Testimony 

Before the Subcommittee on National Security, 

Emerging Threats, and International Relations, 

Committee on Government Reform, House of 

Representatives 

United States General Accounting Office 

GAO

For Release on Delivery 

Expected at 1:00 p.m. EDT 

Tuesday, June 1, 2004 GULF WAR ILLNESSES

DOD’s Conclusions About 

U.S. Troops’ Exposure 

Cannot Be Adequately 

Supported 

Statement of Keith Rhodes, Chief Technologist 

Center for Technology and Engineering, Applied Research 

and Methods 

GAO-04-821T 

On 8/6/04 this testimony was reissued because, beginning on 

page 15, the support for “Some Studies Suggest an Association 

between Chemical Warfare Exposure and Gulf War Illnesses” was 

inadvertently omitted. 
www.gao.gov/cgi-bin/getrpt?GAO-04-821T.

To view the full product, including the scope 

and methodology, click on the link above. 

For more information, contact Keith Rhodes 

at (202) 512-6412 or rhodesk@gao.gov. 

Highlights of GAO-04-821T, a report to

Subcommittee on National Security, 

Emerging Threats, and International 

Relations, Committee on Government 

Reform, House of Representatives 

June 2004

GULF WAR ILLNESSES

DOD's Conclusions about U.S. Troops' 

Exposure Cannot Be Adequately 

Supported 

DOD’s and MOD’s conclusion about troops’ exposure to CW agents, based 

on DOD and CIA plume modeling, cannot be adequately supported. The 

models were not fully developed for analyzing long-range dispersion of CW 

agents as an environmental hazard. The modeling assumptions as to source 

term data—quantity and purity of the agent—were inaccurate because they 

were uncertain, incomplete, and nonvalidated. 

The plume heights used in the modeling were underestimated and so were 

the hazard area. Postwar field testing used to estimate the source term did 

not realistically simulate the actual conditions of bombings or demolitions. 

Finally, the results of all models—DOD and non-DOD models—showed wide 

divergences as to the plume size and path. 

DOD’s and VA’s conclusion about no association between exposure to CW 

agents and rates of hospitalization and mortality, based on two 

epidemiological studies conducted and funded by DOD and VA, also cannot 

be adequately supported because of study weaknesses. In both studies, 

flawed criteria—DOD’s plume model and DOD’s estimation of potentially 

exposed troops based on this model—were used to determine exposure. 

This may have resulted in large-scale misclassification. 

Troops under the path of the plume were classified as exposed; those not 

under the path, as nonexposed. But troops classified as not exposed under 

one DOD model could be classified as exposed under another DOD model. 

Under non-DOD models, however, a larger number of troops could be 

classified as exposed. Finally, as an outcome measure, hospitalization rate 

failed to capture the types of chronic illnesses that Gulf War veterans report 

but that typically do not lead to hospitalization. 

Since the end of the Gulf War in 

1991, many of the approximately 

700,000 U.S. veterans have 

experienced undiagnosed illnesses. 

They attribute these illnesses to 

exposure to chemical warfare (CW) 

agents in plumes—clouds released 

from bombing of Iraqi sites. But in 

2000, the Department of Defense 

(DOD) estimated that of the 

700,000 veterans, 101,752 troops 

were potentially exposed. GAO was 

asked to evaluate the validity of 

DOD, the Department of Veterans 

Affairs (VA), and British Ministry of 

Defense (MOD) conclusions about 

troops’ exposure. 

This testimony summarizes a 

report GAO is issuing today. 

GAO is recommending that the 

Secretary of Defense and the 

Secretary of Veterans Affairs not 

use the plume-modeling data for 

any other epidemiological studies 

of the 1991 Gulf War. VA concurred 

with our recommendation. DOD 

did not concur but we have 

clarified the recommendation to 

address DOD’s concerns as we 

understand them. GAO also 

recommends that the Secretary of 

Defense require no additional 

plume modeling of Khamisiyah and 

other sites. DOD concurred with 

our recommendation. 

The Central Intelligence Agency 

(CIA) did not concur with our 

report, stating it could not review 

the draft report in the time allotted. 
Page 1 GAO-04-821T 

June 1, 2004 

Mr. Chairman and Members of the Subcommittee: 

We are pleased to participate in this international hearing by presenting 

our assessment of the plume modeling, conducted by the Department of 

Defense (DOD) and the Central Intelligence Agency (CIA), to determine 

the number of U.S. troops that might have been exposed to the release of 

chemical warfare agents during the Gulf War in 1990. We presented our 

preliminary results to you in our testimony on June 2, 2003.1

 My statement 

today is based on our final report, entitled Gulf War Illnesses: DOD’s 

Conclusions about U.S. Troops’ Exposure Are Unsupported, which is 

being issued today.2

As you know, many of the approximately 700,000 veterans of the Persian 

Gulf War have experienced undiagnosed illnesses since the war’s end in 

1991. Some fear they are suffering from chronic disabling conditions 

because of wartime exposures to vaccines, as well as chemical warfare 

agents, pesticides, and other hazardous substances with known or 

suspected adverse health effects. When the issue of the possible exposure 

of troops to low levels of chemical warfare agents was first raised, during 

the summer of 1993, DOD and the CIA concluded that no U.S. troops were 

exposed because (1) there were no forward-deployed Iraqi chemical 

warfare agent munitions and (2) the plumes—clouds of chemical warfare 

agents—from the bombing that destroyed the Iraqi chemical facilities 

could not have reached the troops. 

This position was maintained until 1996, when DOD publicly disclosed that 

U.S. troops destroyed a stockpile of chemical warfare agent munitions 

after the Gulf War in 1991, at a forward-deployed site, Khamisiyah, in Iraq. 

Consequently, DOD and the CIA conducted several analyses using 

computer modeling, in an effort to estimate the number of troops that 

might have been exposed to chemical warfare agents. Recognizing that 

actual data on the source term—such as the quantity and purity 

 1

U.S. General Accounting Office, Gulf War Illnesses: Preliminary Assessment of DOD 

Plume Modeling for U.S. Troops’ Exposure to Chemical Agents, GAO-03-883T

(Washington, D.C.: June 2, 2003). www.gao.gov. 

2

U.S. General Accounting Office, Gulf War Illnesses: DOD’s Conclusions about U.S. Troops 

Exposure Cannot Be Adequately Supported, GAO-04-159 (Washington, D.C.: June 1, 2004). 

www.gao.gov. 
Page 2 GAO-04-821T 

(concentration) of the agent—and the meteorological conditions—such as 

the wind and the weather patterns—were not available,3

 in 1996 and 1997, 

DOD and the CIA conducted field-testing and modeling of the demolition 

of Khamisiyah, to determine the size and path of the plume, as well as the 

number of U.S. troops exposed to chemical warfare agents within the area 

of the modeled plume’s path. During these initial modeling efforts, DOD 

also asked the Department of Energy’s (DOE) Lawrence Livermore 

National Laboratories (LLNL) to conduct modeling. In 1997, DOD and the 

CIA also combined the results of five different meteorological and 

dispersion models into a composite simulation of the plume area. They 

conducted additional simulations, using meteorological and dispersal 

models, to estimate the path of exposure from plumes during the 

bombings of sites other than Khamisiyah—Al Muthanna, Muhammadiyat, 

and Ukhaydir. In 2000, DOD revised its modeling estimates for the 

destruction of chemical warfare agents at Khamisiyah, and estimated that 

101,752 U.S. troops had potentially been exposed. 

In response to your request, we evaluated how well conclusions—about 

the extent of exposure of U.S. troops and the association between CW 

exposure and troops’ hospitalization and mortality rates—are supported 

by available evidence. Specifically, we have assessed the following: 

1. How valid is the DOD and MOD conclusion---based on CIA and DOD 

plume-modeling results—about U.S. and British troops’ exposure to 

CW agents? 

2. What were the costs for the CIA’s and DOD’s various plume modeling 

efforts? 

3. How valid are the DOD and Department of Veterans Affairs (VA) 

conclusions from epidemiological studies, based on DOD’s plume 

modeling results, that there was no association between CW exposure 

at Khamisiyah and the troops’ hospitalization and mortality rates? 

 3

Observations were few because Iraq stopped reporting weather station measurement 

information to the World Meteorological Organization in 1981. As a result, data on the 

meteorological conditions during the Gulf War were sparse. The only data that were 

available were for the surface wind observation site, 80 to 90 kilometers away, and the 

upper atmospheric site, about 200 kilometers away. 
Page 3 GAO-04-821T 

To determine the validity of DOD’s conclusion—that U.S. troops’ 

exposures to chemical warfare agents were as DOD estimates suggested—

based on its plume-modeling analysis, we examined the meteorological 

and dispersion models DOD used to model chemical warfare agent 

releases from the U.S. demolition of Khamisiyah and Coalition bombings 

of Al Muthanna, Muhammadiyat, and other sites in Iraq during the Gulf 

War deployment period. We evaluated the basis for the technical and 

operational assumptions DOD made in (1) conducting the modeling for the 

bombing and demolition of Iraqi sites and 

(2) estimating the specific data and information used in the modeling, 

relating to source term, meteorological conditions, and other key 

parameters. We also evaluated the efforts of the CIA and DOD to collect 

and develop data on source term and other key parameters used in the 

modeling efforts. 

We interviewed DOD and CIA modelers and officials involved with the 

modeling and obtained documents and reports from DOD’s Deployment 

Health Support Directorate. We also interviewed and received documents 

from DOE officials who were involved with the modeling at LLNL. In 

addition, we interviewed officials and obtained documents from the 

Institute for Defense Analyses (IDA) concerning the IDA expert panel 

assessment of CIA’s modeling of Khamisiyah. We also interviewed U.S. 

Army officials at Dugway Proving Ground, Utah, to determine how 

chemical warfare agents might have been released during the Khamisiyah 

pit area demolitions. Finally, we interviewed officials at the U.S. Army 

Center for Health Promotion and Preventive Medicine, to determine how 

specific troop unit exposures were identified, and officials of the United 

Nations Monitoring, Verification, and Inspection Commission (UNMOVIC), 

to obtain information on source term data from the United Nations Special 

Commission’s (UNSCOM) analyses and inspections of the Khamisiyah, Al 

Muthanna, Muhammadiyat, and other sites. 

To determine the validity of DOD’s and the Department of Veterans 

Affairs’ (VA) conclusions—based on epidemiological studies—that there 

was no association between Khamisiyah exposure and the rates of 

hospitalization or mortality, we reviewed published epidemiological 

studies in which hospitalization and mortality among exposed and 

nonexposed U.S. troops were analyzed. We also interviewed the study 

authors and researchers and examined the Gulf War population databases 

provided to the researchers by DOD in support of these studies. We 

interviewed Veterans Benefits Administration officials and obtained 

documents and reports on their analyses of DOD’s population databases. 

Scope and 

Methodology 
Page 4 GAO-04-821T 

We did not examine whether plume modeling data were being used by VA 

to determine eligibility for treatment or compensation. 

In an effort to identify the total costs associated with modeling and related 

analyses of chemical warfare agent releases during the Gulf War; we 

interviewed relevant officials and collected cost data from various DOD 

agencies and DOD contractors who supported the modeling efforts. 

To determine the extent of British troops’ exposure to chemical warfare 

agent-related releases during the Gulf War, we interviewed British Ministry 

of Defense (MOD) officials in London and at Porton Down, and reviewed 

U.K. Ministry of Defense reports concerning the potential effects of 

exposure to chemical warfare agent-related releases on British forces. 

We conducted our work from May 2002 through May 2004 in accordance 

with generally accepted government auditing standards. 

DOD and MOD’s conclusions, based on DOD’s plume-modeling efforts 

regarding the extent of U.S. and British troops’ exposures to chemical 

warfare agents, cannot be adequately supported. Given the inherent 

weaknesses associated with the specific models DOD used and the lack of 

accurate and appropriate meteorological and source term data in support 

of DOD’s analyses, we found five major reasons to question DOD and 

MOD’s conclusions. First, the models were not fully developed for 

analyzing long-range dispersion of chemical warfare agents as an 

environmental hazard. Second, assumptions regarding source term data 

used in the modeling—such as the quantity and purity of the agent—were 

inaccurate, since they were based on (1) uncertain and incomplete 

information and (2) data that were not validated. Third, the plume heights 

from the Gulf War bombings were underestimated in DOD’s models. 

Fourth, postwar field testing at the U.S. Army Dugway Proving Ground, to 

estimate the source term data, did not reliably simulate the actual 

conditions of either the bombings or the demolition at Khamisiyah. Fifth, 

there is a wide divergence in results among the individual models DOD 

selected, as well as in the unselected DOD and non-DOD models, with 

regard to the size and path of the plume and the extent to which troops 

were exposed. Given these inherent weaknesses, DOD and MOD cannot 

know which troops were and which troops were not exposed. 

The total costs for the various plume-modeling efforts to analyze the 

potential exposure of U.S. troops—from the demolition at Khamisiyah and 

the bombing of several other sites in Iraq—cannot be estimated. DOD 

Results in Brief 
Page 5 GAO-04-821T 

organizations and other entities involved with the plume-modeling efforts 

could provide only direct costs (that is, contractors’ costs), which totaled 

about $13.7 million. However, this amount does not include an estimate of 

the considerable indirect costs associated with the salaries of DOD, VA, 

and contractors’ staff or costs of facilities, travel, and equipment. We 

requested, but DOD could not provide, this estimate. In addition, the CIA 

would not provide direct and indirect costs for Gulf War plume modeling 

because, in its view, our request constituted oversight of an intelligence 

matter, beyond the scope of GAO authority. The CIA’s contractor, the 

Science Applications International Corporation (SAIC), also did not 

respond to our request for cost data. 

DOD’s and VA’s conclusions—that there is no association between 

exposures to chemical warfare agents from demolitions at Khamisiyah and 

rates of hospitalization and mortality among U.S. troops—also cannot be 

adequately supported. DOD and VA based these conclusions on two 

government-funded epidemiological studies, one conducted by DOD 

researchers, the other by VA researchers.4

 In each of these studies, flawed 

criteria were used to determine which troops were exposed. For example, 

in each study, the criteria used were based on (1) DOD plume modeling of 

exposures from postwar demolition of the Khamisiyah munitions depot 

and (2) DOD’s estimates, using this modeling, of which troops were under 

the path of the plume. Troops under the path of the plume were classified 

as exposed, those not under the path as nonexposed. However, troops 

classified as nonexposed under one DOD model could be classified as 

exposed under another DOD model, thereby confounding the results. In 

the DOD models, a small area was identified as being under the path of the 

plume, resulting in a small number of troops identified as exposed. But in 

other modeling not selected for consideration, such as that performed at 

the LLNL, for example, a much larger, as well as different area, was 

identified as under the path of the plume, resulting in the potential 

classification of a larger number of troops as having been exposed. In 

addition, these exposed troops included different troops from those in the 

DOD models–that is, troops classified as exposed in the DOD selected 

models would have been classified as nonexposed in the other models, 

even though the area of coverage was much greater. 

 4

G. C. Gray and others, “The Postwar Hospitalization Experience of Gulf War Veterans 

Possibly Exposed to Chemical Munitions Destruction at Khamisiyah, Iraq,” American 

Journal of Epidemiology 150 (1999); H. K. Kang and T.A. Bullman, “Mortality Among U.S. 

Veterans of the Persian Gulf War: 7 Year Follow-up,” American Journal of Epidemiology 

154 (2001): 399-409. 
Page 6 GAO-04-821T 

These flaws may have resulted in large-scale misclassification of the 

exposure groups—that is, a number of exposed veterans may have been 

classified as nonexposed, and a number of nonexposed veterans may have 

been misclassified as exposed. In addition, in the hospitalization study, the 

outcome measure—number of hospitalizations—would not capture the 

chronic illnesses that Gulf War veterans commonly report, but which 

typically do not lead to hospitalization. Several published scientific studies 

of exposure involving Gulf War suggest an association between low-level 

exposure to chemical warfare agents and chronic illnesses. 

In our report, we are recommending that the Secretary of Defense and the 

Secretary of Veterans Affairs not use the plume-modeling data for future 

epidemiological studies of the 1991 Gulf War, since VA and DOD cannot 

know from the flawed plume modeling who was and who was not 

exposed. 

We are also recommending that the Secretary of Defense require no 

further plume-modeling of Khamisiyah and the other sites bombed during 

the 1991 Gulf War in order to determine troops’ exposure. Given the 

uncertainties in the source term and meteorological data, additional 

modeling of the various sites bombed would most likely result in 

additional costs, while still not providing any definitive data on who was 

or was not exposed. 

We obtained comments our draft of this report from VA, DOD, and CIA. 

VA concurred with recommendation that VA and DOD not use the plumemodeling data for future epidemiological studies, since VA and DOD 

cannot know from the flawed plume modeling who was and who was not 

exposed. DOD did not concur with the recommendation, indicating that to 

them it called for a blanket prohibition of plume modeling in the future. 

The intent of our recommendation is only directed at epidemiological 

studies involving the DOD and CIA plume modeling data from the 1991 

Gulf War and not a blanket prohibition of plume modeling in future. We 

have clarified the recommendation along these lines. DOD concurred with 

our second recommendation, indicating that despite enhancements in the 

models, uncertainties will remain. CIA did not concur with our report, 

indicating that it could not complete its review in the time allotted. 

According to the CIA, modeling is the art and science of using 

interconnected mathematical equations to predict the activities of an 

actual event. In this case, modeling was used to determine the direction 

Background 
Page 7 GAO-04-821T 

and extent of the plume from chemical warfare agents. In environmental 

hazard modeling, simulations recreate or predict the size and path (that is, 

the direction) of the plume, including the potential hazard area, and 

potential exposure levels are generated. 

In addition to identifying the appropriate event to model, modeling 

requires several components of accurate information: 

• the characteristics or properties of the material that was released and its 

rate of release (for example, quantity and purity; the vapor pressure; the 

temperature at which the material burns; particle size; and persistency and 

toxicity); temporal information (for example, whether chemical agent was 

initially released during daylight hours, when it might rapidly disperse into 

the surface air, or at night, when a different set of breakdown and 

dispersion characteristics would pertain, depending on terrain, plume 

height, and rate of agent degradation); 

• data that drive meteorological models during the modeled period (for 

example, temperature, humidity, barometric pressure, dew point, wind 

velocity and direction at varying altitudes, and other related measures of 

weather conditions); 

• data from global weather models, to simulate large-scale weather patterns, 

and from regional and local weather models, to simulate the weather in 

the area of the chemical agent release and throughout the area of 

dispersion; and 

• information on the potentially exposed populations, animals, crops, and 

other assets that may be affected by the agent’s release. 

Various plumes during the 1991 Gulf War were estimated using globalscale meteorological models, such as the National Centers for 

Environmental Prediction Global Data Assimilation System (GDAS) and 

the Naval Operational Global Atmospheric Prediction System (NOGAPS). 

Regional and local weather models were also used, including the Coupled 

Ocean-Atmosphere Mesoscale Prediction System (COAMPS), the 

Operational Multiscale Environmental Model with Grid Adaptivity 

(OMEGA), and the Mesoscale Model Version 5 (MM5). 

Information for Modeling 

Types of Models Used 
Page 8 GAO-04-821T 

Transport and diffusion models were also used during the 1991 Persian 

Gulf War plume simulation efforts.5

 These models estimate both the path 

of a plume and the degree of potential hazard posed by the chemical 

warfare agents. Dispersion models used during the Gulf War included the 

Hazard Prediction and Assessment Capability (HPAC) along with its 

component, the Second-order Closure Integrated Puff (SCIPUFF) model; 

the Vapor, Liquid, and Solid Tracking (VLSTRACK) model; the NonUniform Simple Surface Evaporation (NUSSE) model; and the 

Atmospheric Dispersion by Particle-in-Cell (ADPIC) model. 

DOD’s conclusion about the extent of U.S. troops’ exposure to chemical 

warfare agents during and immediately after the Gulf War, based upon 

DOD and CIA plume model estimates, cannot be adequately supported. 

This is because of uncertainty associated with the source term data and 

meteorological data. Further, the models themselves are neither 

sufficiently certain nor precise to draw reasonable conclusions about the 

size or path (that is, the direction) of the plumes. 

In particular, we found five reasons to question DOD’s conclusion. First, 

the models DOD and the CIA selected were in house models not fully 

developed for analyzing long-range dispersion of chemical warfare agents 

as environmental hazards. DOD and CIA officials selected several in-house 

models to run plume simulations. For Khamisiyah and the other Iraqi sites 

selected for examination, DOD selected the COAMPS and OMEGA 

meteorological models and the HPAC/SCIPUFF and VLSTRACK dispersion 

models. However, these models were not at the time fully developed for 

modeling long-range environmental hazards. 

Second, the assumptions about the source term data used in the models 

are inaccurate. The source term data DOD used in the modeling for sites at 

Khamisiyah, as well as Al Muthanna and Muhammadiyat, contain 

significant unreliable assumptions. DOD and the CIA based assumptions 

on field testing, intelligence information, imagery, UNSCOM inspections, 

and Iraqi declarations to UNSCOM. However, these assumptions were 

based on limited, nonvalidated, and unconfirmed data concerning (1) the 

nature of the Khamisiyah pit demolition, (2) meteorology, (3) agent purity, 

(4) amount of agent released, and (5) other chemical warfare agent data. 

In addition, DOD and the CIA excluded from their modeling efforts many 

 5

We use dispersion in this report to refer to both transport and diffusion models. 

DOD’s Conclusion 

about U.S. Troops’ 

Exposure to Chemical 

Warfare Agents 

Cannot Be Adequately 

Supported 
Page 9 GAO-04-821T 

other sites and potential hazards associated with the destruction of binary 

chemical weapons, vast stores of chemical warfare agent precursor 

materials, and the potential release of toxic byproducts and chemical 

warfare agents from other sites.6

Third, in most of the modeling performed, the plume heights were 

significantly underestimated. Actual plume height would have been 

significantly higher than the height DOD estimated in its modeling of 

demolition operations and bombings. The plume height estimates that the 

CIA provided for demolition operations at the Khamisiyah pit were 0 to 

100 meters. However, neither DOD nor the CIA conducted testing to 

support estimated plume height associated with the bombings of Al 

Muthanna, Muhammadiyat, or Ukhaydir. According to DOD modelers, 

neither plume height nor any other heat or blast effects associated with 

these bombings were calculated from the models; instead, these data were 

taken from DOD’s Office of the Special Assistant for Gulf War Illnesses. In 

addition, according to a principal Defense Threat Reduction Agency 

modeler, DOD’s data on plume height were inconsistent with other test 

data for the types of facilities bombed. 

Fourth, postwar field testing at the U.S. Army Dugway Proving Ground, in 

Utah, to estimate the source term data did not realistically simulate the 

actual conditions of the demolition operations at Khamisiyah or the effects 

of the bombings at any of the other sites in Iraq. For field testing to be 

effective, conditions have to be as close to the actual event as possible, but 

these tests did not provide more definitive data for DOD and CIA’s models. 

The tests did not realistically simulate the conditions of the demolition of 

122 mm chemical-filled rockets in Khamisiyah. The simulations took place 

under conditions that were not comparable with those at Khamisiyah. 

There were differences in meteorological and soil conditions; the 

construction material of munitions crates; rocket construction (including 

the use of concrete-filled pipes as rocket replacements to provide inert 

filler to simulate larger stacks); and the number of rockets, with far fewer 

rockets and, therefore, less explosive materials. In addition, in the tests, 

the agent stimulant used had physical properties different from those of 

the actual agent. 

 6

A binary weapon mixes two less-toxic materials to create a toxic nerve agent within the 

weapon when it is fired or dropped. 
Page 10 GAO-04-821T 

Finally, there are wide divergences—with regard to the size and path of 

the plume and the extent to which troops were exposed—among the 

individual models DOD selected. The models DOD used to predict the 

fallout from Khamisiyah and the other sites showed great divergence, even 

with the same source term data. While the models’ divergences included 

plume size and paths, DOD made no effort to reconcile them. The IDA 

expert panel observed that the results were so divergent that it would not 

be possible to choose the most exposed areas or which U.S. troops might 

potentially have been exposed. IDA therefore recommended a composite 

model, which DOD adopted.7

 However, this approach only masked 

differences in individual model projections with respect to divergences in 

plume size and path. In addition, DOD chose not to include in the 

composite model the results of the LLNL simulation, performed at the IDA 

expert panel’s request. The LLNL simulation estimated a larger plume size 

and different path from DOD’s models. The IDA panel regarded the LLNL 

model as less capable than other models because it modeled atmospheric 

phenomena with less fidelity. A modeling simulation done by the Air Force 

Technical Applications Center (AFTAC) also showed significant 

divergences from DOD’s composite model. 

According to British officials, the MOD did not collect any source term or 

meteorological data during the 1991 Persian Gulf War. It also did not 

independently model the plume from Khamisiyah, relying instead on the 

1997 DOD and CIA modeling of Khamisiyah. However, according to British 

MOD officials, they were reassessing the extent of British troops’ 

exposure, based on DOD’s revised 2000 remodeling of Khamisiyah. We 

requested from the British MOD, but did not receive, information on the 

findings from this reassessment. 

The MOD also determined that a number of British troops were within the 

boundary of the plume in the DOD and CIA composite model. The MOD 

estimated that the total number of British troops potentially exposed was 

about 9,000 and the total number of troops as “definitely” within the path 

of the plume, however, was about 3,800. In addition, of 53,500 British 

troops deployed, at least 44,000 were estimated as “definitely not” within 

the path of the plume. However, since the MOD relied exclusively on 

DOD’s modeling and since we found that DOD could not know who was 

 7

The composite approach DOD used is also known as the ensemble approach. 

MOD Relied on U.S. 

Plume Modeling to 

Determine Their 

Troops’ Exposure to 

Chemical Warfare 

Agents 
Page 11 GAO-04-821T 

and who was not exposed, the MOD cannot know the extent of British 

troops’ exposure. 

The DOD and CIA were the primary agencies involved in the modeling and 

analysis of U.S. troops’ exposure from the demolition at Khamisiyah and 

bombing of chemical facilities at Al Muthanna, Muhammadiyat, and 

Ukhaydir, but several other agencies and contractors also participated. 

Funding to support the modeling efforts was provided to various DOD 

agencies and organizations, the military services, and non-DOD agencies 

and contractors. We collected data on the direct costs these agencies 

incurred or funds they spent. As shown in table 1, direct costs to the 

United States for modeling the Gulf War were about $13.7 million. 

Total U.S. PlumeModeling Costs 
Page 12 GAO-04-821T 

Table 1: U.S. Direct Costs for Modeling Gulf War Illnesses 

Agency or contractor Direct costsa Work done 

BAHR Inc. $11,796 Reviewed (1) processes and technology used to produce estimates of U.S. 

forces potentially exposed and (2) draft reports on Khamisiyah 

Central Intelligence Agency b Computer-modeling analysis 

Chemical Biological Defense 

Command, Aberdeen Proving 

Ground 

140,000 Wood-surface evaporative modeling and environmental data support efforts

Defense Threat Reduction Agency 870,000 Computer-modeling analyses with HPAC/SCIPUFF dispersion and OMEGA 

weather models 

Institute for Defense Analyses 149,429 Convened a panel of experts to review Khamisiyah pit modeling analyses 

Lawrence Livermore National 

Laboratory 

60,000 Computer-modeling analyses with ADPIC dispersion and MATHEW 

weather models 

National Center for Atmospheric 

Research 

308,000 Computer-modeling simulations using MM5 weather model 

Naval Research Laboratory 1,090,000 Meteorological analysis to identify downwind hazard assessment with 

NOGAPS and COAMPS weather models. 

Naval Surface Warfare Center 522,000 Computer-modeling analyses with VLSTRACK dispersion and COAMPS 

weather models 

Office of the Special Assistant to the 

Deputy Secretary of Defense for Gulf 

War Illnesses 

7,980,000 Internal costs for producing case narratives for Al Muthanna, Khamisiyah, 

Muhammadiyat, and Ukhaydir 

Science Applications International 

Corporation 

c Computer-modeling analysis 

U.S. Army Center for Health 

Promotion and Preventative Medicine 

731,000 Exposure assessment and environmental modeling to determine U.S. 

troops’ exposed to chemical releases from multiple incidents during the Gulf 

War 

U.S. Army Dugway Proving Ground 1,861,950 Field trials and laboratory testing using 122 mm chemical-simulant filled 

rockets to develop source term data for modeling 

White Sands Missile Range 2,600 Missiles for testing at Dugway Proving Ground 

Total $13,726,775 

Sources: Agency and contractor responses provided to GAO regarding their modeling and analysis costs. 

a

Direct costs for agencies includes funding for contracts provided by the Office of the Special 

Assistant to the Deputy Secretary of Defense for Gulf War Illnesses. 

b

The CIA denied our request for its costs for modeling chemical releases from Khamisiyah, as well as 

Al Muthanna, Muhammadiyat, and Ukhaydir. 

c

SAIC did not respond to our requests for information. 
Page 13 GAO-04-821T 

DOD and VA each funded an epidemiological study on chemical warfare 

agent exposure—DOD’s on hospitalization rates and VA’s on mortality 

rates. From the hospitalization study, conducted by DOD researchers, and 

the mortality study, conducted by VA researchers, on exposed and 

nonexposed troops, DOD concluded that there was no significant 

difference in the rates of hospitalization and VA concluded no significant 

difference in the rates of mortality. These conclusions, however, cannot be 

supported by the available evidence. These studies contained two inherent 

weaknesses: (1) flawed criteria for classifying exposure, resulting in 

classification bias, and (2) an insensitive outcome measure, resulting in 

outcome bias. In addition, in several other published studies of 1991 

Persian Gulf War veterans, suggest an associations between chemical 

warfare exposure and illnesses and symptoms have been established. 

In the two epidemiological studies, DOD and VA researchers used DOD’s 

1997 plume model for determining which troops were under the path of 

the plume—who were estimated to be exposed—and which troops were 

not—those who were estimated to be nonexposed. However, this 

classification is flawed, given the inappropriate criteria for inclusion and 

exclusion. 

In the hospitalization study, the DOD researchers included 349,291 Army 

troops “coded” as being in the Army on February 21, 1991. However, the 

researchers did not report cutoff dates for inclusion in the study—that is, 

they did not indicate whether these troops were in the Persian Gulf 

between January 17, 1991, and March 13, 1991, the period during which the 

bombings and the Khamisiyah demolition took place. Although we 

requested this information, DOD researchers failed to provide it. Finally, 

the total number of 349,291 troops is misleading because many troops left 

the service soon after returning from the Persian Gulf and therefore would 

not have been hospitalized after the war in a military hospital—another 

criterion for inclusion in the study. Moreover, the researchers did not 

conduct any analyses to determine what number or percentage of those 

who left active duty were in the exposed or nonexposed group (including 

uncertain low-dose exposure or estimated subclinical exposure). Given all 

the methodological problems in this study, it is not possible to accurately 

estimate the total size or makeup of the exposed and nonexposed 

population that may have sought or may have been eligible for care 

leading to military hospitalization. 

In the mortality study, the VA researchers included 621,902 Gulf War 

veterans who arrived in the Persian Gulf before March 1, 1991. Troops 

DOD’s and VA’s 

Epidemiology-Based 

Conclusions on 

Chemical Warfare 

Exposure and Rates 

for Hospitalization 

and Mortality Cannot 

Be Adequately 

Supported 

DOD and VA Used Flawed 

Criteria for Determining 

Troops’ Exposure 
Page 14 GAO-04-821T 

who left before January 17, 1991—the beginning of the bombing of Iraqi 

research, production, and storage facilities for chemical warfare agents—

were included in the study. This group was not likely to have been 

exposed. Therefore, including them resulted in VA’s overestimation of the 

nonexposed group. 

Troops who came after March 1, 1991—the period during which 

Khamisiyah demolition took place—were excluded from the VA study. The 

Defense Manpower Data Center (DMDC) identified 696,000 troops 

deployed to the Persian Gulf, but the mortality study included only the 

621,902 troops deployed there before March 1, 1991. This decision 

excluded more than 74,000 troops, approximately 11 percent of the total 

deployed. In addition, 693 troops who were in the exposed group were 

excluded because identifying data, such as Social Security numbers, did 

not match the DMDC database. VA researchers did not conduct follow-up 

analysis to determine whether those who were excluded differed from 

those who were included in ways that would affect the classification. 

Hospitalization rates—the outcome measure used in the hospitalization 

study—were insensitive because they failed to capture the chronic 

illnesses that 1991 Persian Gulf War veterans commonly report, but that 

typically do not lead to hospitalization. Studies that rely on this type of 

outcome as an end point are predetermined to overlook any association 

between exposure and illness. 

Based on DOD’s 1997 plume model, DOD’s hospitalization study compared 

the rates for 1991 Persian Gulf War veterans who were exposed with the 

rates for those who were nonexposed. This study included 349,291 active 

duty Army troops who were deployed to the Persian Gulf. However, DOD 

researchers did not determine the resulting bias in their analyses, because 

they did not account for those who left the service. 

The Institute of Medicine noted that the hospitalization study was limited 

to Army troops remaining on active duty and to events occurring in 

military hospitals. Conceivably, those who suffered from Gulf War-related 

symptoms might leave active duty voluntarily or might take a medical 

discharge. Hospitalization for this group would be reflected in VA or 

private sector databases, but not in DOD databases. The health or other 

characteristics of active duty troops could differ from those of troops who 

DOD and VA Used an 

Insensitive Outcome 

Measure for Determining 

Hospitalization Rates 
Page 15 GAO-04-821T 

left active duty and were treated in nonmilitary hospitals. Moreover, 

economic and other factors not related to health are likely to affect the use 

of nonmilitary hospitals and health care services.8

This limiting of the study to troops remaining on active duty produced a 

type of selection bias known as the healthy warrior effect.9

 It strongly 

biased the study toward finding no excess hospitalization among the 

active duty Army troops compared with those who left the service after 

the war. 

We found some studies that suggest an association between chemical 

warfare agent exposure and Gulf War illnesses. Each of these studies has 

both strengths and limitations. 

In a privately funded study, Haley and colleagues reported an association 

between a syndromic case definition of Gulf War illnesses, developed to 

model the ill veterans’ symptomatic complaints, with exposure to CW 

agents.10 In this study, the authors developed questionnaires on symptoms 

and environmental exposure identified in pilot studies of ill Gulf War 

veterans, similar to epidemic investigations by the Centers for Disease 

Control and Prevention (CDC).11 These questionnaires were given to 249 

troops from a U.S. Navy Mobile Construction Battalion that participated in 

the Gulf War. Factor analysis of the data on symptoms was used to derive 

 8

Institute of Medicine, Gulf War Veterans: Measuring Health (Washington, D.C.: National 

Academy Press, 1999), p. 36. 

9

R. W. Haley, “Point: Bias from the ‘Healthy-Warrior Effect’ and Unequal Follow-Up in 

Three Government Studies of Health Effects of the Gulf War,” American Journal of 

Epidemiology 148 (1998): 315–38. 

10R. W. Haley and T. L. Kurt, “Self-Reported Exposure to Neurotoxic Chemical 

Combinations in the Gulf War,” JAMA 277 (1997): 231–37. 

11See Michael B. Gregg, ed., Field Epidemiology, 2nd ed. (New York: Oxford University 

Press, 2002). 

Some Studies Suggest an 

Association between 

Chemical Warfare 

Exposure and Gulf War 

Illnesses 

Gulf War Veterans Studies 
Page 16 GAO-04-821T 

a case definition identifying six syndrome factors.12 Three syndrome factor 

variants found to be the most significant were (1) impaired cognition, 

(2) confusion-ataxia, and (3) arthro-myo-neuropathy. 

Impaired cognition (syndrome 1) was associated with troops’ having worn 

flea collars that contained chlorpyrifos.13 Confusion-ataxia (syndrome 2), 

the most severe clinically, was associated with three risk factors.14 The 

first was likely CW exposure; the second was the geographic location near 

the Saudi-Kuwaiti border around the fourth day of the air war, conducted 

January 18–23, 1991, when Czech chemical detection units detected sarin 

and mustard in ambient air near the Saudi-Kuwaiti border; and the third 

was side effects experienced after taking pyridostigmine. There was also a 

significant synergistic association between likely exposure to CW agents 

and the number of side effects from pyridostigmine.15 Arthro-myoneuropathy (syndrome 3) was associated with the amount of exposure to 

95 percent DEET in ethanol insect repellent and with the number of side 

effects of pyridostigmine.16

 12R. W. Haley and others, “Is There a Gulf War Syndrome? Searching for Syndromes by 

Factor Analysis of Symptoms,” JAMA 277 (1997): 215–22. The six syndrome factors were 

impaired cognition, confusion-ataxia, arthro-myo-neuropathy, phobia-apraxia, feveradenopathy, and weakness-incontinence. 

13Impaired cognition is characterized by problems with attention, memory, and reasoning, 

as well as insomnia, depression, daytime sleepiness, and headache. (Study results showed 

relative risk 8.2, 95 percent, CI 2.9–23.5, p = 0.001.) 

14Confusion-ataxia is characterized by problems with thinking, disorientation, balance 

disturbances, vertigo, and impotence. 

15(1) CW exposure, relative risk 7.8, 95 percent, CI 2.3–25.9, p < 0.0001; (2) geographic 

location, relative risk 4.3, 95 percent, CI 1.9–10.0, p = 0.004; (3) pyridostigmine side effects, 

dose-response trend up to relative risk 32.4, 95 percent, CI 7.8–135.0, p < 0.0001; (4) 

synergistic association, Rothman synergy statistic 5.3, 95 percent, CI 1.04–26.7, p < 0.05. 

See Jonathan B. Tucker, “Evidence Iraq Used Chemical Weapons during the 1991 Persian 

Gulf War,” The Nonproliferation Review 4:3 (Spring–Summer 1997): 114–22. Center for 

Nonproliferation Studies, Monterey Institute of International Studies, 

http://cns.miis.edu/pubs (Apr. 28, 2004); and U.S. Department of Defense, Office of the 

Special Assistant for Gulf War Illnesses, Coalition Chemical Detections and Health of 

Coalition Troops in Detection Area (Washington, D.C.: Aug. 5, 1996). 

http://www.gulflink.osd.mil/czech_french/czfr_refs/n08en011/coalitn.html (Apr. 28, 2004). 

16Arthro-myo-neuropathy is characterized by joint and muscle pains, muscle fatigue, 

difficulty lifting, and paresthesias of the extremities. (Results showed for exposure, doseresponse effect to relative risk 7.8, 95 percent, CI 2.4–24.7, p < 0.0001; for side effects, doseresponse effect to relative risk 3.9, 95 percent, CI 1.3–12.1, p < 0.0001.) 
Page 17 GAO-04-821T 

The inference that these risk-factor associations represent causal effects is 

supported by (1) the large, highly significant relative risks; (2) the doseresponse effects; and (3) the synergistic effect of the risk factor 

associations with the syndromic case definition. Risk factors found not to 

be significantly associated with the case definition include environmental 

pesticides, pesticides in uniforms, antibiotic or antimalarial prophylaxis, 

multiple immunizations, smoke from oil well fires, fumes from jet fuel, 

fumes from burning jet fuel in tents, petroleum in drinking water, depleted 

uranium munitions, smoking, alcohol use, and combat exposure. 

Another study of Gulf War veterans by Nisenbaum and colleagues, funded 

by CDC, examined the risk factors in 1,002 Air Force reservists.17 They 

found, first, that the case definition of Fukuda and colleagues of 

“multisymptom illness” was strongly associated with at least one of the 

three chronic symptom groups fatigue, mood/cognition, and 

musculoskeletal pain. And, next, they found that reported exposure to CW 

agents was most strongly associated with the “severe illness” case 

definition of Fukuda and colleagues and less strongly associated with their 

“mild–moderate illness” case definition.18

Both case definitions were less strongly associated with the use of insect 

repellent (p = 0.006), the use of pyridostigmine (p = 0.01), and having an 

injury requiring medical attention (p = 0.03). But neither case definition 

was associated with smoke from oil well fires, coming under attack, seeing 

casualties, or having adverse health events in the family. The findings were 

attributed to the effects of stress but offered no empirical support for the 

explanation. 

In a study that VA funded, Proctor and colleagues compared the exposure 

histories of 186 Gulf War veterans from Fort Devens, Massachusetts, and 

66 from New Orleans, including 48 who deployed only to Germany. 

Collectively, the 252 veterans are known as the Massachusetts–New 

 17R. Nisenbaum and others, “Deployment Stressors and a Chronic Multisymptom Illness 

among Gulf War Veterans,” Journal of Nervous and Mental Disease 188 (2000): 259–66. 

18Association with “severe illness,” adjusted OR 3.46, 95 percent, CI 1.73–6.91, p < 0.0001; 

association with “mild–moderate illness,” adjusted OR 2.25, 95 percent, CI 1.54–3.27, p < 

0.0001. See K. Fukuda and others, “A Chronic Multisymptom Illness Affecting Air Force 

Veterans of the Persian Gulf War,” JAMA 280 (1998): 981–88. 
Page 18 GAO-04-821T 

Orleans cohort.19 The case definition was a set of eight body-system 

symptom scores (BSS, distributed from 0 to 4), each constructed by 

summing the 5-point frequency-of-occurrence scales (0 = occurs never, 4 = 

occurs almost every day) for three symptoms typical of a particular body 

system. The eight body systems were cardiac, dermatological, 

gastrointestinal, musculoskeletal, neurological, neuropsychological, 

psychological, and pulmonary. Post-traumatic stress disorder (PTSD) was 

diagnosed with the structural clinical interviews, Clinician Administered 

Posttraumatic Stress (CAPS) disorder scale, or a Mississippi Scale score of 

>89. The symptoms were obtained from the 52-item Expanded Health 

Symptom Checklist, the exposure measures from an environmental 

exposure questionnaire and an Expanded Combat Exposure Scale (CES) 

questionnaire. Multiple regression analysis—controlling for age, sex, 

education, study site, Expanded CES score, and PTSD status—was used to 

develop a risk-factor model for each BSS scale. 

Exposure to CW agents and debris from SCUD missiles was associated 

with four BSS scales; exposure to smoke from tent heaters, with three BSS 

scales; exposure to pesticides, vehicle exhaust, and burning human waste, 

with two BSS scales; the Expanded CES, with only one BSS scale; and 

exposure to pyridostigmine bromide (antinerve gas pills) and smoke from 

oil well fires, with no BSS scale. Controlling for depression scores and 

excluding veterans diagnosed with PTSD did not substantially affect the 

associations. 

Three additional studies conducted with VA and DOD funding extended 

the risk-factor research for the Massachusetts–New Orleans cohort. The 

association of self-reported CW agent (nerve agent) exposure was tested 

with different formulations of the case definition. White and colleagues 

used psychological and neuropsychological tests to define illness. They 

found that exposure to CW agents was associated with abnormal measures 

of mood, memory, and attention or executive function.20 Associations 

remained significant after controlling for age, sex, race, years of education, 

repeated grade in school, head injury, medication use, diagnosis of current 

 19S. P. Proctor and others, “Health Status of Persian Gulf War Veterans: Self-Reported 

Symptoms, Environmental Exposures, and the Effect of Stress,” International Journal of 

Epidemiology 27 (1998): 1000–10. 

20R. F. White and others, “Neuropsychological Function in Gulf War Veterans: Relationships 

to Self-Reported Toxicant Exposures,” American Journal of Industrial Medicine 40 

(2001): 42–54. 
Page 19 GAO-04-821T 

PTSD (by CAPS), diagnosis of current depression (by structural clinical 

interviews), active duty versus Reserve or Guard status, seeking disability 

rating, and Vietnam service. 

Lindem and colleagues developed multiple regression models for 

neuropsychological test measures as case definitions of Gulf War 

illnesses.21 Chemical warfare agent exposure was found to be associated 

with attention and executive function (continuous performance test), 

delayed verbal recall (California Verbal Learning Test and Visual 

Reproduction Test), and confusion and fatigue (Profile of Mood States). 

These associations remained significant when controlling for age, 

education, and PTSD diagnosis (by CAPS). 

Wolfe and colleagues, studying 945 troops from the Massachusetts–New 

Orleans cohort, found that the CDC case definition of multisymptom 

illness was most strongly associated with having smelled a chemical odor, 

having taken up to 21 antinerve gas pills, or having experienced up to 10 

formal alerts for CW agent attack.22

Kang and colleagues conducted a random sample mail survey that VA 

funded. Obtaining responses from 11,441 Gulf War veterans and 9,476 

nondeployed Gulf War era veterans, they developed a case definition by 

factor analysis of symptoms measured by their questionnaire.23 The first 

three syndrome factors closely resembled those that Haley and others 

derived (noted earlier). Finding that syndrome 2 was unique to the sample 

that had been deployed in the Gulf War (found in the deployed, but not the 

nondeployed, sample) and that the component symptoms were 

neurological in character, the researchers termed their syndrome 2 a 

possible unique Gulf War neurological syndrome. Four symptoms—

blurred vision, loss of balance or dizziness, tremor or shaking, and speech 

difficulties—were associated with syndrome 2 only in the deployed 

sample. Consequently, Kang and colleagues established their case 

 21K. Lindem and others, “Neuropsychological Performance in Gulf War Era Veterans: 

Traumatic Stress Symptomatology and Exposure to Chemical-Biological Warfare Agents, 

Journal of Psychopathology and Behavioral Assessment 25:2 (2003): 105–19. 

22Chemical odor, OR = 6.2, 95 percent, CI 3.9–9.9; antinerve gas pills, OR = 3.7, 95 percent, 

CI 2.4–5.6; formal alerts for CW attack, OR = 2.7, 95 percent, CI 2.0–3.7. See J. Wolfe and 

others, “Risk Factors for Multisymptom Illness in U.S. Army Veterans of the Gulf War,” 

Journal of Occupational and Environmental Medicine 44:3 (2002): 271–81. 

23H. K. Kang and others, “Evidence for a Deployment-Related Gulf War Syndrome by Factor 

Analysis,” Archives of Environmental Health 57:1 (2002): 61–68. 
Page 20 GAO-04-821T 

definition as having all four of these symptoms. In the deployed sample, 

277 met the case definition and 6,730 who had none of the four symptoms 

constituted the control group. Of a large number of risk factors analyzed, 

only nine were associated with the case definition, with an odds ratio 

greater than 3.0. Of these, perceived exposure to nerve agent had the 

strongest association (odds ratio 15.1, 95 percent, CI 11.5–19.9, p < 

0.000001). This finding—a neurological syndrome appearing as the second 

factor in a factor analysis and being the most strongly associated risk 

factor, 15 times more common in ill veterans meeting the case definition 

than in controls—closely parallels the findings of Haley and colleagues. 

The finding received little notice, however, because the VA-funded mail 

survey did not (1) provide the odds ratio values in the table reporting the 

risk factor analysis results and (2) describe the finding in the text or 

abstract of the paper. When we noticed the finding, we manually 

calculated the odds ratios from the raw data in the table. 

Smith and colleagues showed that hospitalization rates for several ICD-9 

diagnoses were higher in veterans categorized in the Khamisiyah 2000 

plume than in those not in the plume, and the association for cardiac 

arrhythmias was statistically significant. However, this study suffers from 

the same deficiencies as the earlier study that we cited: use, 

inappropriately, of hospitalization outcome measures rather than 

measures of Gulf War illness, which usually do not result in 

hospitalization, and use of plume modeling based on flawed data.24 

The 2002 Kang and Bullman study has not been published in a peerreviewed journal and therefore should not have been included in a review 

of the scientific epidemiologic literature. The DOD studies were invalid for 

two reasons: (1) Hospitalization and mortality were inappropriate 

outcomes because they do not measure Gulf War illnesses, which often do 

not lead to hospitalization, and (2) The DOD studies, no matter how 

powerful their techniques, could not control for the selection bias that 

resulted from the disproportionate early discharge of the ill Gulf War 

veterans soon after the Gulf War. Including only DOD hospital records of 

service members remaining on active duty resulted in the exclusion of 

veterans who left service for poor health. No amount of sophisticated 

 24T. C. Smith and others, “Gulf War Veterans and Iraqi Nerve Agents at Khamisiyah: 

Postwar Hospitalization Data Revisited,” American Journal of Epidemiology 158 (2003): 

457–67.
Page 21 GAO-04-821T 

techniques can correct for this selection bias toward finding no 

difference.25

In one genetics study, Haley and colleagues found an association between 

the case definition of Gulf War illnesses in U.S. Gulf War veterans and low 

blood levels of the Q-type isoenzyme of the paraoxonase/arylesterase 

enzyme group (PON).26 The PON group of enzymes is a potentially 

important predisposing factor in Gulf War illnesses because one of its 

major functions in normal body physiology is to protect the nervous 

system from organophosphate chemical toxins, such as pesticides and 

nerve agents. This finding was remarkable because the only function of Q 

type of the PON enzyme group is to protect the nervous system from nerve 

agents sarin, soman, tabun, and VX. The R-type isoenzyme has as its main 

function protection from organophosphate pesticides, such as diazinon, 

malathion, and parathion. Thus, an association between Gulf War illnesses 

and blood levels of only the Q-type isoenzyme of PON points specifically 

to nerve agent exposure. In addition, the total PON level—that is, the sum 

of the Q and R isoenzyme levels—was not associated with the illnesses. 

And the genotype (QQ, QR, or RR) was only marginally associated with 

them, as expected, because the level of the Q-type isoenzyme is a more 

important determinant of susceptibility to nerve agents than the genotype. 

In another genetics study, Mackness and colleagues reported lower blood 

levels of total PON in ill British Gulf War veterans than in civilian controls 

in a previously published study; however, they did not measure the blood 

levels of the Q and R isoenzymes of PON, needed for a definitive study of 

Haley’s hypothesis.27 This finding could indicate that ill British Gulf War 

veterans represented a mixture of some with low Q-type PON and others 

with low R-type PON. In some veterans, the illness would be associated 

with exposure to nerve agents; in others, with exposure to pesticides. 

Alternatively, the difference in total PON levels may have resulted from 

differences in the assays or in the veterans, since (1) the enzyme assays in 

 25H. K. Kang and T. A. Bullman, Mortality among U.S. Gulf War Veterans Who Were 

Potentially Exposed to Nerve Gas at Khamisiyah, Iraq (Washington, DC: Department of 

Veterans Affairs, May 2002).

26R. W. Haley and others, “Association of Low PON1 Type Q (Type A) Arylesterase Activity 

with Neurologic Symptom Complexes in Gulf War Veterans,” Toxicology and Applied 

Pharmacology 157 (1999): 227–33. 

27B. Mackness and others, “Low Paraoxonase in Persian Gulf War Veterans Self-Reporting 

Gulf War Syndrome,” Biochemical and Biophysical Research Communications 276 

(2000): 729–33. 

Genetics Studies 
Page 22 GAO-04-821T 

the controls were performed years before those for the ill veterans and (2) 

the controls were civilians studied in an entirely different setting. 

In yet a third genetics study, Hotopf and colleagues reported results of 

tests for total PON levels in blood samples—obtained in a study by Unwin 

and colleagues—for four groups of British troops: (1) ill veterans of the 

Gulf War, (2) well veterans of the Gulf War, (3) ill nondeployed veterans of 

the Gulf War era, and (4) ill veterans of the Bosnian conflict.28 The case 

definition of illness was a score below 72.2 on the SF-36 Physical Status 

questionnaire. Again, the researchers did not measure the levels of the Q 

and R isoenzymes of PON, making the findings difficult to interpret. The 

researchers found a low mean level of total PON in both ill and well 

groups deployed to the Gulf War and higher levels in the Gulf War era and 

ill Bosnian groups. 

The depressing of the total PON level, the researchers suggested, might be 

the result of some deployment-related exposures. However, instead of 

looking at exposure to CW agents, the researchers investigated the 

possible effect of multiple immunizations on total PON levels and found 

no evidence for it. An alternative explanation is that total PON level in 

both ill and well deployed veterans was the result of misclassification of 

veterans by the case definition. A score of 72.2 on the SF-36 scale is not a 

very low score, particularly in ill Gulf War veterans, and it is a nonspecific 

measure of illness, given that a low score indicates illness from any 

cause.29 Consequently, many veterans ill from causes unrelated to the war 

would be misclassified as cases of Gulf War illness and, conversely, many 

ill from the war but with less disability would be misclassified as controls. 

This conclusion is supported by a nonsignificant trend showing that ill 

veterans who had been deployed to the Gulf War had a lower median total 

PON level than well veterans who had also been deployed to the Gulf War. 

The many flaws of design and methodology in both British studies of PON 

levels do not contribute to an understanding of the PON hypothesis and 

leave the finding of Haley and colleagues in need of better replication. 

 28See Matthew Hotopf and others, “Paraoxonase in Persian Gulf War Veterans,” Journal of 

Occupational and Environmental Medicine 45 (2003): 668-75, and C. Unwin and others, 

“Health of UK Servicemen Who Served in the Persian Gulf War,” Lancet 353 (1999): 169–78. 

29R. W. Haley and others, “Severely Reduced Functional Status in Veterans Fitting a Case 

Definition of Gulf War Syndrome,” American Journal of Public Health 92 (2002): 46–47. 
Page 23 GAO-04-821T 

A series of laboratory studies with animals have established the biological 

plausibility that brain cell damage results from low-level exposure to sarin. 

Husain and colleagues demonstrated in two studies at the Division of 

Pharmacology and Toxicology at the Defense Research and Development 

Establishment in Gwalior, India, that repetitive administration of low-dose 

sarin (approximately 0.25 LD50) daily for 10 days caused delayed onset 

damage to neurons in the spinal cords and brains of mice exposed by 

inhalation and of hens exposed by subcutaneous injection.30

Privately funded studies by Abou-Donia and colleagues demonstrated that 

combinations of organophosphates and similar cholinesterase-inhibiting 

chemicals in hens produce greater neurotoxic effect on brain and nerve 

tissue than any of the agents alone.31 Abou-Donia’s subsequent work, 

funded by DOD, extended the findings to synergistic combinations 

involving sarin at moderate concentrations (0.5 LD50).32 A similar study by 

Husain and Somani, also funded by DOD, on the delayed brain effects of 

low-dose sarin (0.05 LD50) in combination with pyridostigmine and 

exercise, confirmed these findings. In particular, it demonstrated that the 

neuronal damage from very low doses of sarin affected primarily the basal 

ganglia region of the brain (striatum).33

A study by Henderson and colleagues, with DOD funding, found that 

repeated inhalation exposure to low-level sarin at subsymptomatic doses 

 30K. Husain and others, “Delayed Neurotoxic Effect of Sarin in Mice after Repeated 

Inhalation Exposure,” Journal of Applied Toxicology 13 (1993): 143–45, and “A 

Comparative Study of Delayed Neurotoxicity in Hens Following Repeated Administration 

of Organophosphorus Compounds,” Indian Journal of Physiology and Pharmacology 39 

(1995): 47–50. 

31Mohamed B. Abou-Donia and others, “Neurotoxicity Resulting from Coexposure to 

Pyridostigmine Bromide, DEET, and Permethrin,” Journal of Toxicology and 

Environmental Health 48 (1996): 35–56, and “Increased Neurotoxicity Following 

Concurrent Exposure to Pyridostigmine Bromide, DEET, and Chlorpyrifos,” Fundamentals 

of Applied Toxicology 34 (1996): 201–22. 

32Mohamed B. Abou-Donia and others, “Combined Exposure to Sarin and Pyridostigmine 

Bromide Increased Levels of Rat Urinary 3-Nitrotyrosine and 8-Hydroxy-2’-

Deoxyguanosine, Biomarkers of Oxidative Stress,” Toxicology Letters 123 (2001): 51–58; 

“Disruption of the Blood-Brain Barrier and Neuronal Cell Death in Cingulate Cortex, 

Dentate Gyrus, Thalamus, and Hypothalamus in a Rat Model of Gulf-War Syndrome,” 

Neurobiology of Disease 10 (2002): 306–26; and “Sarin: Health Effects, Metabolism, and 

Methods of Analysis,” Food and Chemical Toxicology 40 (2002): 1327–33. 

33K. Husain and S. Somani, “Delayed Toxic Effects of Nerve Gas Sarin and Pyridostigmine 

under Physical Stress in Mice,” Journal of Burns and Surgical Wound Care 2 (2003): 2–19. 

Animal Studies 
Page 24 GAO-04-821T 

(0.1 LCt50) for 5 or 10 days, with or without heat stress, produced no 

immediate effects.34 But at 30 days after exposure to sarin, damage was 

produced to cholinergic receptors in several brain regions, including the 

basal ganglia. In the same study, Henderson and colleagues identified 

evidence of an autonomic nervous system injury affecting the function of 

T-cells in the immune system as well.35 In addition, chronic abnormalities 

of neuronal metabolism in the basal ganglia have been implicated in ill 

Gulf War veterans by several investigators through the use of magnetic 

resonance spectroscopy.36

Two recent laboratory studies at the U.S. Army Medical Research Institute 

of Chemical Defense, Aberdeen Proving Ground, support the animal 

studies. Scremin and colleagues demonstrated that moderate doses of 

sarin (0.5 LD50) in combination with pyridostigmine bromide produced 

prolonged elevations in rats’ cerebral blood flow but that neither agent 

alone had a prolonged effect on cerebral blood flow.37 A companion study, 

by Roberson and colleagues, demonstrated that repeated administration of 

sarin to guinea pigs in doses of 0.2 or 0.4 LD50 produced no immediate ill 

effects on behavior, weight, body temperature, flinch threshold, or EEG 

brain wave activity. But at 100 days postdosing, abnormal brain function 

was found, indicating neurochemical or pathological brain cell changes 

that affect behavior.38

 34R. F. Henderson and others, “Response of F344 Rats to Inhalation of Subclinical Levels of 

Sarin: Exploring Potential Causes of Gulf War Illness,” Journal of Toxicology and 

Industrial Health 17 (2001): 294–97 and 18:1 (2002): 48. 

35See Henderson and others, “Response of Rats to Low Levels of Sarin,” and “Subclinical 

Doses of the Nerve Gas Sarin Impair T Cell Responses through the Autonomic Nervous 

System,” Journal of Toxicology and Applied Pharmacology 184 (2002): 82–87. 

36See R. W. Haley and others, “Brain Abnormalities in Gulf War Syndrome: Evaluation by 1

H 

Magnetic Resonance Spectroscopy,” Radiology 215 (2000): 807–17, and “Effect of Basal 

Ganglia Injury on Central Dopamine Activity in Gulf War Syndrome: Correlation of Proton 

Magnetic Resonance Spectroscopy and Plasma Homovanillic Acid,” Archives of Neurology 

57 (2000): 1280–85, as well as D. J. Meyerhoff and others, “Reduced N-Acetylaspartate in 

the Right Basal Ganglia of Ill Gulf War Veterans by Magnetic Resonance Spectroscopy,” 

Proceedings of the International Society of Magnetic Resonance Medicine 9 (2001): 994. 

37O. U. Scremin and others, “Effects of Chronic Exposure to Low Levels of Cholinesterase 

Inhibitors on Cerebral Blood Flow,” paper for the Society for Neuroscience Meeting, 

Orlando, Florida, 2002. 

38Melinda Roberson and others, “Depression of Cholinesterase Activity by Low-Dose Sarin 

Exposure May Lead to Persistent Changes That Influence Behavior,” Society for 

Neuroscience, Washington, D.C., Program no. 205.3 (Abstract, 2002). 
Page 25 GAO-04-821T 

In evaluating the plume models used, the results from the DOD and CIA 

modeling can never be definitive. Plume models can allow only estimates 

of what happens when chemical warfare agents are released in the 

environment. Such estimates are based on mathematical equations, which 

are used to predict an actual event—in this case, the direction and extent 

of the plume. However, in order to predict precisely what happens, one 

needs to have accurate data on relative to both source term and 

meteorological conditions. DOD had neither of these. 

Given the unreliability of the input data, the lack of individual troop 

location information, and the widely divergent results of the simulations 

conducted based on varying models, DOD’s analyses cannot adequately 

estimate the extent of U.S. troops’ exposure to chemical warfare agents 

and other related releases. In particular, the models selected were not fully 

developed for projecting long-range environmental fallout, and the 

assumptions used to provide the source term data were inaccurate or 

flawed. Even when models with the same source term data were used, the 

results diverged. In addition, the models did not include many potential 

exposure events and exposures to some key materials—for example, 

binary chemical weapons, mustard agent combustion by-products, and 

chemical warfare agent precursor materials. It is likely that if models were 

more fully developed and more credible data for source term and 

meteorological conditions were included in them, particularly with respect 

to plume height as well as level and duration of exposure, the hazard area 

would be much larger and most likely would cover most of the areas 

where U.S. troops and Coalition forces were deployed. However, given the 

lack of verifiable data for analyses, it is unlikely that any further modeling 

efforts would be more accurate or helpful. 

The results of DOD’s modeling efforts were, nonetheless, used in 

epidemiological studies to determine the troops’ chemical warfare agent 

exposure classification—i.e., exposed versus nonexposed. As we noted in 

1997, to ascertain the causes of veterans’ illnesses, it is imperative that 

investigators have valid and reliable data on exposure, especially for lowlevel or intermittent exposures to chemical warfare agents.39 To the extent 

that veterans are misclassified as to exposure, relationships will be 

obscured and conclusions misleading. In addition, DOD combined the 

 39U.S. General Accounting Office, Gulf War Illnesses: Improved Monitoring of Clinical 

Progress and Reexamination of Research Emphasis Are Needed, GAO/NSIAD-97-163

(Washington, D.C.: June 23, 1997). 

Conclusions 
Page 26 GAO-04-821T 

results of individual models that showed smaller plume size and ignored 

the results of the LLNL which showed much larger plume size and 

divergent plume path. Given the uncertainties in source term data and 

divergences in model results, DOD cannot determine or estimate—with 

any degree of certainty—the size and path of the plumes or who was or 

who was not exposed. 

In our report, we are recommending that the Secretary of Defense and the 

Secretary of Veterans Affairs not use the plume-modeling data for future 

epidemiological studies of the 1991 Gulf War, since VA and DOD cannot 

know from the flawed plume modeling who was and who was not 

exposed. 

We are also recommending that the Secretary of Defense require no 

further plume-modeling of Khamisiyah and the other sites bombed during 

the 1991 Persian Gulf War in order to determine troops’ exposure. Given 

the uncertainties in the source term and meteorological data, additional 

modeling of the various sites bombed would most likely result in 

additional cost, while still not providing DOD with any definitive data on 

estimating who was or was not exposed. 

We obtained comments on a draft of this report from VA, DOD, and CIA. 

VA concurred with the recommendation that VA and DOD not use the 

plume-modeling data for future epidemiological studies, since VA and 

DOD cannot know from the flawed plume modeling who was and who was 

not exposed. DOD did not concur with the recommendation, indicating 

that to them it called for a blanket prohibition of plume modeling in the 

future, where the limitations of the 1991 Gulf War may not apply. The 

intent of our recommendation is only directed at epidemiological studies 

involving the DOD and CIA plume modeling data from the 1991 Gulf War 

and not a blanket prohibition of plume modeling in the future. We have 

clarified the recommendation along these lines. DOD concurred with our 

second recommendation, indicating that despite enhancements in the 

models, uncertainties will remain. CIA did not concur with our report, 

indicating that it could not complete its review in the time allotted. 

Recommendations for 

Executive Action 
Page 27 GAO-04-821T 

If you or your staff have any questions about this testimony or would like 

additional information, please contact me at (202) 512-6412 or Sushil 

Sharma, Ph.D., Dr.PH., at (202) 512-3460. We can also be reached by e-mail 

at rhodesk@gao.gov and sharmas@gao.gov. Individuals who made key 

contributions to this testimony were Venkareddy Chennareddy, Susan 

Conlon, Neil Doherty, Jason Fong, Penny Pickett, Laurel Rabin, and 

Katherine Raheb. James J. Tuite III, a GAO consultant, provided technical 

expertise. 

Keith Rhodes, Chief Technologist 

Center for Technology and Engineering 

 Applied Research and Methods 

(460566) 
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