1991 PERSIAN GULF WAR: DIRECT AND INDIRECT CHEMICAL WARFARE AGENT AND RELATED EXPOSURES
James J. Tuite, III
I. INTRODUCTION
Since the initial modern use of chemical warfare agents during the First World War, military planners have been acutely aware of their effects and the need to both protect personnel from them and to effectively prevent the enemy from using them. Over the succeeding years, military researchers developed agents that were increasingly powerful and deadly. These developments have enabled battlefield commanders to use fewer, more stable munitions with maximum effect. This enhanced lethality creates a difficult problem for today's military planners. How do you target and destroy the facilities producing and storing these vast quantities of chemical warfare agents, denying the enemy their use, and at the same time prevent the deadly poisons stored at these locations from killing, injuring, or sickening nearby civilian population centers and your own forces? As the stockpiling of these agents becomes more commonplace throughout the world, this dilemma should be of increasing concern to the scientific community because of the potential military, environmental, and medical implications.
In the years prior to the 1991 Persian Gulf War, Iraq focused on the development of weapons of mass destruction, including the development and production of thousands of metric tons of chemical warfare agents and their precursor compounds. The dilemma cited above was one that the coalition of forces assembled against Iraq had to confront directly. Having had clear air superiority and believing that not targeting these facilities would result in widespread Iraqi use of chemical warfare agents, the decision was made to destroy them. Sortie after sortie was directed against storage and production facilities, ammunition bunkers, and other suspected chemical and biological warfare facilities.
Prior to the war, according to representatives of both Sandia and Livermore National Laboratories, there was sufficient concern over the fallout from the bombings of Iraqi weapons of mass destruction facilities among military planners that both the U.S. Army and U.S. Air Force commissioned studies on the subject by these laboratories. Footnote1 The studies and their findings remain classified by the U.S. government. However, prompted by concerns expressed by their own experts, the Soviet Embassy contacted the U.S. Department of State on January 17, 1991, to officially express concern that leakage from the Iraqi chemical and nuclear plants would actually reach parts of the Soviet Union. Footnote2 While portions of the U.S. intelligence reports regarding this issue remain classified, on January 18, 1991, an internal staff report from the Office of the Director for Joint Staff Intelligence confirms that several major chemical weapons facilities had already been targeted. The report went on to confirm that it was unknown if the U.S. was able to monitor the extent of radiological, chemical, or biological contaminants in Iraq. This lack of knowledge, according to the report, was "due to the absence of ground assets in proximity to these facilities. Footnote3 The Soviet government was told: "We have no reason to believe [my emphasis] that the damage caused by U.S./Coalition forces on nuclear, biological, or chemical targets presents a threat to the Soviet Union." Footnote4 These reports confirm that the absence of an ability to collect evidence resulted in an official response suggesting that there was evidence of absence of fallout from the bombings.
Also in the months prior to the conflict, there were reports that Iraqi military personnel had removed chemical agent materials from central production and storage facilities, consistent with the deployment pattern established prior to their use against Iran in the 1980-1988 Iran-Iraq War. Footnote5
On January 7, 1991, intelligence reports confirm that additional chemical weapons were removed from the Samarra Chemical and Biological Warfare Research, Production, and Storage facility. The number of weapons removed and the location to which they were deployed remains unknown. The Defense Intelligence Agency evaluated the activity to be a production run to replace depleted stocks of unstable chemical agent munition fills. Footnote6 Hundreds of tons of bulk chemical warfare agent, precursor materials, munitions, and other hazardous materials were sitll at these facilities when the bombings began
After the initiation of the bombings on January 17, 1991, chemical nerve and blister agents began being detected throughout the region occupied by the coalition forces. Satellite observations show both the direction of fallout distribution and weather anomalies corresponding to the pattern of reported low-level chemical warfare agent detections in areas occupied by coalition forces. Scientific and instrumental observations involving wet chemistry, mass spectrometry, ion mobility spectrometry, chemical and biochemical reaction, and ionization, all indicated the locations to which the materials progressed. The properties of the materials targeted and the types of weapons used in the effort to destroy them and other reports of the absence of medical effects in areas where they were expected and the presence of medical effects in areas impacted by the observed phenomena all support the hypothesis outlined in this paper that allied bombings of Iraqi chemical warfare agent facilities pumped chemical weapons agents, their precursor materials, and their toxic by-products, into the passing weather patterns, which carried the toxins into allied-occupied areas before they returned to the earth's surface.
METHODOLOGY: An examination of the events of the 1991 Persian Gulf War as if it were a scientific experiment requires identifying the location of the materials involved, understanding the physical properties of the materials involved; understanding the method of material destruction; verifying the reliability of the sensor technology deployed and related data collected; and examining satellite, surface weather, and constant pressure data regarding meteorological patterns; and, examining undefined variables and available animal and human subject data. Two periods of weather data are examined: conditions during a meteorological phenomena that occurred from January 17 - January 24, 1991, and the prevailing meteorological patterns during the remainder of the war.
This factual data, discussed in detail below, supports the hypothesis that many coalition forces were exposed to varying levels of chemical warfare agents over the period of the war as a result of the coalition bombings of Iraqi chemical warfare agent facilities. Other cases in which these materials were reliably detected or discovered at locations other than those disclosed by the coalition governments thus far are also examined in Annex 1.
GOAL: To determine the hazard associated with the stockpiling and deployment of chemical weapons and the problems inherent in denying a potential adversary their use.
X. HUMAN EXPOSURE ISSUES
Chemical nerve agents are organophosphate poisons that operate by disrupting the metabolic process, causing the buildup of a chemical messenger (acetylcholine) by inhibiting the production of acetylcholinesterase, a key regulator of neurotransmission. According to material safety data sheets prepared by the U.S. Army Chemical Research, Development and Engineering Center, Aberdeen Proving Grounds, Maryland, the inhibition of cholinesterase enzymes throughout the body by nerve agents is more or less irreversible, so that their effects are prolonged. Until the tissue cholinesterase enzymes are restored to normal activity, probably a very slow regeneration over a period of weeks or 2 to 3 months if damage is severe, there is a period of increased susceptibility to the effects of another exposure to any nerve agent. During this period the effects of repeated exposures are cumulative; after a single exposure, daily exposures to concentrations of nerve agent insufficient to produce symptoms may result in the onset of symptoms after several days. Continued daily exposure may be followed by increasingly severe effects. The degree of exposure required to produce the recurrence of symptoms, and the severity of these symptoms, depends on the duration of exposure and time intervals between exposures. Increased susceptibility is not specific to the particular nerve agent initially absorbed. Footnote19 See MSDS for Soman, Sarin, Tabun, and VX in Appendix A.
Many soldiers became sick during the air war, at the same time that the chemical alarms began sounding repeatedly. This illness became widely known among the soldiers as the "Saudi flu." This illness was characterized by the soldiers as causing a flu-like illness and many also claimed to have rashes, consistent with over-exposure to organophosphate poisons. The soldiers also began taking the nerve agent pre-treatment pill, pyridostigmine bromide, during this period. In some cases, it is hard to differentiate what caused the Saudi flu, since according to Army medical studies, the pills are believed to have caused adverse side effects in about 50% of those to whom they were administered.
Further, pyridostigmine bromide (a carbamate rather than an organophosphate cholinesterase inhibitor, and believed to have reversible effects), while improving the survival of animals exposed to soman and treated with atropine and 2-PAM, may actually make individuals more vulnerable to other nerve agents, such as VX and sarin. Footnote20 In addition, many of the individuals who reportedly were ill, did not take the pills at all. It is also interesting to note that, according to A Comparative Study of Warfare Gases: Their History, Description, and Medical Aspects, by H.L. Gilchrist, published as an Army Medical Bulletin in 1923, "in [mild] poison gas cases similar conditions are noted as in influenza cases."
In 1974, Dr. Karlheinz Lohs, then the Director of the Institute of Toxicology of the German Democratic Republic's Academy of Sciences, in a review of the literature, concluded that mustard chemical warfare agents are capable of producing a wide range of mutagenic, carcinogenic, hepatoxic, and neurotoxic effects. Studies conducted of the delayed toxic effects on individuals exposed to organophosphorous chemical nerve agents and pesticides were summarized by Dr. Lohs. He grouped the types of symptoms observed as follows: Footnote21
Group 1: suffered from pathologies resulting from acylation -- the inhibition of cholinesterase, chiefly acetylcholinesterase. The symptoms are similar to those in acute cases of poisoning, including constriction of the pupil, visual adjustment spasms, bronchoconstriction, bronchospasm, lowered pulse rate, nausea, vomiting, abdominal cramps, diarrhea, urinary and fecal incontinence, pallor, increased salivation, perspiration, tearing, increased blood pressure, tremor, muscular weakness, cramps, possible paralysis, insufferable headaches, feelings of anxiety, speech and balance disorders, and depression of the respiratory center.
Group 2: suffered from pathologies resulting from alkylation of DNA or the biogenic amines of the central nervous system, or both. They take the form of delayed and permanent pathologies of the central nervous system. Teratogenic (referring to deformities in embryo development), mutagenic, carcinogenic, hepatoxic, and hematoxic symptoms also arise.
Group 3: suffered from pathologies not individually known -- metabolites, and so on. The major clinical manifestations take the form of impotence, paralysis, and eye diseases.
According to this literature, actual clinical manifestations of any known case of organophosphorous poisoning are compounded from each of these groups to varying extents. Other symptoms described as neurological or psychopathological are tinnitus (ringing in the ears); speech difficulties; memory defects, especially slowness in recall; weakness; insomnia; drowsiness; concentration difficulty; mental confusion; uneasiness; and somnambulism with excessive dreaming. Dissociation and schizophrenia have also been noted in some cases. The manifestation of these symptoms are subject to marked individual variation.
XI. SCOPE OF THE ILLNESS
Early in the investigation into this issue, only U.S. soldiers were believed to be ill. However, at present similar cases are known to exist in the U.K., the Czech Republic, Canada, Australia, Kuwait, and Iraq, suggesting that the illness is the result of some sort of regional or environmental problem.
XII. RECENT STUDIES
Neurological Damage in Persian Gulf War Veterans
On March 27, 1996, Dr. Goran Jamal, from the Southern General Hospital, at the University of Glascow, Scotland, published in the Journal of Neurology, Neurosurgery, and Psychiatry of the British Medical Association the results of a study he conducted regarding neurological dysfunctions as they relate to Gulf War Syndrome. In the study, Dr. Jamal reports on a group of fourteen gulf war veterans with unexplained illness who were randomly selected from a large list. He compared the functional integrity of the peripheral and central nervous system with a group of age and sex matched healthy controls using pre-determined outcome measures. The latter included
scoring of symptoms and clinical neurological signs; quantitative sensory testing of heat, cold, and vibration sensibility; motor and sensory nerve conduction studies on upper and lower limb; needle electromyography of distal and proximal muscles; and, multi-modality evoked potentials (Visual, brain stem and somatosensory). Four parameters, all related to peripheral nerve function, showed statistically significant abnormalities between the populations at the 95% confidence limit, while a further two parameters were different at the 99% level. Jamal and his associates have concluded that there is evidence of peripheral nervous system damage in the Gulf War veterans.
In subsequent press interviews, Jamal, known for his work on occupational organophospate poisoning and post viral fatigue, said the damage observed was similar to that caused by exposure to organophosphate poisons, but he has not claimed to have identified the direct cause of the damage.
Immunologic Anomalies
On March 28, 1996, in testimony before the U.S. House of Representatives Subcommittee on Human Resources and Intergovernmental Relations, Dr. Howard B. Urnovitz, a research microbiologist from California, released the results of a new study investigating the underlying causes of Persian Gulf War Related Illnesses (PGWRI). Dr. Urnovitz presented data on the failure of veterans to mount an expected antibody response to a booster vaccine that many of the veterans received.
The study was designed to test whether military personnel who had developed symptoms of Persian Gulf War Related Illnesses (PGWRI) had the expected antibody responses to the oral polio vaccine which military personnel were given, according to government records. The serum survey was conducted on age-matched subjects in three groups: 1) 345 randomly selected non-military civilians, 2) 134 subjects deployed to the Persian Gulf -- many of whom have symptoms consistent with PGWRI (35 veterans from California and 99 >from Arkansas) -- and 3) 32 Arkansas veterans who were not deployed.
The response of the random civilian population showed the expected level of antibody to all three strains of polio virus. Only a small difference was noted among the test groups with respect to the antibody response to polio serotype 1. In contrast, the serum from the military test groups (both those deployed and not deployed to the Persian Gulf), showed an unexpectedly low antibody response to polio serotype 2. Moreover, only the deployed military personnel showed a low antibody response to polio serotype 3. The levels found in the non-deployed group of veterans were not significantly different from that of the general public.
According to this research, the immunologic abnormality of the antibody response to polio vaccines in deployed veterans raises serious questions about the ability of Gulf War veterans to contain common microbial infections. The toxic exposure to chemical agents may have had multiple effects directly and indirectly on the body's ability to ward off what are commonly referred to as "opportunistic infections". It is not clear whether, in addition to nerve tissue damage, immune-related tissue was also directly damaged by chemical agent exposure.
There is a real concern that the unexplained illnesses associated with the Gulf War veterans put themselves and family members at risk for infections of unknown origin. It is difficult to discern whether the continued unresolved central and peripheral nervous system, gastrointestinal, muscle and skin disorders are a result of direct chemical agent exposure, such as described in the literature related to organophospate induced delayed neuropathies (OPIDN), a possible secondary manifestation of "post viral fatigue syndrome," or more likely, a combination of both. The anecdotal reports of family members with unexplained illnesses and a concern for an increase in birth defects raises the level of these concerns.
XIII. SUMMARY OF CHEMICAL WARFARE AGENT EXPOSURE DURING THE WAR
PERIOD ONE: JANUARY 17, 1991 - JANUARY 24, 1991
During this critical period, coalition forces targeted and bombed the key Iraqi chemical warfare research, production, and storage facility at Samarra (Muthanna) on 17 January 1991, major chemical warfare agent production and storage facilities at Habbaniyah I, Habbaniyah II, and Habbaniyah III ( also known as Fallujah I, II, III) on 17-18 January 1991, and chemical weapons storage facilities at An Nasiriyah and Ubaydah Bin Al Jarrah Airfield on 17 January 1991. This pattern of chemical weapons facility bombing activity is likely incomplete, but the bombings of these critical targets are confirmed in contemporaneous intelligence reports. The pattern of bombing activity, and particularly the bombing of the major production and storage facilities at Habbaniyah I, II, III on January 17-18, 1991, was concealed by omission in a report by the Defense Intelligence Agency (DIA) to the Defense Science Advisory Board Task Force investigating Desert Storm Syndrome. Footnote22
Satellite Data
Shortly after the initiation of the air war and throughout the period covered in this section (January 17-24, 1991) a low pressure system over Iraq and a high pressure center over the Indian Ocean resulted in a stationary frontal pattern and the development of low-level cloud and fog activity directly over the area occupied by coalition forces. The following datasets identify meteorological imagery from NOAA-11 that provide contemporaneous visual evidence of this activity which stalled the free movement of vapor and air >from Iraq directly over positions occupied by deployed troops.
Pattern of Reliable Detector/Sensor Activity
No single detection of chemical warfare agents viewed in isolation can reveal a pattern of activity, particularly a pattern of fallout activity. However, a broader overview analysis of this period provides detailed insight into the cause of many of the reported detections, the associated phenomena, and the widespread reporting of dead animals, flu-like illnesses, rashes, and M8A1 ionization alarm soundings. In addition to the M8A1 alarm, a broad array of equipment used varying technologies to detected and confirmed the presence of chemical warfare agents as well as to identify the specific agents present. The following is a listing of the different physical principles used by this equipment::
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