Mycotoxins and Gulf War Illness: A Possible Link

by Jonathan B. Tucker, Ph.D.

A tantalizing unsolved mystery of the Persian Gulf War took place on the early morning of January 19, 1991, the third day of the Coalition air campaign against Iraq. Nearly 750 construction specialists (Seabees) with the 24th Naval Mobile Construction Battalion were housed in two camps near the port of Al Jubayl in northern Saudi Arabia. Camp 13, also known as Camp Rohrbach, was situated west of the commercial port, while a smaller Air Detachment was located south of the port, at King Abdul Aziz Naval Air Station.

At about 3:00 AM on the morning of January 19, a brilliant flash of red light appeared in the cloud-covered sky over the port of Al Jubayl. The flash was followed by a loud double-explosion and a shockwave powerful enough to knock over tents at Camp 13 and awaken the sleeping troops. According to one eyewitness, "The concussion was so strong that it knocked me to my knees." [1]

Almost immediately, the general-quarters alarm began to sound. Thomas Harper, communications chief for the Air Detachment, heard a warning message come over the camp radio net: "Alpha 6 Bravo [the unit's call sign], we have a confirmed chemical agent." The radio then broadcast a message to all stations ordering the troops to don their gas masks and chemical-protective suits and proceed to bunkers. There was also a call for chemical decontamination teams. [2]

Near-panic broke out as the Seabees struggled to pull on their masks and rubberized suits. As the troops emerged from their tents and ran to the bunkers, they smelled a sharp, acrid odor and saw a dense yellowish mist floating over the camp. Many individuals did not mask in time or failed to achieve a good seal. They began to choke, and a few had profuse nasal secretions that fouled their masks. Fred Willoughby felt his mouth, lips, and face go numb, a sensation similar to Novocain at a dentist's office. Roy Morrow and Nick Roberts experienced a burning sensation on their exposed skin and a strange metallic taste, "like sucking on a penny." [3]

A half-hour later, the all-clear sounded. The Seabees emerged from the bunkers and ran to the water buffaloes to wash their burning skin, which had become red and inflamed. Although many troops were convinced they had been exposed to a chemical attack, their commanding officers told them the explosion had been the "sonic boom" of a jet fighter passing overhead and ordered them to stop discussing the incident and return to barracks. Radio operators in the command bunkers were later ordered to burn their log pages covering the period of the incident. [4]

When the sun rose later that morning, Nick Roberts observed a thin coating of yellow powder on tents and vehicles. Other Seabees noticed that an area near the entrance to the commercial port of Jubayl had been cordoned off with yellow hazard tape, and that a fenced-in herd of animals nearby had died. Later that day, the battalion's chemical officers collected each soldier's chemical-protective suit and replaced it with a new one, the only time such a gear exchange took place during the war. Because of a shortage of equipment, routine replacement of chemical suits was extremely rare during the Gulf War, if it occurred at all.

Within a few days after the mysterious double-explosion, those Seabees who had experienced burning skin, facial numbness, and choking began to suffer from flu-like symptoms, including fever, sweating, diarrhea, and muscle cramps and spasms. Areas of skin that had been exposed during the incident broke out in rashes, welts, and small blisters, which eventually burst and turned into ulcerating sores that scabbed over and healed but later recurred. The Seabees' joints also began to ache, and the pain became progressively worse. Several developed painfully swollen lymph nodes.

For many of those affected, the symptoms have persisted ever since. According to a telephone survey conducted by The New York Times in September 1996, of 152 veterans of the 24th Naval Mobile Construction Battalion who were contacted, 114 said they were sick with chronic illnesses they attributed to the war. The symptoms they reported were strikingly consistent: chronic diarrhea, joint pain, muscle spasms, mysterious tumors and skin rashes, chronic fatigue, recurrent headaches, and memory loss. Dozens of veterans said they had been hospitalized repeatedly and had been forced to give up their jobs and careers. [5] Nick Roberts has been diagnosed with non-Hodgkin's lymphoma, a cancer of the lymphatic system, and he claims that several other Seabees who served at Al Jubayl have developed lymphatic cancers as well. [6] The Pentagon's Explanation

The Department of Defense (DoD) now contends that the loud noise heard by the Seabees on the early morning of January 19, 1991 was probably the explosion of an Iraqi Scud missile, contradicting the initial explanation by unit commanders that it had been a sonic boom. According to a Pentagon statement, a review of battle records indicates that "a Scud missile aimed toward Dhahran [Saudi Arabia] was intercepted at high altitude in the area [of Al Jubayl] around the time of the... incident."" [7] DoD officials deny that the Scud carried a chemical warhead, since the burning skin and other acute symptoms reported by victims are not consistent with the effects of standard chemical-warfare agents. [8] Mustard gas, for example, does not cause an immediate burning sensation on the skin, facial numbness, or a metallic taste in the mouth; instead, it induces painful skin blisters that appear between three and eight hours after exposure.

The alternative explanation offered by the Pentagon is that the Seabees may have been exposed to a toxic propellant released from an intercepted Iraqi Scud as it broke up in the atmosphere. [9] It is known that the Iraqis used red fuming nitric acid (RFNA), a highly corrosive chemical, as an oxidizer for the kerosene fuel in their ballistic missiles. When a Scud was damaged by a Patriot missile, the RFNA remaining in the oxidizer tank was often dispersed. As a result, individuals downwind of a Scud intercept may have been exposed to droplets of nitric acid and toxic vapors of nitrogen dioxide, the reddish-brown smoke that RFNA gives off as it evaporates.

According to a CIA analysis, individual exposures to RFNA released from an intercepted Scud would depend on several factors, including proximity to the impact site, level of shelter and chemical protection, the amount of RFNA remaining in the fuel tank, the amount released when the missile broke up, and the prevailing atmospheric conditions. The worst-case hazard area could be as large as 2-3 kilometers downwind and 100 to 200 meters wide. Toxicological studies of nitrogen oxides indicate that the first symptoms of exposure appear after a period of 4 to 30 hours, during which victims feel extremely fatigued and show signs of abnormally low blood pressure. After this latent period, acute symptoms develop, including headache, dizziness, lassitude, nausea and vomiting, cyanosis (a blue tinge to the mucous membranes), anxiety, difficulty breathing, and suffocation. [10]

There are three problems with the Pentagon's hypothesis, however. First, the U.S. intelligence community did not detect an Iraqi Scud launch against Saudi Arabia in the early morning of January 19, 1991. The U.S. Central Command Nuclear, Biological and Chemical (NBC) Desk Log makes no mention of a Scud launch associated with the Al Jubayl incident. Similarly, the intelligence chronology kept by the 11th Air Defense Artillery Brigade reports four Scud launches against Israel that night, but none against Saudi Arabia. [11]

A second problem with the Pentagon's explanation is that although RFNA is a highly corrosive acid, none of the exposed troops observed any damage to their rubber gas masks, protective garments, weapons, ponchos, canteen containers, or tents. Third, whereas nitrogen oxides produce a reddish-brown smoke, eyewitnesses of the Al Jubayl attack have consistently reported a "yellow-green fog or mist floating through the air." [12]

These discrepancies suggest that the Al Jubayl attack may have come from another source. Although a notarized affidavit prepared by eyewitness Thomas Harper reports the rumor that an Iraqi MiG jet fighter was shot down over the port of Al Jubayl, it is possible that some other type of aircraft was involved. [13]

According to Theodore Myers, who was present at Al Jubayl that night and has since developed symptoms of Gulf War illness, two Patriot missiles were launched during the incident. According to Myers's eyewitness account:

"I was at Fleet Hospital 5 [in Al Jubayl] when my rack [ed note: In USMC jargon a rack is a bed] shook so hard it moved at least a foot. As I stood there startled, the Marines that patrolled our perimeter shoulted into the tents to go to the bunkers, since two Patriots from across the street had been fired. We went to the bunkers without putting on any protection, as there were no alarm sirens going off. We were there about 10 or 15 minutes when our security people told us to go back to the tents, that everything was all-clear. When I got back in the tent, our sirens went off and we went to MOPP-4. Too late though, since we had just spent at least 10 minutes standing outside unprotected. I never did get all my gear on, nor did many others . . . Later that day, I had to go tot the base for something and as I passed the Patriots, I noticed that all the [missile] casings were green, except for two that were yellow. I don't know if that means they were fired or replaced. [14]

Although the Patriot system served primarily to intercept Iraqi Scuds during the Gulf War, it was originially developed as an air-defense weapon and was presumably more effective in this mode. Thus, it is possible that the two Patriots launched at Al Jubayl the night of the incident were aimed at an intruding Iraqi aircraft rather than a Scud missile.

What type of Iraqi aircraft could have been involved in a chemical/biological attack on Al Jubayl? One clue comes from a declassified U.S. intelligence report, dated October 1991, which states that an Iraqi Su-22 Sukhoi Fitter is the export version of the Su-17M, a single-seat variable-geometry ground attack fighter manufactured by the former Soviet Union. [15] The U.S. intelligence report includes the following observations:

A photograph taken during the multinational invasion of Iraq, at [Tallil] airbase approximately 10 kilometers southwest of An Nasiryah, reveals a possible chemical/biological spray tank on the inboard port side pylon of a probable Su-22 aircraft. The jet aircraft bears an Iraqi flag and appears to have been either hit or blown in-place by coalition gunfire/bombs. Enlargements of the original picture reveal a possible 'air scoop' on the top-front of the tank, thus the hypothesis of a possible C/B spray tank. This tank also has an access panel on its port side. Additionally depicted are an outboard fuel tank, a jack holding up the port side wing, and a blown vehicle to the left of the aircraft. [16]

The accompanying analysis notes that the design of the tank seen in the photo was consistent with a "dry agent spray tank" (such as would be used to deliver a freeze-dried biological toxin) and that the jack holding up the left wing suggested that the Iraqis were trying to remove something important under the wing. Further, the blown-up vehicle next to the aircraft was not a standard chemical decontamination truck but "did contain hoses and tubing which could indicate a non-standard decon vehicle for C/B munitions." [17]

A second mention of the Iraqi Su-22 as a possible biological weapons delivery system occurs in a declassified 1992 CIA document on "Iraqi BW mission planning," also posted on GulfLINK. The sanitized document reads as follows:

In the fall of 1990, Iraqi President Saddam Husayn ordered that plans be drawn up for the airborne delivery of a biological warfare (BW) agent . . . The plan called for a test mission of three MiG 21's to conduct an air raid [deleted] using conventional high-explosive ordnance. If these aircraft were able to penetrate [deleted] air defenses and successfully bomb [deleted] thena second mission was to take off within a few days of the first, using the same flight path and approaches. The second mission, also composed of three MiG 21's carrying conventional ordnance, was to serve as a decoy for a single Su-22 aircraft following the same route but flying between 50 and 100 meters altitude. Optimal delivery altitude for the BW agent was judged to be 50 meters at a speed of 700 kilometers an hour. While wind and weather conditions would be critical to the effectiveness of a BW mission, for security reasons there was no intention to involve air force meteorologists in mission planning. [portion deleted] Shortly after hostilities began . . . the three-MiG mission took off from Tallil Airfield, near An Nasariyah. All three aircraft were shot down early in the mission, and as a result plans to launch the Su-22 armed with a biological agent and flying under cover of a second, decoy mission were cancelled. [18]

Despite the concluding sentence of this report, it is possible that another Su-22 equipped with a biological spray tank did manage to penetrate Coalition air defenses and attack the port of Al Jubayl before it was shot down by the Patriot missiles. Another hypothesis is that an Iraqi propeller-driven aircraft was intercepted over Al Jubayl. A 4:40 AM entry in the U.S. Central Command NBC Desk Log, recorded an hour and a half after the double explosion, notes that a British liaision officer near Al Jubayl "herd [sic] a propeller driven aircraft in the area" shortly before the incident. [19] Iraq was known to possess several Swiss-made Pilatus PC-7 or PC-9 propeller-driven planes, which were based at Umm Qasr (near Basra in southern Iraq) and used to deliver chemical weapons during the Iran-Iraq War. [20] A GulfLINK document dated February 2, 1991, also reports that "chemical bombs" were stored at Umm Qasr airfield during the Persian Gulf War. [21]

Pentagon officials insist that no Iraqi aircraft could have penetrated Saudi airspace as far south as Al Jubayl, since it would have been detected by an AWACS radar aircraft stationed over the Persian Gulf and intercepted immediately by U.S. fighters. The possibility remains, however, that a low-flying Iraqi plane or an unmanned drone could have been misidentified as an allied aircraft or simply lost in the ground clutter. Indeed, the famous flight of the young German pilot Mathias Rust, who flew a propeller plane from West Germany to Moscow's Red Square in May 1987 without being detected, suggests that even the densest air-defense networks can be fallible when it comes to small, low-flying aircraft.

In sum, it is conceivable that a single Iraqi aircraft (either an Su-20 or a Pilatus PC 7/9) may have penetrated Coalition air defenses in northern Saudi Arabia and disseminated a toxic agent over the commercial port of Al Jubayl, after which the plane was shot down by two Patriot missiles. The detonation of the Patriot warheads, followed shortly thereafter by the explosion of the plane's gas tanks, would account for the reported double blast (detonation-concussion) and shockwave. A cloud of toxic agent may then have drifted downwind, exposing the Seabees in the two camps near the port.

If such a scenario did occur, what type of toxic agent could have been involved? None of the standard chemical-warfare agents (blister agents such as mustard or lewisite, nerve agents such as sarin or VX) have either acute and chronic effects consistent with those reported by victims of the Al Jubayl incident. Only one known family of biochemical agents can cause many of the symptoms experienced by the affected troops: mycotoxins, a broad class of naturally occurring fungal poisons associated with serious illness and death in humans. Two families of mycotoxins are potential suspects, the aflatoxins and the trichothecenes. Aflatoxins

Aflatoxins are a family of toxins produced by the fungal mold Aspergillus, which infects peanuts and other food grains. Although aflatoxins are generally considered to be non-lethal in humans, they are of medical concern because they are extremely potent inducers of liver cancers, which may develop months to years after exposure. Ingestion of large amounts of aflatoxin may also result in severe liver damage and acute symptoms, including death. According to a U.S.Army field manual on chemical and biological warfare agents, "Aflatoxins are not only toxic; they also induce cancers, malformations, and mutations. Because their effects, although severe, are relatively slow to appear, aflatoxins may not be viable as [warfare] agents." [22]

In 1995, four years after the end of the Gulf War, inspectors with the United Nations Special Commission on Iraq (UNSCOM), the U.N. agency responsible for uncovering and eliminating Iraq's weapons of mass destruction, determined that Iraq had produced large quantities of aflatoxin. According to an UNSCOM status report released in October 1995, Iraq admitted that it had begun studies of aflatoxin in May 1988 at a biological weapons laboratory near the town of Al Salman. The U.N. report notes, "Research was conducted into the toxic effects of aflatoxins as biological warfare agents and their effect when combined with other chemicals." [23] To this end, Iraqi scientists studied the effects of these toxins on sheep, donkeys, monkeys, and dogs in the laboratory and in a special inhalation chamber, as well as in the field. Iraqi Production and Weaponization of Aflatoxin

Iraq also admitted to UNSCOM that it had engaged in the large-scale production and weaponization of aflatoxin. Beginning in 1988, Iraq cultivated the toxin-producing mold Aspergillus in five-liter flasks at the Al Salman facility. In 1989, production of aflatoxin for biological-weapons purposes was moved to another plant near the town of Fudaliyah. Here, between April and December 1990, Iraqi scientists produced a total of about 1,850 liters of concentrated aflatoxin in solution. [24]

In November 1989 and in May and August 1990, Iraq conducted weaponization trials of aflatoxin in 122mm artillery rockets and R400 aerial bombs. In December 1990, aflatoxin and two other biological-warfare agents (anthrax spores and botulinum toxin) were filled into R400 aerial bombs and warheads for the Al-Hussein missile, an extended-range version of the Soviet Scud. To date, Iraq has admitted producing a total of 2,200 liters of concentrated aflatoxin, of which 1,580 liters were filled into 16 aerial bombs and two missile warheads. [25]

Baghdad claims that all of its biological weapons, including those filled with aflatoxin, were deployed in early January 1991 at sites well north of the Kuwait Theater of Operations (KTO) and remained unused throughout the Gulf War. According to Iraqi declarations, the aerial bombs filled with biological agents were deployed to three remote airfields, where they were placed in open pits, covered with canvas, and buried with dirt to shield them from attack. The biological warheads for the Al-Hussein missiles were reportedly hidden in a railroad tunnel and in earth-covered pits near the Tigris canal. [26] Given Iraq's long record of falsehood and deception with respect to its biological-warfare capabilities, however, these statements should not necessarily be taken at face value.

Military Utility of Aflatoxin

Iraq's motivation for producing and weaponizing aflatoxin remains unclear. It is possible that Iraq may have sought to induce long-term illnesses in Coalition troops, an approach that would be consistent with Iraq's strategy of attrition against Iran during the 1980-88 Iran-Iraq War. Alternatively, aflatoxin have been intended to function as an incapacitant or a lethal agent in large doses. Some Western experts speculate that the Iraqis learned from animal testing that high concentrations of aflatoxin, disseminated as an aerosol, have far more immediate and devastating effects than the slow induction of liver cancers associated with the ingestion of small doses. [27]

According to a CIA report on intelligence and Gulf War illnesses, published on the Internet in August 1996,

With the possible exception of aflatoxin, all declared Iraqi agents were intended to cause rapid death or incapacitation. The only documented effects of aflatoxin in humans are liver cancer months to years after it is ingested and symptoms--possibly including death--caused by liver damage from ingestion of large amounts. Effects of aerosolized aflatoxin are unknown. UNSCOM assesses that Iraq looked at aflatoxin for its long-term carcinogenic effects and that testing showed that large concentrations of it caused death within days. We have no information that would make us conclude that Iraq used aflatoxin or that it was released in the atmosphere when bombing occurred. [28] [emphasis added]

The italicized sentences indicate that (1) little is known about the toxic effects of aflatoxin aerosols, and (2) the CIA has not obtained conclusive evidence that aflatoxins were either used deliberately by Iraq or were released inadvertently as a result of Coalition bombing of production or storage facilities. Since it is doubtful that the CIA and Department of Defense have conducted a thorough investigation of this issue, the negative formulation reporting a lack of information does not rule out possible exposures. As the saying goes, "Absence of evidence does not mean evidence of absence." Trichothecene Mycotoxins

Trichothecene (pronounced "tri-ko-thee-seen") mycotoxins are a large family of fungal toxins that produce nausea, vomiting, diarrhea, skin irritation, and internal bleeding. Fusarium, Stachybotrys, and other trichothecene-producing molds can infect food grains such as corn, rye, barley, oats, and millet, as well as straw and hay. Historically, trichothecene mycotoxins have been known to cause severe health problems in humans and animals who have eaten contaminated food. [29] In 1944, for example, 30 percent of the population of Orenburg district, near Siberia, was affected by alimentary toxic aleukia (ATA), an often fatal disease caused by the ingestion of trichothecenes.

T-2 toxin and diacetoxyscirpenol (DAS) are the most potent members of the trichothecene family. They have an estimated lethal dose in humans of 3 to 35 milligrams (thousands of a gram), making them moderately toxic compared to chemical nerve agents such as sarin. Nevertheless, microgram doses of T-2 toxin and DAS are sufficient to cause vomiting, sustained nausea, and skin and eye irritation. According to one source, trichothecenes are approximately 10 to 500 times more potent than mustard gas in inducing skin necrosis. [30]

Harvesting and extraction of infected grain can yield large quantities of trichothecenes for warfare purposes. Crude extracts of Fusarium containing a mixture of trichothecenes are more potent than pure T-2 toxin, and aflatoxin interacts synergistically with trichothecenes to increase their combined toxicity. [31]

Military dissemination of these toxins would probably be in the form of a powder or smoke aerosol or, alternatively, sprayed in large, liquid drops as a ground contaminant. Trichothecenes can enter the body by absorption through the skin or eyes, inhalation (in aerosol form), or ingestion in contaminated food or water. When solubilized in the solvent dimethylsulfoxide (DMSO), T-2 toxin and DAS are readily absorbed through the skin. [32] It is also known that trichothecenes are about 10 times more toxic when inhaled as an aerosol than by oral or subcutaneous administration. [33]

An advantage of the trichothecenes from a military standpoint are that they are extremely stable, particularly in dry powder form. They can be stored for years at room temperature with no loss of activity and retain their full potency even after being boiled in water for an hour. Accordingly, these toxins are difficult to decontaminate from clothing and equipment and are highly persistent in the environment, although they are eventually broken down by soil bacteria. [34]

Symptoms of Trichothecene Poisoning

Trichothecenes exert their toxic effects by inhibiting protein synthesis, and are therefore able to harm multiple organ systems simultaneously. They do the most damage to rapidly dividing cells such as those in the lining of the gastrointestinal tract, the bone marrow, and the lymph nodes, giving rise to symptoms similar to those of radiation poisoning. Because there is a large gap between the incapacitating dose and the lethal dose of trichothecenes, many casualties will become sick but not die. The delay in the appearance of symptoms after exposure depends on the dose and the means of delivery. Initial symptoms may occur within an hour of inhalation or as long as 12-24 hours after skin contact. After a single low-level exposure, the peak effects tend to occur in one to three days. [35]

Initial symptoms of trichothecene poisoning are burning and irritation of the mucous membranes, including conjunctivitis (eye inflammation), nasal irritation (with or without bleeding), and sore throat. If the agent is delivered as an aerosol, coughing and shortness of breath are accompanied by burning of the lungs and secondary pulmonary edema. Nausea and persistent vomiting are common, as are diarrhea (which may be bloody) and dehydration. Damage to exposed areas of skin is often extensive: the symptoms range from redness and inflammation to the formation within several hours of small (1 centimeter diameter), hard, fluid-filled blisters. [36] Other early symptoms are shortness of breath, dizziness, chest pain, low blood pressure and rapid heartbeat.

Delayed symptoms of high-dose trichothecene exposure include hemorrhage and necrosis of the mucous membranes, such as the lining of the gastrointestinal tract, resulting in bloody diarrhea; neurological disorders, and depressed bone-marrow activity leading to immune-system impairment and increased susceptibility to multiple bacterial and viral infections. [37]

Because there are no known antidotes to the trichothecenes, treatment is limited to supportive care. Decontamination is possible if the victim washes extensively with large amounts of soap and water, but must be performed immediately after exposure. [38] Although T-2 toxin and DAS are broken down by the body, some of the resulting metabolic products--such as HT-2 toxin--are also highly toxic. (HT-2 toxin is about two-thirds as toxic as T-2 toxin. [39]) Studies have also shown that both T-2 toxin and DAS are lipid-soluble and may persist for weeks in skin and fat tissue. [40] Unfortunately, little research has been done on the chronic effects of sublethal trichothecene exposures. Alleged Use in Southeast Asia

Beginning in the 1930s, the Soviet Union did extensive research on trichothecene mycotoxins, which were responsible for serious epidemics in Russia resulting from the consumption of contaminated grain. In 1981, the U.S. government accused the Soviets and their Vietnamese and Lao communist allies of employing mixtures of trichothecenes (popularly known as "yellow rain") for warfare purposes against resistance forces in Laos, Cambodia, and Afghanistan. [41] The State Department subsequently published two white papers laying out a wide variety of evidence to support these allegations, including analyses of samples of toxic material and of victims' blood and tissue, refugee testimony, defector reports, and classified intelligence such as communications intercepts. [42] A group of independent scientists detected gaps and inconsistencies in the government's case and managed to undermine its credibility with the general public.[43] To this day, however, members of the U.S. intelligence community stand by their conclusions and insist that the allegations of Soviet mycotoxin warfare were true. [44]

Some of the immediate and delayed symptoms associated with reported low-level exposures to "yellow rain" in Laos and Cambodia in the late 1970s are similar to those described by Seabees who experienced the mysterious incident at Al Jubayl. Victims in Southeast Asia who were exposed to a yellow powder, mist, smoke, or dust sprayed from low-flying aircraft experienced an immediate burning sensation on the skin, an acrid odor, and began to retch and vomit in a matter of minutes. Unlike traditional vomiting agents, the vomiting induced by yellow rain was protracted over hours to days and often contained blood. Victims also experienced severe diarrhea, passing bloody stools up to eight times a day. Other symptoms included dizziness, rapid heartbeat, low blood pressure, chest pain, loss of far-field vision, and the blistering of exposed skin. At higher doses, bleeding under the fingernails and around the eyes, severe bruising of the skin, and bleeding gums were also reported. Finally, people who had been exposed to lethal doses of yellow rain suffered massive internal bleeding from the gastrointestinal tract, bloody vomiting, and death within a few days. [45] Iraqi Involvement with Mycotoxins

Some Western analysts suspect that the former Soviet Union may have transferred chemical and biological weapons technology and expertise to Iraq, possibly including mycotoxin agents. Unsubstantiated evidence also suggests that Iraq may have used trichothecene mycotoxins against Iranian troops during the 1980-88 Iran-Iraq War. According to one account, Iraqi forces employed trichothecenes along with standard nerve and blister agents (tabun, mustard, and lewisite) during a massive attack on Iranian troops at Majnoon Island in March 1984. [46] Belgian chemical-weapons expert Aubin Heyndrickx also reported in 1989 that he had detected trichothecene mycotoxins in the blood, urine, and feces of Iranian soldiers treated as gas victims from the Majnoon Island battle. [47] Heyndrickx's findings were controversial, however, and have not been confirmed by other scientists.

Despite the lack of solid scientific evidence for Iraqi military use of trichothecene mycotoxins during the Iran-Iraq War, the following items are suggestive of a strong Iraqi interest in trichothecene mycotoxins for warfare purposes:

1. One of the chief scientists in Iraq's biological warfare program, Dr. Rihab Rashid Taha al-Azawi, was a specialist in biological toxins who obtained her doctorate in toxicology from the University of East Anglia in England.
2. In 1986, the Iraqi government paid nearly 30,000 West German marks to purchase samples of four trichothecene mycotoxins from Sigma-Chemie in Munich, a subsidiary of a St. Louis-based company that manufactures specialty biochemicals for research institutions. [48] The West German government licensed this sale on the grounds that the quantities of toxin were too small to be useful for military purposes. During subsequent hearings in the German Parliament, however, a representative of the Federal German Intelligence Service testified that Iraq could have made effective use of small quantities of mycotoxins for military research, and that trichothecenes are particularly well suited for sabotage missions and terrorist attacks. [49]
3. In the summer of 1989, Iraq purchased a fungus from an unidentified source in The Netherlands for the production of mycotoxins, according to a declassified U.S. government intelligence report. The report also notes: "The mycotoxins are being developed in a high security laboratory at the Saddam University (332100N/04425000E), Baghdad, IZ [Iraq] for possible biological warfare use." [50]
4. A captured pre-war Iraqi military record, dated April 10, 1990, refers specifically to trichothecene mycotoxins ("yellow rain"). The document is a communication addressed from Tank Battalion Headquarters, 55 Republican Guards, to the chemical company of the Tawakalna Ala Allah Forces Command of the Republican Guards. This record, written on the back of a Form 102 (a receipt for chemical weapons-related equipment) in the space titled "Weapons and assignment numbers, important characteristics of weapons and assignments, quantities, and other remarks," reads as follows:
5. In reference to your letter... dated April 2, 1990, we are sending you our commissioner ([Warrant Officer] Ghanem Nohad Jamell) who has 4 Forms 102. Please give him the yellow rain manual (fungal toxins) number /894 delivered to our unit pursuant to delivery plan number 17. Please review and respond. [51]
6. This document indicates that the Iraqi Chemical Corps had prepared an entire manual devoted to offensive and/or defensive operations with trichothecene mycotoxins, suggesting a major Iraqi military effort in this area. A declassified U.S. Defense Intelligence Agency (DIA) document dated March 1993 describes Iraqi research on a trichothecene-related illness in humans. The report states that Iraqi scientists discovered the first known instance in humans of a chronic diaper dermatitis (skin inflammation) caused by the fungus Stachybotrys atra, which produces reridin A, a trichothecene mycotoxin known to produce disease in animals. The Iraqi scientists reported incidents of humans becoming sick after exposure to Stachybotrys-contaminated straw, and found reridin A to be toxic at a dose of only 0.0001 nanogram. A DIA field note attached to the report states:
1. Identifying a new trichothecene producer could well be related to [Iraqi] CBW research. The agent suspected of being employed in Southeast Asia is T-2, a trichothecene which is a potent "blister-agent-like" toxin. Also of interest is that these scientists mentioned sickness resulting from human exposure. This may well be legitimate work in identifying diaper dermatitis; however, given the admitted stance that Iraq was working on BW agents, this research should be noted for future CBW targeting. [52]
7. In December 1994, the Iraqi government sponsored a conference in Baghdad on "Post-War Environmental Problems in Iraq." At this conference, Iraqi scientists reported that analyses of samples of vegetation, water, and soil had revealed the presence of high levels of five trichothecene mycotoxins that did not occur naturally in the areas of Iraq where the samples were taken. Both T-2 toxin and HT-2 toxin (a metabolite) were also reportedly found in the blood and urine of Iraqi civilians complaining of vomiting, fever, headache, backache, swollen eyes, and chest pain. [53] Based on these findings, Baghdad accused the United States of conducting mycotoxin warfare against Iraq. On its face, the Iraqi allegation is implausible. Moreover, given the difficulty of identifying trichothecenes even with sophisticated analytical techniques, the claimed Iraqi detections must be viewed with skepticism. Nevertheless, it is at least conceivable that mycotoxin weapons were produced and stockpiled by Iraq and then dispersed by U.S. bombing of munitions bunkers and/or forward-deployed bermed munitions, causing collateral exposures to Iraqi civilians as well as Coalition troops. (Crudely bermed open-air storage sites would produce much greater fallout than munitions destroyed in steel-reinforced concrete bunkers.)
8. In 1995, Iraq admitted to UNSCOM that it had done research on milligram quantities of two trichothecene mycotoxins, T-2 toxin and DAS, although it denied any large-scale production of these agents. [54] Given Baghdad's long history of lies and deception, however, this statement should not necessarily be taken at face value. Iraq has already admitted the large-scale production of aflatoxin, and it is at least possible that significant quantities of trichothecene mycotoxins were secretly produced and weaponized as well.

Toxin Weapons and Iraqi Military Doctrine

One possible Iraqi motivation for producing and employing mycotoxins would be to debilitate enemy forces, an approach that Baghdad appears to have seriously considered. Iraqi military planners understood that it is more disruptive to injure rather than kill enemy troops, since dead soldiers require far less attention and resources than wounded ones. According to a U.S. defense analyst, "Perhaps the greatest problem is created when soldiers are physically or mentally incapacitated in such a way that renders them unfit for combat, and without the commander necessarily realizing what has happened or why." [55] The insidious use of toxin-warfare agents would have been consistent with Saddam's overall strategy during the Gulf War, which was to "bleed" the Coalition forces by inflicting high casualties. The Iraqi leader calculated that large numbers of dead or injured American troops would generate strong political pressures from U.S. public opinion to end the war, forcing the Bush Administration to reach a political settlement on Baghdad's terms. [56]

Revealing insights into Iraq's offensive biological-warfare doctrine can be drawn from Iraqi military manuals translated by the U.S. Armed Forces Medical Intelligence Center (AFMIC), now part of the Defense Intelligence Agency. In particular, the Iraqi manuals stress the use of chemical or biological agents to produce non-fatal casualties rather than deaths, with the aim of disrupting the enemy's operations and overburdening his medical and logistical infrastructure. For example, a field manual published by the Iraqi Chemical Corps in 1984, titled Chemical, Biological and Nuclear Operations, discusses the tactical utility of incapacitating biological and toxin agents:

It is possible to select anti-personnel biological agents in order to cause lethal or incapacitating casualties in the battle area or in the enemy's rear areas.... Incapacitating agents are used to inflict casualties which require a large amount of medical supplies and treating facilities, and many people to treat them. Thus it is possible to hinder the opposing military operations. [57]

This doctrine is consistent with Iraq's avowed experimentation with several incapacitating biological-warfare agents, including three non-lethal viruses: hemorrhagic conjunctivitis virus (which produces extreme eye pain and temporary blindness), rotavirus (which causes acute diarrhea that could lead to dehydration), and camelpox (which causes fever and skin rash in camels but may induce a non-fatal illness in humans who are not natives of the Middle East). [58]

Since the end of the Gulf War, senior Iraqi officials have insisted that their biological weapons were strictly weapons of last resort, intended for retaliation against the major cities of regional adversaries (such as Riyadh and Tel Aviv) in the event of a nuclear attack on Baghdad. They have also stated that Saddam Hussein predelegated the authority to launch aerial and missile strikes with biological weapons to the subordinate commanders of the bases where the weapons were deployed. Thus, if Baghdad's communications were cut off or the Iraqi military command destroyed in a "decapitating" enemy attack, a retaliatory strike could still be carried out. [59] In an interview in October 1995, Iraqi Oil Minister Amer Rashid insisted that Iraq would have used biological weapons only in retaliation. "Iraq had no intention of using biological weapons unless the allies or Israel attacked Baghdad with nuclear weapons," he said. [60]

Nevertheless, the veracity of such statements is open to doubt. For example, although Iraqi officials have assured UNSCOM that they destroyed all of their biological weapons after the Gulf War, they have been unable to provide any physical or documentary evidence to back up this claim. Senior UNSCOM officials now believe that the Iraqi statement is false, and that as many as 16 Scud missiles armed with biological warheads may still be hidden on fast-moving trucks to evade detection.[61]

Although UNSCOM has no concrete evidence that any of Iraq's biological and toxin weapons were actually used, none of the weapons has yet been accounted for. Moreover, the fact that Iraq possessed a retaliatory biological-warfare option does not rule out the first use of the same capability, nor does it constitute proof that Iraq's biological arsenal was strictly a weapon of last resort. In any event, Baghdad would clearly have nothing to gain, and much to lose both politically and economically, by admitting that it employed chemical or biological weapons during the Gulf War. In particular, such an admission would make it much less likely that the U.N. Security Council would ever vote to lift the crippling economic sanctions imposed on Iraq in the aftermath of the war. Links to the Al Jubayl Incident

U.S. forces in the Gulf did not possess any field monitoring systems capable of detecting or identifying aflatoxin or trichothecene mycotoxins. At the time of Operation Desert Storm, the only biological agents that U.S. intelligence believed Iraq had weaponized--and that U.S. forces were equipped to detect--were anthrax and botulinum toxin. (The jury-rigged U.S. biological detection system involved the collection of particulate air samples at regular intervals, followed by an antibody-based analysis technique. Because the system did not operate in real-time, it would have detected exposures of U.S. troops to anthrax or botulinum only afteran attack had occurred.) Moreover, although thousands of U.S. troops were vaccinated against anthrax and botulinum toxin, no vaccine or antidote against mycotoxins was (or is) available.

It is known that U.S. Army Technical Escort teams conducted extensive environmental and biomedical sampling for chemical and biological warfare agents in Iraq, Kuwait, and Saudi Arabia during and after the Gulf War. These samples were analyzed at the Naval Forward Laboratory in Al Jubayl or shipped back to Army laboratories in the United States for more sophisticated analysis. The results of most of these analyses remain classified, however, and have not been released even to the Marine units that collected some of the samples. [62]

Despite the lack of sampling data available in the public domain, several unusual characteristics of the Al Jubayl incident, recounted by eyewitnesses, are consistent with possible Iraqi use of trichothecene mycotoxins:

1. Victims of the Al Jubayl attack reported an immediate itching and burning sensation on exposed areas of skin, followed by the formation of small blisters after a delay of several hours, as well as nausea, vomiting, diarrhea, fever, and lassitude. These symptoms are consistent with low-level exposure to trichothecenes. (Unlike mustard gas, which produces painful blisters after a delay of three to eight hours, trichothecenes cause an immediate burning sensation on the skin).
2. The "metallic taste" reported by several eyewitnesses is suggestive of the use of the organic solvent dimethylsulfoxide (DMSO), which facilitates the dissemination of trichothecenes as a fine mist and their rapid absorption through the skin of exposed individuals. [63] After dispersal, the volatile solvent would evaporate, leaving a dry powder residue on exposed surfaces.
3. The "yellow powder" that Nick Roberts observed coating tents and vehicles on the morning after the attack is suggestive of a crude extract of Fusarium fungus, which contains a yellow pigment in addition to a mixture of potent trichothecene toxins.
4. Some wives and children of veterans suffering from Gulf War illnesses report that they have come down with similar symptoms, suggesting that the causative agent may be transferable from one individual to another, perhaps in contaminated clothing or through intimate contact. In addition, several civilian army depot workers who were never deployed to Saudi Arabia but were assigned to clean or repair military vehicles and other equipment returned from the theater have developed characteristic symptoms of Gulf War illnesses. [64] Similar illnesses have also been reported among embalmers who handled the remains of dead U.S. soldiers in the military morgue at Dover Air Force Base. These mysterious phenomena suggest the presence either of an unusually rugged infectious agent or a persistent toxic contaminant. Since mycotoxins are known to be highly stable and difficult to decontaminate, they could provide a possible explanation.

Anomalies

Two anomalies remain to be explained. Shortly after the Al Jubayl attack, Harold Jerome Edwards, the chemical NCO with the Air Detachment of the 24th Naval Mobile Construction Battalion, detected blister agent (e.g., mustard gas or lewisite) in the air using M-256 kits, disposable "chemical labs on a card" that are considered highly reliable. Edwards told Senate investigators in 1994 that after the explosion over the port, he had conducted three M-256 tests. Two of the tests were positive for chemical blister agent; the third test was negative, but was done in a sheltered area between two rows of tents.[65] The U.S. Central Command NBC Desk Log for the period covering the Al Jubayl attack also includes an entry stating that a nearby British unit reported detections of blister agent about an hour after the double-explosion, using two detection methods (M-9 paper and a hand-held Chemical Agent Monitor).[66] As noted above, however, the symptoms reported by sick veterans are not consistent with blister-agent exposure.

There are three possible explanations for this discrepancy. First, although the M-256 kit is not designed to detect mycotoxins, it is possible the presence of these toxins in the air could cause the kit to give a positive reading for blister agent. Controlled laboratory testing would be needed to test this hypothesis. Second, the M-256 kits used at Al Jubayl may have generated a false-positive reading for blister agent if they were beyond their expiration dates. Third, it is possible that the Iraqis used a mixed-agent attack against Al Jubayl involving a "cocktail" of dusty mustard and a crude extract of mycotoxins (trichothecenes and/or aflatoxin). Indeed, the October 1995 UNSCOM status report states that Iraq did research on "the toxic effects of aflatoxins as biological warfare agents and their effect when combined with other chemicals" [emphasis added].

The second anomaly is that U.S. Marine units who were deployed in the same area near Al Jubayl as the affected Seabees--and hence should have experienced a similar toxic exposure--have not reported a high incidence of symptoms typical of Gulf War illnesses. This discrepancy may perhaps be explained by the fact that while most of the Seabees were reservists, most of the Marines were active-duty and thus less likely to report illness for fear of receiving a medical discharge. In any event, there is a need for an epidemiological study comparing the incidence of chronic illnesses in the two groups. Conclusions and Recommendations

A large proportion of the Seabees who were exposed to the mysterious attack at Al Jubayl have developed chronic symptoms considered typical of Gulf War illnesses: severe fatigue, joint aches, memory loss, mysterious gastrointestinal ailments, and skin rashes. Although the evidence for Iraqi use of aflatoxin and/or trichothecene mycotoxins at Al Jubayl remains circumstantial, this hypothesis warrants further investigation.

Iraq has admitted to large-scale production and weaponization of aflatoxin but insists it only did research on small quantities of trichothecene mycotoxins. Given Iraq's record of deceit and deception, however, it would be premature to rule out the secret large-scale production of trichothecenes. UNSCOM should pursue this possibility in future interrogations of senior Iraqi officials.

The results of the extensive chemical and biological sampling operations undertaken by U.S. forces during and after Operation Desert Storm should be declassified and released to the public. If environmental or biomedical samples were found to contain aflatoxins or trichothecene mycotoxins not indigenous to Iraq, this data would provide strong evidence of Iraqi use of toxin weapons.

Scientific knowledge about the physiological effects of low-dose exposures to the trichothecene mycotoxins (particularly in aerosol form) is seriously lacking. More research is clearly needed to assess the long-term medical consequences, if any, of such exposures.

Finally, since lipid-soluble trichothecenes such as T-2 toxin and DAS may persist in fatty tissues for several weeks, if not longer, it would be worthwhile to analyze for mycotoxin residues in blood samples or fat or skin biopsies taken from veterans shortly after they developed symptoms of Gulf War illnesses. Since the half-life of mycotoxins in the body is limited, their absence would not necessarily rule out exposures. Conversely, the discovery of mycotoxin residues in the body fluids of sick Gulf War veterans would provide strong support for the hypothesis presented here.

Jonathan B. Tucker, Ph.D., directs the Chemical and Biological Weapons Nonproliferation Project at the Center for Nonproliferation Studies, Monterey Institute of International Studies (Monterey, CA).

End Notes

1. Philip Shenon, "Many Veterans of the Gulf War Detail Illnesses from Chemicals," The New York Times, September 20, 1996, pp. A1, A12.
2. Thomas L. Harper, notarized affidavit, Meriwether Country, Georgia, June 7, 1993.
3. Author's telephone interviews with Roy Morrow and Nick Roberts, sick Gulf War veterans.
4. Thomas L. Harper affidavit.
5. Shenon, New York Times, p. A12.
6. Author's telephone interview with Nick Roberts.
7. Shenon, New York Times, p. A12.
8. Ibid.
9. Ibid.
10. Central Intelligence Agency, Ballistic Vehicle Analysis Branch, declassified memorandum on "Gulf War Illnesses" dated July 19, 1995.
11. 11th Air Defense Artillery Brigade, Desert Shield/Desert Storm After-Action Report, p. II-B-166.
12. Shenon, New York Times, p. A12.
13. Harper affidavit, op. cit.
14. E-mail message to Patrick Eddington from Theodore Myers, President of Gulf War Veterans of Virginia, December 25, 1996.
15. Mark Lambert, ed., Jane's All the World's Aircraft, 1992-93 (Coulsdon, UK: Jane's Information Group Ltd., 1992), pp. 236-237.
16. Defense Intelligence Agency, "Possible Chemical/Biological Warfare Spray Tank on Su-22 Aircraft," Serial IIR 2 201 0067 92, GulfLINK filename 22010067.92.a
17. Ibid
18. Central Intelligence Agency, "Iraqi BW Mission Planning," 1992, GulfLINK filename 062596_cia_74624_01.txt
19. . Central Command, Nuclear, Biological and Chemical (NBC) Desk Log, Operation Desert Storm, January 19, 1991 (declassified June 9, 1994).
20. Defense Intelligence Agency, "Iraq: Air Force Capability to Deliver Chemcial Weapons As of 4 Jan 91," January 14, 1991, GulfLINK filename 72928819.
21. Defense Intelligence Agency, "Locations of All KNown or Supsected Chemical Storage Sites in the KTO," February 2, 1991, GulfLINK filename 0175pgv.91d.
22. Army Field Manual No. 3-9, Potential Military Chemical/Biological Agents and Compounds (Washington, D.C.: Headquarters, Department of the Army, 12 December 1990), p. 77.
23. United Nations Special Commission on Iraq, Status report, October 11, 1995, p. 26.
24. Ibid, p. 27.
25. Ibid, p. 29.
26. "CIA Report on Intelligence Related to Gulf War Illnesses," August 2, 1996, posted on GulfLink [DoD website on Gulf War illnesses], p. 7.
27. Alan George, "Saddam's Cancer Bombs Scare," Jane's Intelligence Review, December 1996, p. 5.
28. "CIA Report on Intelligence Related to Gulf War Illnesses," p. 7.
29. See Mary Kilbourne Matossian, Poisons of the Past: Molds, Epidemics, and History (New Haven: Yale University Press, 1989).
30. Kenneth S.K. Chinn, Trichothecenes: Are They Potential Threat Agents? (Dugway, Utah: U.S. Army Dugway Proving Ground, DPG-S-83-502 [Sanitized Version], June 1983), pp. 11-13.
31. Colin G. Rousseaux, "Trichothecene Mycotoxins: Real or Imaginary Toxins?" Comments on Toxicology vol. 2, no. 1 (1988), p. 42.
32. B.W. Kemppainen, J.G. Pace, and R.T. Riley, "Comparison of in vivo and i>in vitro percutaneous absorption of T-2 toxin in guinea pigs," Toxicon, vol. 25 (1987), pp. 1153-1162.
33. Rousseau, p. 42.
34. U.S. Army Field Manual 3-9, p. 89.
35. Ibid.
36. Ibid.
37. William B. Burck and Louise-Marie Cote, "Trichothecene Mycotoxins," in Handbook of Natural Toxins, Vol. 6: Toxicology of Plant and Fungal Compounds, edited by Richard F. Keeler and Anthony T. Tu (New York: Marcel Dekker, 1991), pp. 523-555
38. National Research Council, Protection Against Trichothecene Mycotoxins (Washington, D.C.: National Academy Press, 1983), pp. 158-164.
39. Ibid, p. 127.
40. Burck and Cote, op. cit.
41. Elisa D. Harris, "Sverdlovsk and Yellow Rain: Two Cases of Soviet Noncompliance?" International Security, vol. 11, no. 4 (Spring 1987), pp. 41-95.
42. U.S. Department of State, Chemical Warfare in Southeast Asia and Afghanistan: Report to Congress from Secretary of State Alexander M. Haig, Jr., Special Report No. 98, March 22, 1982; and Chemical Warfare in Southeast Asia and Afghanistan: An Update, Report from Secretary of State George P. Schultz, Special Report No. 104, November 1982.
43. Julian Robinson, Jeanne Guillemin, and Matthew Meselson, "Yellow Rain in Southeast Asia: The Story Collapses," in Susan Wright, ed., Preventing a Biological Arms Race (Cambridge, MA: MIT Press, 1990), pp. 220-238.
44. Author's interview with Gary Crocker, Bureau of Intelligence and Research, U.S. Department of State, October 9, 1996.
45. Special National Intelligence Estimate No. 11/50/37-82, Use of Toxins and Other Lethal Chemicals in Southeast Asia and Afghanistan, Volume II -- Supporting Analysis, February 2, 1982 [Declassified with redactions in November 1987], pp. E-1, E-2.
46. Hooshang Kadivar and Stephen C. Adams, "Treatment of Chemical and Biological Warfare Injuries: Insights Derived from the 1984 Iraqi Attack on Majnoon Island," Military Medicine, 1991, vol. 156, no. 4, pp. 171-177.
47. A. Heyndrickx, N. Sookvanichsilp, and M. Van den Heede, "Detection of Triochothecene Mycotoxins (Yellow Rain) in Blood, Urine, and Faeces of Iranian Soldiers Treated as Victims of a Gas Attack," Rivista di Tossicologia Sperimentale e Clinica, 1989, vol. 19, no. 1-3, pp. 7-11.
48. The order was for 500 milligrams of T-2 toxin, 100 milligrams of HT-2 toxin, 100 milligrams of verrucarol, and 2,000 milligrams of diacetyoxyscirpenol (DAS). See Deutcher Bundestag, Drucksache 11/4172, March 13, 1989.
49. "Hundertmal Toedlicher als C-Waffen," Der Spiegel, vol. 43, no. 5 (January 30, 1989), pp. 16-18.
50. Joint Staff, Washington, DC, "Iraq Acquires Fungus for Possible BW Use,"Serial IIR 2 762 0035 90, December 6, 1989.
51. Captured Iraqi military record, "Manual Receipt: Army Form/Sample/Number 102," GulfLINK filename 3tr41_44.m24.
52. U.S. Defense Intelligence Agency, "Iraqi Research on New Mycotoxicosis in Humans," March 3, 1993, Serial IIR 2 201 0507 93, GulfLINK filename 22010507.93a.
53. Foreign Broadcast Information Service, "Iraq: Study Alleges U.S. Used Chemical Weapons in Gulf War," Baghdad INA in English, 08:45 GMT, July 2, 1995.
54. United Nations Special Commission on Iraq, Status report, October 11, 1995, p. 26.
55. Joseph D. Douglass, Jr., "Beyond Nuclear War," Journal of Social, Political and Economic Studies, vol. 15, Summer 1990, p. 149.
56. Interview with General (ret.) Bernard Trainor of Harvard University during the PBS Frontline special, "The Gulf War, Part I,"broadcast on January 9, 1996.
57. Armed Forces Medical Intelligence Center, translation of Manual: Chemical, Biological and Nuclear Operations by Col. Sameem Jalal Abdul Latif, Training Department, Iraqi Chemical Corps, 1984 (Fort Detrick, MD: Foreign Armies Studies Series No. 21, AFMIC-HT-101-92, January 12, 1992), p. 6.
58. United Nations Special Commission on Iraq, Status report, October 11, 1995, pp. 27-28.
59. Reuters, "Iraq targeted 'enemy capitals' if Baghdad nuked," September 21, 1995.
60. Farouk Choukri, "Interview with Iraqi Oil Minister Amer Rashid," Agence France Presse, October 18, 1995.
61. Associated Press, "Weapons inspector: Iraq may be hiding biological-warhead missiles," The Washington Times, March 21, 1996, p. A15.
62. Captain T. F. Manley, Marine Corps NBC Defense in Southwest Asia (Quantico, VA: Marine Corps Research Center, Research Paper No. 92-0009, July 1991), p. 11.
63. H. B. Schiefer, "The Possible Use of Chemical Warfare Agents in Southeast Asia," Conflict Quarterly, vol. 3 (1983), p. 36.
64. U.S. Senate, Committee on Banking, Housing, and Urban Affairs, Hearing: United States Dual-Use Exports to Iraq and Their Impact on the Health of the Persian Gulf War Veterans, May 25, 1994, p. 264.
65. Ibid, p. 294.
66. U.S. Central Command, Nuclear, Biological, Chemical (NBC) Desk Log, Operation Desert Storm, January 19, 1991 (declassified June 9, 1994).