Chapter 1. Iraqi Chemical and Biological Warfare Capability

Over the last ten years, Iraq, a signatory to both the Geneva Protocols of 1925 (prohibiting the use of poisoned gas) and the Biological Warfare Convention of 1972 (banning biological weapons), has expended an enormous amount of research and energy in developing these and other prohibited weapons.

Iraq was believed to have been manufacturing mustard gas at a production facility in Samarra since the early 1980s. It also began an extensive program to produce nerve agent precursor chemicals, taking advantage of its own natural resources. Phosphate mines/industries are at Akashat, Al Qaim, and Rutbah.[1] The Iraqi Al Fallujah gas warfare complex was believed to be capable of producing up to 1,000 tons per month of Sarin, as well as the nerve agent VX[2] In addition, with the assistance of foreign firms, Iraq developed the capability to experiment with hydrogen cyanide, cyanogen chloride, and lewisite.[3] By the start of the Gulf War, Iraqi forces had developed chemical delivery capabilities for rifle grenades, 81mm mortars, 152mm, 130mm, and 122mm artillery rounds; bombs; 90mm air-to-ground rockets; 216 kilogram FROG and 555 kilogram SCUD warheads; and possibly land mines and cruise missiles.[4]

On July 30, 1991, Ambassador Rolf Ekeus, director of the United Nations Special Commission on Iraq (UNSCOM), charged with overseeing the elimination of Iraq's chemical and nuclear arsenals, told the Security Council that U.N. inspectors had found chemical warheads armed with nerve gas. Mr. Ekeus claimed that some warheads found were already fitted onto the SCUD missiles.[5]

Iraq's chemical warfare capability was known to the U.S. government before the war. A month before the war began, then Central Intelligence Agency (CIA) Director William Webster estimated that Iraq possessed 1,000 tons of poisonous chemical agents, much of it capable of being loaded into two types of missiles: the FROG (Free Rocket Over Ground) and the SCUD B (SS1).[6] Jane's Strategic Weapons Systems lists warhead capabilities for the FROG7 as high explosive (HE), chemical, or nuclear, and for the Iraqi versions of the SCUD as probably HE or chemical.[7]

Status of Iraqi Readiness to Use Chemical Weapons Against Coalition Forces

In March 1991, Molly Moore reported from Jubayl, Saudi Arabia that Marine Commanders found no indications of chemical weapons stockpiles on the battlefields of Kuwait. According to a Washington Post report that day, (March 7, 1991), U.S. intelligence analysts claimed that these weapons "never got distributed down to the battlefield" from storage sites north of the Euphrates River.[8] A U.S. military intelligence source stated in March 1991 that "it was a matter of not deploying chemical weapons, rather than not having them, guess ... is they never managed to get it down to division level."[9]

Regarding the presence of chemical weapons and Iraqi readiness to use them against Coalition forces, Committee staff has received the following information:

Dale Glover, of the 1165th Military Police Company, was with the 7th Corps, approximately 75 miles inside Iraq, when they came upon a destroyed artillery site. They entered a bunker that was half uncovered by the bombing. Inside there was a very strong ammonia smell. They discovered leaking chemical munitions inserts packed inside aluminum casings. A test confirmed a blister agent. They went back to their unit and reported what they had found. Mr. Glover recalled that "they didn't get back to us for 2-3 hours, then told us it was a false positive, nothing to be concerned about." However, he said, within hours they were ordered to move from the location where they were camped, about three miles from the bunker. Mr. Glover recalled that they had been at that position only a couple of weeks and had not expected to move that soon. When questioned if the site they discovered was south of the Euphrates, he confirmed that it was.[10]

Another source who identified himself to the Committee but wishes to remain anonymous has informed Committee staff that he also was with the 7th Corps in southern Iraq. Somewhere between As Salman and Bashra (in a position south of the Euphrates River), his unit came upon bunkers containing crates of substances that "made you choke, made you want to throw up, burned your eyes. It smelled like ammonia, only a lot stronger." He could not approach the crates without experiencing immediate breathing problems. He said these crates were leaking.[11]

Chris Alan Kornkven was a Staff Sergeant with the 340th Combat Support Company during the Persian Gulf War. He reported to Committee staff that a U.S. military doctor at the 312th Evacuation Hospital told him that doctors at the hospital had been speaking with Iraqi officers. According to these doctors, the Iraqi officers said that they had chemical weapons at the front, and had authorization to use them, but that the winds in their area were blowing the wrong way.[12]

Several press sources carried reports of encounters with chemical mines by the 2nd Marine Division during the initial mine field breaching operation early on February 24, 1991. According to the Chicago Tribune, which interviewed officers and enlisted Marines involved in the operation, a FOX vehicle confirmed positive readings for a nerve agent and for a mustard gas. A second detecting device gave the same positive reading. General Keys, the 2nd Division commander, and Colonel Livingston, commander of the 6th Marine Regiment, told reporters they believed it was possible that a chemical mine was blown up or hit.[13] General Schwarzkopf told reporters he considered the reports "bogus".[14]

British troops also discovered Iraqi chemical mines on the Gulf battlefield, according to Gannett News Service. A British official (not further identified) said that the incident was reported to Prime Minister John Major's war cabinet; no details were given.[15]

Press reports indicate Iraqi readiness to use these weapons against Coalition forces. The British Sunday Times reported on January 27, 1991, that American intelligence detected greatly increased activity at Iraq's main chemical plant at Samarra in the last week of December, and the British Ministry of Defense said that the Allies believe that Iraq "may have as many as 100,000 artillery shells filled with chemicals and several tons [of bulk agent] stored near the front line." According to the Times report, a British Ministry of Defense official said: "The plant was at peak activity and the chemicals were distributed to the troops in Kuwait and elsewhere in theatre." The Times reported that an unnamed Pentagon source said that Hussein had given front-line commanders permission to use these weapons at their discretion, and that "it was no longer a question of if, but when."[16]

Iraqi soldiers captured by the British units also informed the allies that before the war started, Iraq distributed substantial supplies of chemical weapons along the front lines to be held for the ground war.[17] According to Newsweek, U.S. intelligence sources had reported that Saddam Hussein had ordered his commanders to fire chemical weapons as soon as the allies launched a ground offensive.[18] A British signals officer was reported to have said that "we were tuned into the Iraqi command radio net. We heard them give the release order to their front-line troops to use chemical weapons against Rhino Force if it crossed the border."[19]

Destruction of Iraq’s Chemicals and Chemical Weapons by the United Nations

In April 1993, weapons inspectors from the United Nations charged with locating all of Iraq's nuclear, chemical and biological weapons by UN Resolution 687, confirmed that in Muthanna, 65 miles northwest of Baghdad, Iraq manufactured a form of mustard gas as well as Sarin and Tabun, both nerve agents. This vast desert complex was the nucleus of Iraq's chemical weapons program. During the allied bombing in the early days of the Gulf War, Muthanna was a priority target. It was repeatedly attacked and production sites were destroyed. As United Nations inspectors attempted to destroy Iraq's chemical weapons arsenal, they discovered bombs, missiles, and chemical weapons of mass destruction spread out across this immense complex. Of particular concern were the chemical warheads of Al-Hussein modified SCUD missiles, each filled with five gallons of Sarin. Twenty-eight of these warheads have been drained and destroyed by the UN inspectors. These weapons were not destroyed during the bombings at Muthanna because they had been removed to other locations before the Gulf War started. Their relocation and transfer back to Muthanna was described by UN inspectors as a painstaking process.[20] According to Brigadier General Walter Busbee, U.S. Army Chemical and Materiel Destruction Agency, Aberdeen Proving Grounds, these warheads were exported to Iraq from the former Soviet Union.[21]

Chemical warfare agents which either survived the allied bombing or were inventoried and returned to the Muthanna facility for destruction include:[22]

13,000 155-mm artillery shells loaded with mustard gas;
6,200 rockets loaded with nerve agent;
800 nerve agent aerial bombs;
28 SCUD warheads loaded with Sarin;
75 tons of the nerve agent Sarin;
60-70 tons of the nerve agent Tabun; and,
250 tons of mustard gas and stocks of thiodiglycol, a precursor chemical for mustard gases.

U.N. inspectors have concluded that the Muthanna plant was capable of producing two tons of Sarin and five tons of mustard gas daily. The plant was also capable of manufacturing VX, a nerve gas and one of the most toxic chemicals ever produced.[23]

In addition to Muthanna, chemical agents were destroyed at two airbases: one located 40 miles west of Baghdad and the other located near An Nassiriyah, where a number of 122mm rockets loaded with Sarin (GB) were blown in place. According to UNSCOM sources, many of these weapons were hastily deployed prior to the air war and later returned for destruction. The UN has destroyed hundreds of tons of bulk chemical agents and tens of thousands of chemical munitions. In addition, hundreds of thousands of liters of key chemical precursors which have been identified and destroyed include: 14,600 liters of DF; 121,000 liters of D4 and 153,983 liters of thiodiglycol. According to UNSCOM, the Iraqis were capable of employing both binary and mixed agent weapons. Binary weapons identified used DF. When combined with appropriate chemicals, GB and GF are produced.[24]

UNSCOM also discovered, at various locations, evidence of research into certain biological agents, including botulinus toxin, anthrax, an organism responsible for gas gangrene (clostridium perfringens) and others as identified below. The evidence discovered by the group suggested that this was primarily an offensive biological warfare program.[25]

On February 13, 1994, a clandestine radio service in Iraq, the Voice of the Iraqi People, reported that Saddam, Hussein's government was still attempting to hide chemical and biological weapons from international inspectors by repeatedly relocating them. Citing unidentified individuals, the radio reported that the banned weapons were being hidden in the oil pipelines that have been "out of operation because of the international embargo."[26]

Chemical Warfare Doctrine and the Use of Combined Agent Warfare

There is substantial evidence to suggest that in the use of chemical weapons, as in other military areas, the Iraqi military adhered, at least in part, to Soviet military doctrine. Soviet military doctrine suggested that chemical warfare should be conducted with mixed agents.[27] Mixed agents, often referred to as "cocktails," are intended to enhance the capabilities of nerve agents and defeat the precautions taken by the enemy.[28] Use of mixed agents could account for the wide variety of symptoms displayed by the Gulf' War veterans. Mixed agents can be made by combining a variety of biotoxins, nerve agents, vesicants, blister agents and some biological agents -- such as bacteria and fungi, and others described briefly below.

According to some sources, Iraq used mixed agent weapons combining cyanogen, mustard gas, and tabun against the Kurds. Saddam Hussein stated on April 2, 1990, that Iraq had "double combined chemical" weapons since the last year of the Iran-Iraq War.[29] It was also believed that in 1984 Iraq may have used mixed agent weapons with biological tricothecenes and mycotoxins against Majnoon Island during the Iran-Iraq War.[30]

The utility of chemical weapons and the possibility of exposing one's own troops to indirect chemical weapons effects is an issue which has been seriously debated by both U.S. and Soviet military planners. Soviet doctrine questions the utility of initiating chemical warfare, since chemical weapons produce secondary effects that could obstruct troop advances. U.S. military doctrine warns that, according to its calculations, the use of a nerve agent against a target area of no more than a dozen hectares (a hectare is about 2.47 acres) can, under certain weather conditions, create a hazard zone downwind of up to 100 kilometers in length. Within this downwind area, friendly military units would have to take protective measures .[31]

According to the official military announcements made in the last half of January 1991 and based on the quantity of chemical agents observed by UN inspectors after the war, the scope of coalition bombing against these facilities involved hundreds - if not thousands - of tons of bulk chemical nerve agents, mustard gas, as well as tens of thousands of pieces of chemical munitions. This quantity of chemical warfare agents vastly exceeds the amounts that might be expected to be deployed by a military force in a single chemical attack.

The dispersal of the chemical agents and other hazardous substances is controlled by factors such as topography, wind velocity, direction, temperature, precipitation, vertical temperature gradient and atmospheric humidity. These factors all contribute to the size and type of dispersal pattern which will be observed .[32] In addition, as confirmed by unclassified U.S. satellite imagery, debris from the Coalition bombings were upwardly dispersed, rather than downwardly dispersed as would occur in offensive use, causing chemical agents to be carried by upper atmospheric currents and distributed as "traces" of chemical fallout over "down weather" positions. Czech and French officials confirmed the detections of these chemicals during the war. (See Chapter 3.)

In considering the consequences of the placement of troops in areas downwind (where non-lethal exposure to chemical warfare agents might be expected), it must be remembered that chemical nerve agents, such as Sarin and Soman and other agents, have cumulative effects - often explained as slow rates of detoxification. [33]

Chemical Nerve Agents

Nerve agents kill by disrupting the metabolic processes, causing a buildup of a chemical messenger (acetylcholine) by inhibiting the production of acetylcholine-esterase, a key regulator of neurotransmission. Lethal exposure to chemical nerve agents is generally characterized by drooling, sweating, cramping, vomiting, confusion, irregular heart beat, convulsions, loss of consciousness and coma." [34]

According to a material safety data sheet (MSDS) for Soman (GD), and VX 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 by 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 exposure 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. After symptoms subside, increased susceptibility persists for one to several days. The degree of exposure required to produce recurrence of symptoms. and the severity of these symptoms depend on duration of exposure and time required to produce recurrence of symptoms, and the severity of these symptoms depend on the duration of exposure and the time intervals between exposures. Increased susceptibility is not specific to the particular nerve agent initially absorbed." (See appendix A for MSDS on Soman, Sarin, Tabun, and VX).

Some of the symptoms commonly associated with acute exposure to chemical nerve agents include myosis, frontal headaches, eye pain on focusing, slight dimness of vision, occasional nausea and vomiting, runny nose, tightness in chest, sometimes with prolonged wheezing, expiration suggestive of bronchoconstriction or increased secretion and coughing. Following systemic absorption, these symptoms are identified as typical: tightness in chest, wheezing, anorexia, nausea, vomiting, abdominal cramps, epigastric and substernal tightness, heartburn, diarrhea, involuntary defecation, increased sweating, increased salivation, increased tearing, slight bradycardia, myosis, blurring vision, urinary urgency and frequency, fatigue, mild weakness, muscular twitching, cramps, generalized weakness, including muscles of respiration, with dyspnea and cyanosis, pallor and occasional elevation of blood pressure; giddiness, tension, anxiety, jitteriness, restlessness, emotional lability, excessive dreaming, insomnia, nightmares, headaches, tremors, withdrawal and depression; bursts of slow waves of elevated voltage in EEG (especially on over ventilation), drowsiness, difficulty concentrating, slowness on recall. confusion, slurred speech, ataxia, coma (with absence of reflexes), Cheyne-Stokes respiration, convulsions, depression of the respiratory and circulatory centers, with dyspnea, cyanosis and fall in blood pressure.[35]

The majority of automatic chemical agent detection alarms (M8A1) deployed during the war were not sufficiently sensitive for detecting sustained low levels of chemical agent and monitoring personnel for contamination.[36] US Army Material Safety Data Sheets (MSDS) indicate that chronic exposure to levels of over .0001 mg/m3 for Sarin (GB) is hazardous and required the use of protective equipment. (See appendix A), The minimum level of chemical agent required to activate the automatic chemical agent detection alarm M8A1, commonly in use during the war, exceeds this threshold by a factor of 1,000.[37] As the chemical agent alarms began to sound during the "air war," French, Czech, and many U.S. commanders confirmed that they were sounding from the fallout from the bombings. Over time, even at these levels, after repeatedly being told that there was no danger, U.S. forces failed to take precautionary measures. Others report that the alarms were sounding so frequently that they were turned off.

This increased susceptibility associated with prolonged exposures to non-lethal dosages of nerve gases, suggests that the synergistic effects of the fallout from the bombings of the chemical warfare agent facilities and the administration of the cholinesterase inhibiting drug, pyridostigmine bromide, should be further researched as factors contributing to the symptoms being described by the Gulf War veterans.

The following is a listing of a number of agents which the Iraqi government could have combined or which could have been combined in the atmosphere as a result of Coalition bombings:

Sarin (GB) - A colorless and practically odorless liquid, Sarin dissolves well in water and organic solvents. The basic military use of Sarin is as a gas and a persistent aerosol. A highly toxic agent with a clearly defined myopic effect, symptoms of intoxication appear quickly without any period of latent effect. Sarin has cumulative effects -- that is, a slow rate of detoxification independent of its method of entry into the body. A6cording to Joachim Krause and Charles K. Mallory in Chemical Weapons in Soviet Military Doctrine: Military and Historical Experience, 1915-1991, the progressive signs of initial Sarin intoxication include myosis (contraction of the pupil), photophobia, difficulty breathing and chest pain.[38]

Soman (GD)- A neuro-paralytic toxic agent. Soman is a transparent, colorless, involatile liquid smelling of camphor. Soluble in water to a limited degree, Soman is absorbed into porous and painted surfaces. Soman is similar to Sarin in its injurious effects, but more toxic. When it acts on the skin in either droplet or vapor form, it causes a general poisoning of the organism .[39]

Tabun (GA) - A neuro-paralytic toxic agent. Tabun is a transparent, colorless liquid. The industrial product is a brown liquid with a weak sweetish smell; in small concentrations, it smells of fruit, but in large concentrations, it smells of fish. Tabun dissolves poorly in water but well in organic solvents; it is easily absorbed into rubber products and painted surfaces. Injury occurs upon skin contact with Tabun vapor and droplets. The symptoms of injury appear almost immediately. Marked myosis occurs.[40]

VX - This colorless, odorless, liquid has a low volatility and is poorly soluble in water, but dissolves well in organic solvents. The danger of pulmonary VX intoxication is determined by meteorological conditions and the delivery method used. VX is thought to be very effective against respiratory organs when in the form of a thinly dispersed aerosol. The symptoms of VX intoxication are analogous to those of other nerve agents, but their development is markedly slower. As with other nerve agents. VX has a cumulative effect.[41]

Vesicants and Blood Agents

Lewisite - A vesicant toxic agent, industrial lewisite is a dark-brown liquid with a strong smell. Lewisite is a contact poison with practically no period of latent effect. Lewisite vapors cause irritation to the eyes and upper respiratory tract.[42] According to the Center for Disease Control, lewisite would cause stinging and burning. Its smell, generally characterized as the strong smell of geraniums, could be confused with the smell of ammonia (the reaction to which is regulated by pain fibers rather than smell).[43] Iraqi stores of lewisite were not located after the war according to the Department of Defense.

Cyanogen Chloride - The French first suggested the use of cyanogen chloride as a toxic agent. U.S. analysts have reported that it is capable of penetrating gas mask filters. Partially soluble in water, it dissolves well in organic solvents. It is absorbed easily into porous materials; its military state is a gas. Cyanogen chloride is a quick acting toxic agent. Upon contact with the eyes or respiratory organs, it injures immediately. Lethal exposures result in loss of consciousness. convulsions and paralysis.[44]

Hydrogen Cyanide - A colorless liquid smelling of bitter almonds, hydrogen cyanide is a very strong, quick-acting poison. Hydrogen cyanide affects unprotected humans through the respiratory organs and during the ingestion of contaminated food and water. It inhibits the enzymes, which regulate the intra-cell oxidant-restorative process. As a result, the cells of the nervous system, especially those affecting breathing -- are injured, which in turn leads to quick death. An important feature of hydrogen cyanide is the absence of a period of latent effect. The military state of hydrogen cyanide is a gas. The toxic and physiologic properties of hydrogen cyanide permit it to be used effectively in munitions -- predominantly in rocket-launched artillery. Death occurs after intoxication due to paralysis of the heart. Non-lethal doses do not cause intoxication .[45]

Blister Agents

According to the material safety data sheet (MSDS) for sulfur mustard gas (HD) prepared by the U.S. Army Chemical Research, Development and Engineering Center, Aberdeen Proving Grounds, Maryland, "chronic exposure to HD can cause skin sensitization, chronic lung impairment, cough, shortness of breath, chest pain, and cancer of the mouth, throat, respiratory tract, skin, and leukemia. It may also cause birth defects. (See appendix A for the MSDS sheets on sulfur mustard agents HD and T.) The U.S. Army Chemical and Biological Defense Command lists the current detector sensitivity threshold for the M256A1 kits, a commonly used piece of chemical agent detection equipment in the Gulf War, as 2.0 mg/m3.[46] According to the Material Data Safety Sheets for sulfur mustard, total weight average exposures of greater than .003mg/m3 over an 8-hr period requires the use of protective equipment. (See appendix A.) Therefore, the detection kit would not detect the agent until the amount of agent present exceeded the safety threshold by a factor of over 660. The M8A1 automatic alarms do not detect blister agent.

Mustard Gas - This is a colorless, oily liquid, which dissolves poorly in water, but relatively well in organic solvents, petroleum, lubricant products, and other toxic agents. The injurious effect of mustard gas is associated with its ability to inhibit many enzyme systems of the body. This, in turn, prevents the intra-cell exchange of chemicals and leads to necrosis of the tissue. Death is associated mainly with necrosis of the tissue of the central nervous system. Mustard gas has a period of latent effect (the first signs of injury appear after 212 hours), but does not act cumulatively. It does not have any known antidotes. In military use it can come in gas, aerosol, and droplet form. It therefore acts through inhalation, cutaneously, perorally and directly through the blood stream. The toxic and physico-chemical properties of mustard gas allow it to be used in all types of munitions.[47]

Related Chemical Agent Information

Committee staff has learned that Iraq may have acquired any one of a number of the Soviet binary novachok ("newcomer") series of chemical warfare agent compounds or information relevant to the development of those compounds. This series of chemical warfare agents reportedly contains both lethal and debilitating agents. According to a confidential Committee source, if the Iraqis had obtained samples of these compounds they could be easily analyzed and produced with readily available materials. Several of these compounds are described as agents that even in microdoses can have long lasting effects. These agents are described as inducing myosis, vomiting, memory loss, involuntary motions and internal organ dysfunction. Many of these materials are also described as having mutagenic effects. These materials are, according to the source, stored in the lipids (body fats) and have no known antidotes. In addition, according to the Committee source, the Soviets were believed to have conducted research in a number of dioxin-based chemical warfare agents, and on at least one agent that could be used to contaminate drinking water supplies. Committee staff is conducting further Inquiry to determine if Iraq may have had access to any of these compounds.[48]


Biotoxins are natural poisons, chiefly of cellular structure. A distinction is made between exotoxins, which are given off by an organism while it is alive, and endotoxins, which are given off after a cell's death. The exotoxins cause the injurious effects of biological weapons, but endotoxins guarantee the effects of chemical weapons and do not cause the widespread disease outbreaks associated with biological warfare. Some examples of biotoxins include botulinus toxin and staphylococci enterotoxin.[49]

Biological Warfare Capability

According to the UN, the Iraqi biological warfare program was initiated in mid-1986 at Salman Pak. UNSCOM inspectors discovered evidence of research into certain biological agents including botulinus toxin and anthrax -- as well as organisms responsible for gas gangrene, tetanus and brucellosis, components of a biological weapons program which was not defensive in nature. In four years of work prior to the war, only 10 papers were published. These research programs focused on Iraqi efforts to isolate the most pathogenic spores. They also did research on the aerosolization and on the environmental survivability of some of these biological materials according to the United Nations.[50]

While the Department of Defense maintains that the Iraqi military did not weaponize its biological warfare program, UNSCOM is less certain, reporting that their degree of confidence that weaponization did not occur is low. In fact, readily available high performance agricultural aerosol generators could easily be converted to both decontaminate areas in which chemicals are used and to aerosolize biological and chemical warfare agents.

Other was in which biological materials could have been weaponized include the use of Iraqi 250 and 5001b bombs, aerial rockets, Unmanned aerial vehicles, FAW ground-to-ground missiles, helicopters and Iraqi aircraft. The Committee has received several reports of Iraqi helicopters penetrating Saudi airspace during the war by flying at low levels through the wadis and of Iraqi aircraft penetrating the area over the northern Persian Gulf

According to UNSCOM, indications that suggested that the program was offensive in nature include:

The United Nations said that the first Biological Inspection was initiated on August 8, 1991 at Salman Pak. The inspection was delayed because of the need to extensively immunize the members of the inspection team. The Salman Pak facility was razed one week prior to the arrival of the inspection team.[51]

The United States is aware of the Iraqi potential for using biological weapons. The employment of biological agents in a "cocktail" mix with chemical warfare agents is consistent with Soviet military doctrine. It is clear that biological weapons are much more difficult than chemical weapons to detect and defend against. Some of the symptoms experienced by veterans suffering from Persian Gulf Syndrome are consistent with biological warfare agent use. Verification will require sophisticated medical diagnosis, which to date has not been publicly undertaken.

The question of whether U.S. forces were attacked with a biological agent is problematic. According to Chemical/Biological Program: A Department of Defense Perspective, "It has been recognized that our biological defense program was inadequate. Credible analysis indicated that optimal employment of biological agents could result in a significantly large hazard area." It further cites a memo from the Chairman of the Joint Chiefs of Staff to the SECDEF (Secretary of Defense) noting: "inadequate ability to counter BW (biological warfare) attack/BW defense is a priority requirement."[52] The inadequacy of the current biological defense and detection program was also supported by Deputy Secretary of Defense John Deutch in an unclassified May6, 1994 address delivered at a Department of Defense-sponsored counterproliferation conference at the Los Alamos National Laboratory. According to Deputy Secretary Deutch, the United States has "no biological detection capability deployed with any forces, anywhere."

Novel BW agents created by altering DNA plasmids and vectors are specifically intended to avoid detection. As noted below, several shipments of biological materials that might have been used to carry out such a program were licensed for export from the United States to the Iraq Atomic Energy Commission. In such a program, common intestinal flora such as e. coli could be altered to produce viral, bacterial, or other toxins and would be difficult to treat. If Iraq was successful in developing such agents, diagnosis will continue to elude physicians testing for traditional illnesses. Novel BW agents would certainly elude biological detection devices. There is evidence, based on the nature of the materials imported, that this type of research was being conducted.. Since the Iraqi government managed to dismantle much of its biological warfare program prior to the UNSCOM inspections, we can only speculate on how advanced this program might have been." [53]

It has been suggested that if these problems the veterans are experiencing are Gulf War-related, then we should be seeing even more serious problems among the Iraqis. Since beginning this investigation we have learned that many Iraqi enemy prisoners of war (EPW) suffered skin rashes, sores, nausea, vomiting, coughing and other medical problems while they were being detained in Saudi Arabia. Many members of units who had close contact with these individuals are now reporting to the Committee symptoms consistent with those being suffered by other Gulf War veterans. In addition, Iraq has claimed a dramatic rise in reported cases of communicable diseases since the end of the Gulf War including typhoid, brucellosis, hepatitis and cholera.[54]

Further, reports of Gulf War illnesses being reported is no longer limited to military veterans of the Gulf War. Others reporting manifestation of these symptoms include:

- Department of Defense civilians who served in the Persian Gulf War.

- Department of Defense civilians working at the Anniston (AL) Army Depot and the Sharpsite (CA) Army Depot decontaminating equipment which was returned from the Persian Gulf

- Spouses, particularly the spouses of male veterans, are reporting the following symptoms: chronic or recurring vaginal yeast infections, menstrual irregularities (excessive bleeding and severe cramping), rashes, fatigue, joint and muscle pain, and memory loss.

- Children born to veterans prior to the Gulf War. In many cases both male and female children born prior to the war have experienced symptoms similar to those of the veterans and their spouses.

- Children born following the Gulf War. Some reports have been published which suggest a high rate of miscarriages in the families of Gulf War veterans. Further, sever-al reports have surfaced which suggest that there has been a high rate of physical abnormalities in children born to Gulf War veterans since the war.

U.S. Exports of Biological Materials to Iraq

The Senate Committee on Banking, Housing, and Urban Affairs has oversight responsibility for the Export Administration Act. Pursuant to the Act, Committee staff contacted the U.S. Department of Commerce and requested information on the export of biological materials during the years prior to the Gulf War. After receiving this information, we contacted a principal supplier of these materials to determine what, if any, materials were exported to Iraq which might have contributed to an offensive or defensive biological warfare program. Records available from the supplier for the period from 1985 until the present show that during this time, pathogenic (meaning "disease producing"), toxigenic (meaning "poisonous"), and other biological research materials were exported to Iraq pursuant to application and licensing by the U.S. Department of Commerce. Records prior to 1985 were not available, according to the supplier. These exported biological materials were not attenuated or weakened and were capable of reproduction. According to the Department of Defense's own Report to Congress on the Conduct of the Persian Gulf War, released in April 1992: "By the time of the invasion of Kuwait, Iraq had developed biological weapons. It's advanced and aggressive biological warfare program was the most advanced in the Arab world... The program probably began late in the 1970's and concentrated on the development of two agents, botulinum toxin and anthrax bacteria... Large-scale production of these agents began in 1989 at four facilities near Baghdad. Delivery means for biological agents ranged from simple aerial bombs and artillery rockets to surface-to-surface missiles." [55]

Included in the approved sales are the following biological materials (which have been considered by various nations for use in war), with their associated disease symptoms:[56]

Bacillus Anthracis: anthrax is a disease producing bacteria identified by the Department of Defense in The Conduct of the Persian Gulf War: Final Report to Congress, as being a major component in the Iraqi biological warfare program.

Anthrax is an often-fatal infectious disease due to ingestion of spores. It begins abruptly with high fever, difficulty in breathing, and chest pain. The disease eventually results in septicemia (blood poisoning), and the mortality is high. Once septicemia is advanced, antibiotic therapy may prove useless, probably because the exotoxins remain, despite the death of the bacteria.

Clostridium Botulinum: a bacterial source of botulinum toxin, which causes vomiting, constipation, thirst, general weakness, headache, fever, dizziness, double vision, dilation of the pupils and paralysis of the muscles involving swallowing. It is often fatal.

Histoplasma Capsulatum: causes a disease superficially resembling tuberculosis that may cause pneumonia, enlargement of the liver and spleen, anemia, an influenza-like illness and an acute inflammatory skin disease marked by tender red nodules, usually on the shins. Reactivated infection usually involves the lungs, the brain, spinal membranes, heart, peritoneum, and the adrenals.

Brucella Melitensis: a bacteria which can cause chronic fatigue, loss of appetite, profuse sweating when at rest, pain in joints and muscles, insomnia, nausea, and damage to major organs.

Clostridium Perfringens: highly toxic bacteria, which cause gas gangrene. The bacteria produce toxins that move along muscle bundles in the body killing cells and producing necrotic tissue that is then favorable for further growth of the bacteria itself. Eventually, these toxins and bacteria enter the bloodstream and cause a systemic illness.

In addition, several shipments of Escherichia Coli (E.Coli) and genetic materials, as well as human and bacterial DNA, were shipped directly to the Iraq Atomic Energy Commission.

The following is a detailed listing of biological materials, provided by the American Type Culture Collection, which were exported to agencies of the government of Iraq pursuant to the issuance of an export licensed by the U.S. Commerce Department: [57]

Date : February 8, 1985
Sent to : Iraq Atomic Energy Agency
Materials Shipped:

Ustilago nuda (Jensen) Rostrup

Date: February 22, 1985
Sent to: Ministry of Higher Education
Materials Shipped:

Histoplasma capsulatum var. farciminosum (ATCC 32136) Class III pathogen

Date: July 11, 1985
Sent to: Middle and Near East Regional A
Materials Shipped:

Histoplasma capsulatum var. farciminosum (ATCC 32136) Class III pathogen

Date: May 2, 1986
Sent to: Ministry of Higher Education
Materials Shipped:

    1. Bacillus Anthracis Cohn (ATCC 10)
      Batch # 08-20-82 (2 each)
      Class III pathogen.

    2. Bacillus Subtitles (Ehrenberg) Con (ATCC 82)
      Batch # 06-20-84 (2 each)

    3. Clostridium botulinum Type A (ATCC 3502)
      Batch# 07-07-81 (3 each)
      Class III Pathogen

    4. Clostridium perfringens (Weillon and Zuber) Hauduroy, et al (ATCC 3624)
      Batch# 10-85SV (2 each)

    5. Bacillus subtilis (ATCC 6051)
      Batch# 12-06-84 (2 each)

    6. Francisella tularensis var. tularensis Olsufiev (ATCC 6223)
      Batch# 05-14-79 (2 each)
      Avirulent; suitable for preparations of diagnostic antigens.

    7. Clostridium tetani (ATCC 9441)
      Batch 03-94 (3 each)
      Highly toxigenic.

    8. Clostridium botulinum Type E (ATCC 9564)
      Batch# 03-02-79 (2 each)
      Class III pathogen

    9. Clostridium tetani (ATCC 10779)
      Batch# 04-24-84S (3 each)

    10. Clostridium perfringens (ATCC 12916)
      Batch# 08-14-80 (2 each)
      Agglutinating Type 2.

    11. Clostridium perfringens (ATCC 13124)
      Batch# 08-14-80 (3 each)
      Type A, alpha-toxigenic, produces lecithinase C.J. Appl,

    12. Bacillus Anthracis (ATCC 14185)
      Batch# 01-14-80 (3 each)
      G.G. Wright (Fort Detrick) V770-NPI-R. Bovine anthrax,
      Class III pathogen

    13. Bacillus Anthracis (ATCC 14578)
      Batch# 01-06-78 (2 each)
      Class III pathogen.

    14. Bacillus megaterium (ATCC 14581)
      Batch# 04-18-85 (2 each)

    15. Bacillus megaterium (ATCC 14945)
      Batch# 06-21-81 (2 each)
    16. Clostridium botulinum Type E (ATCC 17855)
      Batch# 06-21-71
      Class III pathogen.

    17. Bacillus megaterium (ATCC 19213)
      Batch# 3-84 (2 each)

    18. Clostridium botulinum Type A (ATCC 19397)
      Batch# 08-18-81 (2 each)
      Class III pathogen

    19. Brucella abortus Biotype 3 (ATCC 23450)
      Batch# 08-02-84 (3 each)
      Class III pathogen

    20. Brucella abortus Biotype 9 (ATCC 23455)
      Batch# 02-05-68 (3 each)
      Class III pathogen

    21. Brucella melitensis Biotype I (ATCC 23456)
      Batch# 03-08-78 (2 each)
      Class III pathogen

    22. Brucella melitensis Biotype 3 (ATCC 23458)
      Batch# 01-29-68 (2 each)
      Class III pathogen

    23. Clostridium botulinum Type A (ATCC 25763)
      Batch# 8-83 (2 each)
      Class III pathogen

    24. Clostridium botulinum Type F (ATCC 35415)
      Batch# 02-02-84 (2 each)
      Class III pathogen

Date: August 31, 1987
Sent to: State Company for Drug Industries
Materials Shipped:

      1. Saccharomyces cerevesiae (ATCC 2601)
        Batch# 08-28-08 (1 each)

      2. Salmonella choleraesuis subsp. choleraesuis Serotype typhi
        (ATCC 6539) Batch# 06-86S (1 each)

      3. Bacillus subtillus (ATCC 6633)
        Batch# 10-85 (2 each)

      4. Klebsiella pneumoniae subsp. pneumoniae (ATCC 10031)
        Batch# 08-13-80 (1 each)

      5. Escherichia coli (ATCC 10536)
        Batch# 04-09-80 (1 each)

      6. Bacillus cereus (11778)
        Batch# 05-85SV (2 each)

      7. Staphylococcus epidermidis (ATCC 12228)
        Batch# 11-86s (I each)|

      8. Bacillus pumilus (ATCC 14884)
        Batch# 09-08-80 (2each)

Date : July 11, 1988
Sent to : Iraq Atomic Energy Commission
Materials Shipped:

    1. Escherichia coli (ATCC 11303)
      Batch# 04-87S
      Phage host

    2. Cauliflower Mosaic Caulimovirus (ATCC45031)
      Batch# 06-14-85
      Plant virus

    3. Plasmid in Agrobacterium Turnefaciens (ATCC37349)
      Ti plasmid for co-cultivation with plant integration vectors in E.
      Coli) Batch# 05-28-85

Date: April 26, 1988
Sent to: Iraq Atomic Energy Commission
Materials Shipped:

    1. Hulambda4x-8, clone: human hypoxanthine
      phosphoribosyltransferase (HPRT) Chromosome(s) X q26.1 (ATCC
      57236) Phage vector; Suggested host: E.coli

    2. Hulambdal4-8, clone: human hypoxanthine
      phosphoribosyltransferase (HPRT) Chromosome(s): X q26.1
      (ATCC 57240) Phage vector; Suggested host: E.coli

    3. Hulambda15, clone: human hypoxanthine
      phosphoribosyltransferase (HPRT) Chromosome(s) X q26.1
      (ATCC 57242) Phage vector; Suggested host: E.coli

Date: August 31, 1987
Sent to: Iraq Atomic Energy Commission
Materials Shipped:

    1. Escherichia coli (ATCC 23846)
      Batch# 07-29-83 (1 each)

    2. Escherichia coli (ATCC 33694)
      Batch# 05-87 (1 each)

Date: September 29, 1988
Sent to: Ministry of Trade
Materials Shipped:

      1. Bacillus anthracis (ATCC 240)
        Batch#05-14-63 (3 each) Class
        III pathogen

      2. Bacillus anthracis (ATCC 938)
        Batch#1963 (3 each)
        Class III pathogen

      3. Clostridium perfringens (ATCC 3629)
        Batch#10-23-85 (3 each)

      4. Clostridium perfringens (ATCC 8009)
        Batch#03-30-84 (3 each)

      5. Bacillus anthracis (ATCC 8705)
        Batch# 06-27-62 (3 each)
        Class III pathogen

      6. Brucella abortus; (ATCC 9014)
        Batch# 05-11-66 (3 each)
        Class III pathogen

      7. Clostridium perfringens (ATCC 10388)
        Batch# 06-01-73 (3 each)

      8. Bacillus anthracis (.ATCC 11966)
        Batch# 05-05-70 (3 each)
        Class III pathogen

      9. Clostridium botulinum Type A
        Batch# 07-86 (3 each)
        Class III pathogen

      10. Bacillus cereus (ATCC 33018)
        Batch# 04-83 (3 each)

      11. Bacillus ceres (ATCC 33019)
        Batch# 03-88 (3 each)

Date : January 31, 1989
Sent to : Iraq Atomic Energy Commission
Materials Shipped:

      1. PHPT31, clone: human hypoxanthine
        phosphoribosyltransferase (HPRT) Chromosome(s) X q26.1
        (ATCC 57057)

      2. plambda5OO, clone: human hypoxanthine
        phosphoribosyltransferase pseudogene (HPRT)
        Chromosome(s): 5 p14-pI3 (ATCC 57212)

Date: January 17, 1989
Sent to: Iraq Atomic Energy Commission
Materials Shipped:

    1. Hulambda4x-8, clone: human hypoxanthine
      phosphoribosyltransferase (HPRT) Chromosome(s) X q26.1
      (ATCC 57237) Phage vector Suggested host: E.coli

    2. Hulambda14, clone: human hypoxanthine
      phosphoribosyltransferase (HPRT) Chromosome(s): X q26.1
      (ATCC 57240) Cloned from human lymphoblast
      Phage vector Suggested host: E.coli

    3. Hulambda15, clone: human hypoxanthine
      phosphoribosyltransferase (HPRT) Chromosome(s) X q26.1
      (ATCC 57241) Phage vector Suggested host: E.coli

Additionally, the Centers for Disease Control has compiled a listing of biological materials shipped to Iraq prior to the Gulf War. The listing covers the period from October 1, 1984 (when the CDC began keeping records) through October 13, 1993. The following materials with biological warfare significance were shipped to Iraq during this period:[58]

Date: November 28, 1989
Sent to: University of Basrah, College of Science, Department of Biology
Materials Shipped:

      1. Enterococcus faecalis

      2. Enterococcus faecium

      3. Enterococcus avium

      4. Enterococcus raffinosus

      5. Enterococcus gallinarium.

      6. Enterococcus durans

      7. Enterococcus hirae

      8. Streptococcus bovis

Date: April 21, 1986
Sent to: Officers City Al-Muthanna, Quartret 710, Street 13, Close 69
House 2811, Baghdad, Iraq
Materials Shipped:

    1. vial botulinum toxoid

Date: March 10, 1986
Sent to: Officers City Al-Muthanna, Quartret 710, Street 13, Close 69
House 28/1, Baghdad, Iraq
Materials Shipped:

      1. 1 vial botulinum toxoid #A2

Date: June 25, 1985
Sent to: University of Baghdad, College of Medicine , Department of Microbiology
Materials Shipped:

    1. 3 yeast cultures
      Candida. sp.

Date : May21, 1985
Sent to : Basrah, Iraq
Materials Shipped:

    1. Lyophilized arbovirus seed
    2. West Nile Fever Virus

Date: April 26, 1985
Sent to: Minister of Health, Ministry of Health, Baghdad, Iraq
Materials Shipped:

    1. 8 vials antigen and antisera
      (r. rickettsii and r. typhi)
      to diagnose rickettsial
      infections (non-infectious)

UNSCOM Biological Warfare Inspections

UNSCOM inspections uncovered evidence that the government of Iraq was conducting research on pathogen enhancement on the following biological warfare-related materials:[59]

In addition, the UNSCOM inspections revealed that biological warfare related stimulant research was being conducted on the following materials:

UNSCOM reported to Committee staff that a biological warfare inspection (BW3) was conducted at the Iraq Atomic Energy Commission in 1993. This suggests that the Iraqi government may have been experimenting with the materials cited above (E.Coli and rDNA) in an effort to create genetically altered microorganisms (novel biological warfare agents).

Biological Warfare Defense

The following section, describing the types, dissemination, and defensive measures against biological agents, is quoted verbatim from a United States Marine Corps Institute document, Nuclear and Chemical Operations, MCI 771113, used in the Command and Staff College's nonresident program. It is clear from this document that the Department of Defense recognizes both the threat and U.S. vulnerability to biological weapons. This document also outlines the Department's understanding of what actions should be taken in the event that a biological weapon has been or is suspected to have been employed.

"Biological agents cannot be detected by the human senses. A person could become a casualty before he is aware he has been exposed to a biological agent. An aerosol or mist of biological agent is born in the air These agents can silently and effectively attack man, animals, plants, and in some cases, materiel. Agents can be tailored for a specific type of target.[60]

Methods of using antipersonnel agents undoubtedly vary so that no uniform pattern of employment or operation is evident. It is likely that agents will be used in combinations so that the disease symptoms will confuse diagnosis and interfere with proper treatment. It is also probable that biological agents would be used in heavy concentrations to insure a high percentage of infection in the target area The use of such concentrations could result in the breakdown of individual immunity because the large number of in micro-organisms entering the body could overwhelm the natural body defenses.[61]

Types of Biological Agents

Different antipersonnel agents require varying periods of time before they take effect, and the periods of time for which they will incapacitate a person also vary. Most of the diseases having antipersonnel employment potential are found on one a group of diseases that are naturally transmitted between animals and man. Mankind is highly vulnerable to them since he has little contact with animals in today's urban society. The micro-organisms of possible use in warfare are found in four naturally occurring groups - the fungi, bacteria; rickettsiae, and viruses.[62]

a. Fungi. Fungi occur in many forms and are found almost everywhere. They range in size from a single cell, such as yeast to multicellularforms, such as mushrooms and puffballs. Their greatest employment potential is against plants, although some forms cause disease in man. A fungus causes the disease coccidioidomycosis in man. Other common infections caused by Fungi include ringworm and "athletes foot ."[63]

b. Bacteria. Bacteria comprise a large and varied group of organisms. They occur in varying shapes, such as rods, spheres, and spirals, but they are all one-celled plants. Some bacteria can assume a resistant structure called a spore, which enables them to resist adverse environmental conditions. Others may produce poisonous substances called toxins. Examples of human disease caused by bacteria are anthrax, brucellosis, tularemia staphylococcus, and streptococcus." [64]

c. Rickettsiae. Rickettsiae organisms have the physical appearance of bacteria and the growth characteristics of viruses. Members of this group must have living tissue for growth and reproduction, whereas most fungi and bacteria can be grown on artificial material. Another characteristic of rickettsiae is that most diseases caused by this group are transmitted by the bite of an insect, such as the mosquito, mite, or tick. Rocky Mountain Spotted Fever, Q fever and typhus are diseases of mankind caused by rickettsiae." [65]

d. Virus. The smallest living things known to mankind are viruses. Viruses me so small than an electron microscope is required to see them. Viruses cannot be grown in the absence of living tissue. Diseases, which are caused by viruses, cannot normally be treated with antibiotics. Viruses cause yellow fever, rabies. and poliomyelitis." [66]

Dissemination of Biological Agents

a. Aerosol. Biological agents may be disseminated on, or over, the target by many means, such as aircraft, missiles, and explosive munitions. These devices produce a biological aerosol, and, if antipersonnel biological agents are ever used, they will probably be disseminated in the form of biological mists or aerosols. This method of dissemination would be extremely effective because the micro-organisms would be drawn into the lungs as a person breathes, and there they would be rapidly absorbed into the blood stream. The hours from dusk until dawn appear to be the best time for dissemination of biological agents. The weather conditions are most favorable for these agents at night, since sunlight will destroy many of them. In field trials, using harmless biological aerosols, area coverages of thousands of square miles have been accomplished The aerosol particles were carried for long distances by air currents.[67] (emphasis added)

b. Living Hosts. Personnel maybe infected by disease carrying vectors, such as insects, rats, or other animals. Mosquitoes may spread malaria yellow fever, or encephalitis; rats spread plague (any mammal may carry rabies). Militarily, specific vectors maybe selected, infected as required, and then released in the target area to seek out their human victims and pass on the disease. Since infection is transmitted through a bite in the skin, protective masks offer no protection. A vectorborne agent may remain in the target area for as long as there are live hosts; thus, a major disadvantage results. The vectorborne agent can become a permanent hazard in the area as the host infects others of his species.[68]

c. Food and Water Contamination. Biological agents could also be delivered to target personnel by placing the agent in food and water supplies (sabotage). This type of attack would probably be directed against small targets, such as industrial complexes, headquarters, or specific individuals. The methods of delivering the attack are many and varied [69]

Defensive Measures

The United States carries out research aimed at improved means of detection of biological agents and treatment and immunization of personnel. Both of these are essential to biological defense.[70]

a .Before an Attack: The inability of the individual to detect a biological attack is perhops the greatest problem. Contributing factors are the delay experienced before the onset of symptoms and the time required to identify specific agents. Without an adequate means of detection, complete defensive measures may not be taken since an attack must first be detected before you can defend against it. Diseases caused by biological agents do not appear until a few days to weeks after contact with the agent. Personnel are protected against biological agents in aerosol form by the protective mask. Ordinary clothing protects the skin from contamination by biological agents. Other means of protection include immunizations; quarantining contaminated areas; cleanliness of the body, clothing, and living quarters: stringent rodent and pest control; proper care of cuts and wounds; and education of troops to eat and drink only from approved sources.[71]

b. After an Attack: After a biological agent attack has occurred, it will be necessary to identify the agent used in the attack so that proper medical treatment may be given to exposed personnel. To perform this identification, it is necessary to collect samples or objects from the contaminated area and send them to a laboratory or suitable facility for processing. Samples may by taken from the air, from contaminated surfaces, or from contaminated water. After the sample is taken, laboratory time will be required to identify the suspected biological agent. The length of time for identification is being significantly shortened through the use of new medical and laboratory techniques. Proper defensive actions taken during a biological attack depend upon the rapid detection of the attack. Biological defense is continuous. You must always be prepared for the employment of these weapons.[72] (emphasis added)

Iraq's Experience in the Use of Chemical Warfare Agents

The fears and the precautions taken prior to the Gulf War were not the product of excessive hysteria. Five United Nations reports have confirmed the use of chemical warfare agents in the Iran-Iraq War.[73] Use of chemical weapons against both the Kurds and Shiite Moslems within Iraq is well documented. Press reports also document Iraqi readiness to use these weapons against Coalition forces during the Persian Gulf War.

In April 1993, two U.S.-based human rights organizations confirmed that they had found residues of chemical weapons used by the Iraqi government of Saddam Hussein against a Kurdish village in northern Iraq in 1988. These groups, Physicians for Human Rights and Human Rights Watch, said they had used advanced analytical techniques to discover the presence of mustard gas and the nerve gas Sarin. Those chemical weapons reportedly were dropped by aircraft on August 25, 1988 and killed four people in the Kurdish village of Birjinni.[74] Testimony from survivors of the Birjinni bombing, who said victims of the raids died writhing and coughing blood, led to accusations that Iraq had gassed its own citizens as part of a campaign against rebellious Kurds that killed tens of thousands.[75] This was the first time that scientists had been able to prove the use of chemical weapons, and especially a nerve gas, through the analysis of environmental residue acquired years after such an attack occurred.[76]

Soil samples were gathered from the 1988 bombing sites and then delivered to a British laboratory. Chemists at Porton Down found traces of mustard gas and Sarin. Dr. Graham Pearson, director of the British Chemical and Biological Defense Establishment, verified these results and confirmed the samples were taken from bomb craters near the northern Iraqi village of Birjinni in June 1992. The byproducts of the breakdown of these poisons are so specific that they provide a "unique fingerprint" in chemical analysis that points directly to a poison gas attack.[77]

An earlier attack had been reported on March 17, 1988 on the village of Halabja. Amnesty International reported that chemical weapons were used in an attack by Iraq, in which "some 5,000 Kurds were killed within an hour.[78] A UN team sent to investigate the attack found evidence of chemical weapons, although they did not rule on who carried out the attack on the town, which had been occupied by Iran since mid-March.[79]

On September 26, 1993, Shiite rebels living in the southern Iraqi marshlands reported an early morning shelling attack by Iraqi forces. The eyewitnesses, who spoke with a New York Times reporter, mentioned that the shells landed with a thud "and not the usual explosion" sending up white clouds. The artillery attack was followed by a ground assault by Iraqi troops who were equipped with gas masks.[80]

A Shiite rebel claimed that upon entering one of the Iraqi armored personnel carriers they found battle orders calling for a chemical attack. Rebel leaders provided a copy of the captured orders. Written in Arabic on the twenty-sixth of September, the orders, numbered 1-15, instructed the Iraqi soldiers to use chemical weapons to "retake the village" and that "each soldier must be instructed on how to respond during the chemical attack."[81]

After the attack, some villagers returned for their belongings, but there was nothing left. They discovered that trees and plants had withered and yellowed. Furthermore, "the cats, the dogs, the birds and even the water snakes had died. But for some reason the victims had been removed by the troops. We saw no bodies."[82]

In November 1993, a nine-member U.N. inspection team arrived to take samples from the area of the alleged chemical attack. The results of the inspection were inconclusive.

It is also suspected that Iraq may have used biological agents (mycotoxins) during the 1984 attack on Majnoon Island, during the Iran-Iraq War, and in 1988 against the Kurds (cholera and typhus). However, no medical verification of Iraqi use of biological warfare agents yet exists.[83]

The above documented instances of chemical weapons use (and suspected use) against Iranians, Kurds, and Shiites undermine Department of Defense assertions that Iraq may not have used these weapons against Coalition forces because they "feared contamination of their own men.[84] Marine Brigadier General Richard Neil said that prisoner debriefings of Persian Gulf War EPWs had "yielded the impression that the Iraqis were not comfortable operating in a chemical environment,...and ... Iraqi soldiers had poor chemical protection equipment of their own."[85] Lt. General Thomas Kelly stated in a press briefing that "the Iraqi Army was very uncomfortable, we are finding out from the POWs, about the use of chemical weapons because they, are not familiar with it.[86] However, as the preceding paragraphs make clear, the Iraqi Army had operational experience with the use of these weapons, unlike their American counterparts.


As the preceding sections of this report make clear, the Government of Iraq possessed a large and sophisticated chemical and biological weapons production complex. Iraq's army, organized and equipped along Soviet lines, also appeared to employ Soviet chemical warfare doctrine, which advocated the use of mixed agent warfare. Iraq used these weapons against its own people in the 1980's, and possibly again in 1993. It should not be surprising that Baghdad would also use every weapon in its arsenal against the much more serious threat to its own survival posed by the massed Coalition forces. Additionally, the release of chemical and biological agents as a result of Coalition bombing should have been expected by the Allied forces, based upon their own doctrine regarding the dispersal of chemical agents.

Several theories have been put forward to explain the cause(s) of Gulf War Syndrome. Most of them lack credibility because they do not explain transmission of similar symptoms across a broad and dissimilar population whose only commonality was the service of a family member in the Persian Gulf theater of operations or contact with returned from that venue. Meanwhile, the passage of over three years since the appearance of the first symptoms, and the inability of the Departments of Defense and Veterans Affairs to find a cause, suggests that the illnesses maybe caused by something that these institutions have not examined. Further, the absence of credible and verifiable published scientific research on the syndrome by these agencies, providing specifies of the types of laboratory research that have been conducted, case histories, and methodologies used, leaves each interested scientist in the dark as to what diagnostic processes have been attempted and which have failed.

There is a growing body of evidence, outlined in detail below, which supports the claims of Gulf War veterans that exposure to chemical and/or biological warfare agents maybe the cause of the complex of illnesses they currently suffer. There appear to be four primary sources of exposure: 1) as a result of direct attack, via missile, rocket, artillery, or aircraft munitions; 2) as a result of intermittent low-level exposure to fallout from Coalition bombing of Iraqi chemical and biological warfare plants and munitions bunkers; 3) as a result of administration of a nerve agent pre-treatment drug that acts in a manner similar to actual nerve agent; and, 4) as a result of continuing contact with the Iraqi enemy prisoners of war (EPWs). In addition, there appear to be two secondary sources of exposure: 1) exposure to occupational/environmental hazards in Southwest Asia and to contaminated materiel returned from the theater of operations, and 2) transmission among family members. Exposure to endemic diseases and illnesses and diseases must also be thoroughly researched.

Hundreds of Gulf War veterans have been interviewed by the Committee staff. The events cited below are included because the veterans reporting them could remember approximately when they occurred, or because there were multiple independent confirming sources. A map showing the location of these events appears at the end of this section.

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