-200 mg intravenous

bolus) and the acetylcholinesterase reactivator, toxogonin (similar, but not

identical to 2 PAM chloride).  These often improved dramatically.  Comatose

casualties who showed signs of significant cardiovascular deterioration (for

example, bradycardia despite administration of standard 2 mg atropine) were not

treated further, as previous experience indicated that they would not recover

probably due to respiratory failure or respirator paralysis.  All of the nerve

agent deaths at the mobile medical points occurred in this group, roughly 1 to

2% of the casualties received.



Toxogonin was in short supply and was considered of dubious value to nerve agent

casualties who arrived hours after exposure similar to the effects of 2 PAM

chloride.  It was mainly given to severe casualties received with 20 to 60

minutes following exposure.  Most nerve agent casualties received only atropine

injections (2 mg/8 hours) and respiratory support as required.  Patients

experiencing cramps were given 30 mg diazepam.  Convulsions were rarely if ever

seen at the medical aid point.  Physicians had no means to determine the nerve

agent dose to which casualties were exposed to the highest agent concentration

never made it to the medical aid point.  



Nerve agent casualties were decontaminated at the medical treatment point by

washing with soap and water and shaving of body hair.  Severe casualties normally

were returned to duty in 4 to 5 weeks, after 2 weeks in rear hospitals and 2 to

3 weeks rest at home.  Troops with significant nerve agent exposure usually were

hospitalized for 1 to 3 days and returned to duty after an additional week's

rest.  Casualties with minor exposures spent 1 to 3 days under observation at a

field hospital and then returned to the front.