Operation Black Dog

[David Guyatt]

Posted as requested and following on from post No. 9 HERE.

OPERATION BLACK DOG

The Gulf war story that no one would publish

By David Guyatt



Source "B" was shaken but not stirred when we first met. The odour of fear and uncertainty was palpable - a fact that was no surprise in view of what I was about to be told. This wasn't my first 007 Bond-like covert rendezvous, but it would certainly be my most startling. We had agreed to meet in order that the source could tell me about a highly secret and even more highly sensitive US operation known as "Black Dog." Neither of us trusted electronic communication and, therefore, a face-to-face meeting was essential.

It was a sunny day and our encounter was in a seamy pub somewhere in the countryside of England. I had watched my back the entire journey - just in case. The meeting followed a story I had written on Gulf War Illness, when I had cautiously been told about a top secret US mission known as "Black Cat." This, I was told, involved a "black" US B52 bomber launching from Offut AFB in Nebraksa, and flying a round-trip to the Persian Gulf.

The hulking bomber carried one bomb packed with VX nerve agent, the most potent chemical weapon in the US CW armoury. The bomb was dropped on elements of the Republican Guard in Southern Iraq, I was informed. Heavy casualties apparently resulted. The operation, directed by the Central Intelligence Agency, was a counter-strike, following an Iraqi Scud that fell on Israel. The missile had contained Sarin and drove the Israeli government almost apoplectic with rage. Fuming, the Israeli's had readied to detonate a nuclear warhead high above Baghdad. Only the swift intervention of President George Bush forestalled what would have been a cataclysmic move destined to unravel the carefully wrought Arab backed Coalition lined-up against Iraqi dictator Saddam Hussein.

To avoid any of the nerve agent being blown back towards coalition troops, the mission involved the launch, from Dhahran of a C130 Hercules carrying one, possibly two, massive five ton Fuel Air bombs. These were detonated above ground zero - the location of the VX chemical agent strike - to ensure all traces of the nerve agent were destroyed. Quite possibly, the Fuel Air Device destroyed all evidence of the illegal counter-strike too, by incinerating bodies. Cleansing by fire is as old as warfare itself.

This information led me to speak to various sources as I searched for corroboration. I was advised to contact Tim Sebastian, former BBC correspondent and well-known author. During a brief telephone call, Sebastian confirmed he also had the same information as I, as recommended I contact the Countess of Mar - a House of Lords representative with a special interest in Gulf War issues. I met Margaret Mar one evening in late summer 1997. A charming and honest individual, she confirmed she had taken Sebastian's information to the Ministry of Defence in private. They later informed her that following consultation with the US Department of Defense officials, no record of the mission had been found. Clearly this was no denial.

Moreover, their explanation didn't gel in other significant ways. The official who responded to the MOD enquiry was Bernard Rostker, the Special Assistant for Gulf War Illness. Hardly, I thought, the person one would expect to be privy to top secret information on a sensitive CIA operation. Besides, I was to later learn that Black Cat almost certainly was subject to a "compartmented" mission name. This simply means that at different levels of the command structure the mission would have been assigned a different name. This nifty device - not dissimilar from Admiral Horatio Nelson holding a telescope to his blind-eye and observing he "sees no ships," - caters nicely to instant deniability, but also helps to identify the level that leaks originate from. Clever. In any event, months later, in December 1997, Tim Sebastian told me that he had fully corroborated Black Cat during a month-long trip to the USA. This was good news but not surprising.

In any event, Source B was concerned not with Black Cat - which I learned he knew about in some detail - but a second, far more sensitive mission known as "Black Dog." This mission had occurred around 25 February 1991 and involved Biological weapons, I was told. Specifically the weapon was a bacterium that resulted in those contaminated drowning in their own bodily fluids. Black Dog involved an aircraft launched from a US carrier in the Red Sea that was targeted on an Iraqi CB weapons plant. The bomb was designed to spread its load via an aerosol spray. Source B provided additional information that cannot be revealed for fear of identifying the individual and other sources.

My first meeting with Lady Mar was predominantly to discuss this second mission. Both she and Tim Sebastian were aware of a second mission that they both knew as "Black Cat 11," but possessed no details. I was not surprised. Some weeks earlier I had contacted a senior US journalist, asking if he would collaborate on my story. I gave him a brief outline of Black Cat, hoping he may stumble on to Black Dog, too. He did, or at least got details of a mission remarkably similar.

Months of investigation resulted in the development of the following mission details:

Original source (B) states that Black Dog entailed the launch of a US Navy warplane from a US Carrier on station in the Red Sea. The source remains unable to identify which of two carriers the aircraft launched from (both the USS Saratoga and the USS Kennedy were on station in the Red Sea during this time-frame: 24/25 February 1991). Nor is source able to provide exact date of this mission. The source further stated that aircrew and ground-crew were CIA.

The source continued by stating that the aircraft dropped biological warfare munition(s) on an Iraqi chemical/biological weapons factory and that numerous deaths resulted. Source states the munition (s) contained a bacteriological agent with a life of no more than 48 hours. The bacterium was not communicable, and had no given name, only a batch number. Those attacked with this weapon drowned in their own bodily fluids, according to the source, who added that the bio-bomb was parachute deployed and its contents dispersed by aerosol spray.

US Sources state that a US Navy S3A Viking aircraft crash landed (presumably as a result of ground fire) behind enemy lines prior to the commencement of the ground war. It is unknown if the aircraft was outward bound on its mission or homebound afterwards. In any event, the spectre of a US "sanitised" aircraft heavily armed with chemical and possibly biological weapons, over-flying hostile territory during time of war logically excludes the possibility this was a training or any other "innocent" mission.

The Viking is used in a long-range recconassaince/anti submarine warfare role. It is thus only lightly armed for defence. In this instance, however, sources say the aircraft was heavily modified with stealth capabilities and was coloured a flat dark grey. The aircraft had no markings, insignia or other identification. Instrumentation was United States manufacture. Bombs were externally attached to wing pylons. The procedure of using unmarked military aircraft (known as “sanitised” i.e., plausible deniability) is known to be consistent with numerous other CIA “black” operations that have reached the public domain.

Sources additionally confirm the mission was conducted under the auspices of the Central Intelligence Agency and that the pilot was an Agency employee (presumably a “sheep-dipped” USN pilot). The aircraft carried, we are told, only two bombs due to “weight considerations.” The downed aircraft had one remaining bomb attached to external pylons. This munition contained a deadly mixture of Tabun, Sarin and Cyclo-Sarin. However, US sources are unable to identify a target or confirm whether this aircraft launched from a USN carrier - giving rise to understandable caution that this was one and the same mission – although the mission profile is similar.

Meanwhile, US sources confirm that the crash site was approximately 60 kilometres behind enemy lines (exact co-ordinates 45.90E – 29.73N) – in a barren wilderness. There the aircraft remained for several days. In the interim, the pilot, who did not eject but came down with his aircraft, was recovered alive.

Following the launch of the Ground War (24 February 1991), US and French divisions swept Iraqi forces away from the general area (As Salman), thereby permitting intact recovery of the aircraft. Consequently, a US two man Black Ops “Search Team” were dispatched from Camp Four, in Saudi Arabia (co-ordinates 44.30E-29.00N) to locate the crashed aircraft and provide exact co-ordinates for recovery.

Camp Four was a large sprawling complex that housed mostly US forces, but some British elements too. It was a jump off point for the US 101 Airborne (Screaming Eagles) into Iraq on the night of 23/24 February 1991. The complex was extensively used to house and repair a variety of equipment.

The two man search team travelled North, into Iraq, by Jeep on or about 27/28 February 1991. Sources state the aircraft crashed approximately one week earlier and that the delay in commencing search and recovery operations was due to the imminent commencement of the ground war. Neither members of the two man search team were US Government employees. In fact, a private US company, almost certainly a CIA proprietary, employed both. Both individuals wore battle-dress but no insignia or other identifying patches – a fact that is again consistent with CIA black operations. An independent British military source has confirmed the presence at Camp Four, of a two man US “Spec Ops” team, in late February 1991. Source stated they were US SpecOps, no insignia or rank apparent and provided a physical description of one individual.

Some distance into Iraq, heading due north along the 45.90 East Latitude co-ordinate the search team observed the downed aircraft from a distance, we are told. Inspection via binoculars showed the right wing of the aircraft to be missing. The left wing was intact. Further observation revealed the presence of one remaining bomb located on the external pylon closest to the fuselage. The bomb was coloured a matt black with no visible marking. It was leaking.

Both team members donned CB protective equipment, we are informed, and approached. The bomb contained a German manufactured fuse designed to ignite the munition above ground. It was identified as a Mark Eleven Seven munition (MC 117) modified for liquid chemical usage and comprised of a steel body with a Mark 131 fin assembly and Central Bursting Tube - according to information made available.

A chemical weapons test with a field test kit (designated “Mary 256”) was conducted and revealed the munition to contain a mixture of Tabun, Sarin and Cyclo-Sarin. It must be stressed that a chemical weapon field test kit would not, repeat not, be capable of detecting the presence of any biological weapon whatsoever. Field detection of biological organisms/bacterium is considerably more complex and requires specialist personnel and equipment. This point is stressed for obvious reasons. The presence of a bacterium as outlined by primary source is neither corroborated, nor ruled out, by these discoveries. However, it is significant that prevailing NATO and Soviet doctrine in the use of biological and chemical weapons, called the use of a “mixed load” – that is to say, munitions would typically carry a varied mixture of inter-acting chemical and biological agents/organisms.

The search team reported their discovery to base, and was ordered to withdraw immediately. Prior to departing the crash site, both team members were puzzled by the presence of a number of dead Iraqi soldiers. All wore face masks (possibly CB protective gear, but may also have been protection against wind-borne sand) and showed no apparent entry wounds or other manifestations of their fatalities. Both team members were said to be sufficiently perplexed by these bodies to take colour photographs of them, we were informed. These photographs and other details were later forwarded to a United Nations source for investigation.

Having left the crash site, the search team were replaced by a US Navy affiliated “Recovery Team.” The latter team recovered the aircraft. The bomb was recovered and transported elsewhere. The damaged aircraft was airlifted – presumably by a Jolly Green Giant helicopter – back to Camp Four and temporarily housed in a compound surrounded with barbed wire. Here, a number of individuals managed to photograph the damaged aircraft on site. Copies of these and other supporting data were privately forwarded to the United Nations for investigation. Meanwhile, other military sources confirm the presence of the barbed wire compound at that location.

The two man Black Ops (search) team were in the Gulf acting under Army Command. Their mission, and, we are told, that of the latter recovery team, was conducted under the orders of General Fred Franks, commander of V11 Corps – the single largest unit in the Gulf war. Both the “Search” and “Recovery” teams formed part of a Special Unit with the designation “SCRSWA” operated under the direct command of Colonel Johnson (attached to AVSCOM – Aviation System Command, US Army). This unit has not been identified, despite a telephone call to the Pentagon library. A Pentagon employee told this writer, with a nervous laugh, that the unit designation is unknown. According to sources, there was a British involvement. This has yet to be identified and confirmed, but it thought possible the bacteriological weapon may have been of British manufacture. In any event, the remaining munition was placed in the custody of Colonel Johnson, sources say. Both members of the search team were specialists in placing, concealing and camouflaging surveillance devices, we were told. These included placing aircraft laser targeting packages.

In November 1997, at my request, the Countess of Mar, in the company of the former Foreign Secretary and Deputy Prime Minister, Lord Howe, met with a senior Ministry of Defence official to discuss Operation Black Dog. The meeting was acrimonious. The result was that the MOD official could neither confirm nor deny the operation but, personally doubted the possibility that a Viking aircraft would be cast in such a role. If this remains the official's only qualitative doubt, I have some advice for him.

A phone call to the premier and highly respected publication, Janes Defence Weekly, will be rewarded with an informative discussion about the aircraft's capability and the US Navy's "Gung Ho" attitude when it comes to "black" operations. One of Jane's expert journalists told me - months prior to the MOD meeting - that there is nothing theoretically to stop a Viking from flying a mission as outlined. The journalist went on to describe other missions even more "apparently" unlikely, including the launch of U2 "spy-planes" from US Navy carriers - amongst other facts.

It remains to be stated that I was advised - from entirely unrelated sources and, in fact, an entirely unrelated story - that a special CIA team of flyers was stationed at Offut AFB during the Gulf war. One of these, a former Navy pilot, and senior team member, is alleged to have been posted to a US aircraft carrier to assume temporary duty (TDY) as Commander Air Group (CAG) during the same time-frame. For a variety of reasons, I now nurture some suspicions that this later information may have been artfully "planted" as disinformation in order to discredit this story. The identity of the senior team member, employed by the CIA and ONI, is known to me, as is his background, and somewhat adds to my concerns. However, I cannot rule out the possibility that this additional information might have reached my attention innocently and coincidentally and, could be accurate?

As our investigation of this story continued, we learned of a possible reason for Black Dog. In late February 1991, an Iraqi Scud had landed in Israel. Sources were able to confirm that the missile contained biological organisms that were "dead on arrival." Whether the organisms were meant to be dead or not wasn't clear, but Iraqi in-expertise in these matters is well-known. This clearly, in the light of the prevailing logic of Black Cat, to be sufficient reason to authorise Black Dog, I believe.

The foregoing, it must be said, is powerful evidence that the US may have engaged in at least two chemical and biological warfare missions during the Gulf war. It is not, however, proof positive. Caution is understandably a key-word amongst the journalistic fraternity. At the same time outside and perverse influence to "spike" or otherwise discredit highly sensitive news stories is increasingly a fact-of-life. Those who might doubt that the media could be so easily seduced need only focus their attention on the consequences of the Gary Webb/San Jose Mercury News "Dark Alliance Series," to witness media timidity.

Having personally worked on the foregoing story for almost nine months, and witnessed numerous editors, journalists and other media representatives shy-away from it for no good reason, I am inclined to conclude that this is one of those stories destined never to reach the light of day.

The hell with that.

[Jan Klimkowski]

David - a fine piece of work, and a gritty account of the challenging lot of the genuine investigative researcher.

Dear old ICI (IcyEye) and British CBW institute Porton Down are responsible for giving us VX, the most lethal known, ie officially disclosed, nerve agent.

If America dropped a VX bomb on the Iraqi Republican Guard in Gulf War I, then it would explain quite a bit about the subsequent conduct of that war. However, it would be absolutely imperative to cover such an event up and destroy - probably incinerate as you suggest - the evidence. Ie the VX-damaged corpses.

VX is technically a V-Series nerve agent. The other major class of nerve agents, the G-Series, are a gift from.... yup, you guessed.... IG Farben.

There was an official investigation into the possible effects of exposure of allied troops to CBW muntions in the aftermath of the destruction of the Khamisiyah Pit in Gulf War I, which concentrated on G-series nerve agents.

It's a whitewash, designed to "establish" that there is no link between exposure to particular chemical weapons and Gulf War Syndrome. The chemical agents concentrated upon are: Sarin and Cyclosarin.

One of the clear risks of chronic or acute exposure to Sarin and Cyclosarin would be organophosphate-induced delayed neuropathy:

http://www.gulflink.osd.mil/khamisiyah_t...Cyclosarin

These "scientific" studies are always regarded as opportunites by military doctors.

[Ed Jewett]

Aw sheee-it, the old delayed neuropathy.


:questionmark:

Now, what was it you were saying?

:nurse:

[David Guyatt]

There was an official investigation into the possible effects of exposure of allied troops to CBW muntions in the aftermath of the destruction of the Khamisiyah Pit in Gulf War I, which concentrated on G-series nerve agents.

It's a whitewash, designed to "establish" that there is no link between exposure to particular chemical weapons and Gulf War Syndrome. The chemical agents concentrated upon are: Sarin and Cyclosarin.

One of the clear risks of chronic or acute exposure to Sarin and Cyclosarin would be organophosphate-induced delayed neuropathy:

Numerous soldiers I spoke to, including those charged with CBW measures for their units, told me that during Gulf War 1, chemical weapons sirens went off time and again, while others watched air blasts of Saddam's missiles showering the troops below with nasty stuff.

It happened regularly - daily and nightly.

But officially it didn't happen at all.

Anyone who asks why the facts, why the fiction, simply needs to be aware that it was the US and Europe who provided Saddam with his CBW capability during the Iraq-Iran war - and turned a nice buck in the process.

[Ed Jewett]

I'm certainly no expert on the matter, but we had -- in Gulf War #1 -- the keys to total victory in our grasp, the mass of the Republican Guard in a small, tightly-closed cinch sack -- shades of the Falaise Gap -- and we failed to take advantage. Was this, then, the Rothschild formula at work? Did we let the boogeyman escape for another round of fun and games, thus putting countless numbers of people in further jeopardy and allowing the development of so much more that followed? [If I am not careful, I am going to revert to playing tabletop war games in order to figure out things for myself...Luckily, the CBW in that arena consists of bread crumbs and coffee spills.]

[Jan Klimkowski]

I've copied the article about Dr Haley into this thread:

Nature + Science
Gulf War Syndrome Is Brain Damage Caused By Nerve Gas, Not Psychological Issues, UT Southwestern Study Proves


By Brantley Hargrove Thu., Sep. 15 2011 at 12:48 PM

Comments (31)

Categories: Local Hero, Nature + Science

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​There's no denying it now: Gulf War Syndrome, characterized by memory loss, lack of concentration, neuropathic pain and depression, is a physiological illness, not a psychological one.A UT Southwestern study, published in the journal Radiology, used a specialized MRI that specifically measures blood flow in the brain and detected marked abnormalities in the brains of those with Gulf War Syndrome. Not only have those abnormalities persisted for 20 years, but in some cases they've worsened.
The findings mark a significant advancement in our understanding of the syndrome, which was for years written off by the Defense Department and the Department of Veterans Affairs as a form of combat stress rather than an objectively diagnosable injury. Dr. Robert Haley, chief epidemiologist at UT Southwestern, and a cadre of clinicians and researchers, have struggled with the government for some 18 years for research funding and to have the syndrome recognized as a legitimate war injury caused by chronic exposure to minimal amounts of sarin gas.
"This was really one of the first techniques to show an objective picture of whether there's really brain damage or not," Haley tells Unfair Park.
In this study, Haley used a neurotransmitter called acetylcholine, which mimics nerve gas and acts to slow the heart rate and blood flow to the brain, making you groggy. For those with receptors damaged by nerve gas, they don't become groggy at all. In fact, sometimes it has the opposite effect. By administering the neurotransmitter and projecting radio waves into the carotid artery, Haley used a kind of MRI to measure blood flow in response. Veterans afflicted with Gulf War Syndrome didn't respond normally by showing decreases in blood flow to the brain you'd expect.
It's no surprise, then, that many of them report sleep difficulties as well. Approximately 20 percent of the population has a weak form of a gene that protects nerve receptors from sarin gas, Haley says. As a result of this study, it's likely no coincidence that at least 25 percent of veterans who were deployed in Iraq are thought to have the syndrome, according to a VA report.
Because of Haley's work, we now know brain damage is involved. But which specific brain cells, and what's wrong with them? Until we understand the underlying pathology, Haley says, we can't treat them. "We're shooting in the dark," he said, referring to potential treatments. "So far, nobody's guessed right.
"But the research is really going to come to a head in the next six to 12 months."
[B]Tags:

Dr. Robert W. Haley, Gulf War Syndrome, UT Southwestern Medical Center[/B]



Comments (31)

[Jan Klimkowski]

Dr Haley is an epidemiologist, and here's a fascinating interview he gave to PBS some years ago:

Note: See reference at the end of this interview to read the studies by Dr. Haley, as well as the published scientific criticism about them.


Q: Dr Haley, are you today convinced there is a real Gulf War Syndrome?


A: In the 24th Navy Mobile Construction Battalion that we studied, there are 30 syndromes, they are very strong and they are due to neurological damage and they are strongly associated with combinations of organic phosphate chemical exposures. That's just undeniable. Now, there's a very good scientific question: is that finding going to be generalizable to the larger group of veterans who served in the war, and that's what our next research project is about.

Q: What was the hypothesis you were testing --

A: The hypothesis we were testing was that what we thought to be vague, non-specific symptoms were in fact a real syndrome. The syndrome was due to brain dysfunction, and that that was caused by exposure to combinations of organophosphates that would work together synergistically. Whereas people who were exposed to just one, would probably not be sick, but those exposed to two or three would be the ones who were sick. That was the hypothesis that we put out ahead of time.


Q: And these organophosphates would produce what's called a neuropathy?


A: Organophosphates are known to produce two syndromes. The failure to recognize these two syndromes has been another thing that stood in the way of understanding this problem. Everybody, every doctor knows, and the military is well aware, that exposure to organophosphates can produce an acute, immediate, very serious reaction that can kill you. And that's due to the paralysis or binding of an enzyme in your body called cholinesterase, and it causes you to have trouble breathing, to have diarrhea and tearing and finally you stop breathing and you can die. If you get over it however you're supposed to -- you have -- you're totally ??... because the enzyme regenerates and you're back functioning normally. And that was what people had in mind.


It was unknown to almost every doctor and to most people in the Defense Department and throughout the country, that there is another syndrome, that is being exposed to some organophosphates, but not all -- whether or not you have that initial syndrome, you can have a delayed reaction where several weeks or months later you can develop a spectra of neurological dysfunctions, which can be permanent. And these are on a spectrum from a very florid peripheral neuropathy where your nerves in your hands and feet stop working, and you can even become somewhat paralyzed. Also involvement of the spinal chord when you develop spasticity, and in some people, particularly where the exposure is long term, periodic and long term and low level, they might not get these peripheral manifestations but they might only get a disorder of the lower part of the brain in the brain stem which produces just psychiatric-like symptoms, vague symptoms like dizziness, difficulty concentrating, and the sorts of things that we see in the Gulf War veterans.


Q: As far as I can tell, the Presidential Advisory Committee and the other panels know abut this work. They just don't think of it as very relevant or in some cases very good. There's a value judgment being made about what this work means. They have considered it and dismissed it. I don't think it's just ignorance.


A: No. I don't think it's ignorance. But I couldn't comment on what it is.


Q: Let's move on to discuss your study and some of the comments scientists have made. One criticism that has been made by a number of epidemiologists is that you had sample bias.



A: Yes. It's been written. The criticism that our study contained a selection bias because not all of the members of the battalion participated is an invalid criticism and has been shown so in our responses to those comments.


What we did in the study is, 41 percent of the members of this battalion participated in the study. You'd like to have 100% and you know if fewer than 100% participate then the ones who didn't participate might be different from the ones that did participate. This is very common in epidemiologic studies to have less than 100% participation and so what we typically do is do a secondary study, a background study, to study the participants and the non-participants and compare them to see if they are different. We did that and published that in the paper, and found that in fact they're identical on age, race, sex, educational levels, jobs that they performed in the Gulf War, various risk factors. The only way they differed was on the probability that they had a serious illness, some kind of illness after the war. But it was not like night and day. It was 70% in the participants and 40% in the non-participants. What that means is that there is going to be a bias in our estimates of the prevalence, but since the risk factors were balanced, that means there's not going to be a bias in our estimation of the relative risks, looking at the risk factors, or in identifying the syndromes. It's only in estimates of the prevalence of the syndromes.


So, in the paper we correct our estimates of the prevalence for the fact that there was a disparity in the degree of illness. Those were corrected in the paper, but they were not noticed by the critics. Once we pointed that out there I think all the scientists that reviewed it felt that answered the question and there was not a selection bias.


Q: Let me go on to the risk factor issue. This is another thing you've been criticised for is the way you assessed exposure. Basically, the way you assessed exposure was asking people whether they thought they were exposed to various chemicals. Now, the critics argue as follows:-- it's one thing to rely on self reporting for somebody's sexual history for an AIDS patient, or a Legionnaires' Disease case, it's another thing to rely on self-reporting as a way of getting exposure data in an area like this where, especially in a political area where these things have such volatility, where strong suggestions have already appeared in the media.


A: Right.


Q: So, is asking somebody whether they've been exposed to chemical weapons remotely comparable to asking whether somebody had intercourse without a condom. How do the vets know whether they've been exposed to chemical weapons?


A: Okay, the questions about chemical weapon exposures referred to were there incidents in which the chemical weapon or arms that were supposed to infect sarin -- organophosphates-- alarms sounded -- the marines went around yelling this is not a drill, this is not a drill, put on your MOP4 protective suits, and then people had symptoms of gastroenteritis for the next 24 hours. I mean --if I ask you, did you have an experience like that, you would know whether you had experience like that. And so -- what our study is saying is that veterans who have experiences like that are much more likely to be the most severely ill of the veterans.


Q: Are you implying though an experience like that means you've been exposed to chemicals?


A: If that experience-- is highly associated with having the illness, it is a clue to the etiology. Now then to take the next step and say what that actually means, that's a much more complex issue getting into laboratory animal studies and collateral evidence of what chemical weapons were on the battlefield if they were, what clouds went over and so forth, and that's not really our area of ex-expertise and as you know that's well -- highly disputed at this point.


Let me say, it's not my expertise to evaluate evidence on chemical uses in the war, and military evidence, intelligence evidence, that's not my expertise, so I can't comment on that. Other than to say that I find very frustrating all the confusion and I'm not sure that we're ever going to have documentation of what actually happened in the war. But I don't think that's necessarily very important. I think what is important is to focus on the ills of war veterans.


What I think is going to solve this is a systematic population study of the 700,000 deployed veterans and the 1.4 million non-deployed veterans at the same time, who didn't go over to the war. Random sample surveys of those in which we test further our neurotoxic hypothesis. And we are actually planning such a study and the Defense Department is contributing funding to it. So we will actually pick a random sample of these two groups, survey them with our instruments and repeat ??... cases and controls back to Dallas, do intensive testing neurologically of the same kind of blinded conditions as before, look at those factors and try to repeat the study in a representative sample of the population. I think if that were to come out with something similar to what we found before I think it would be very convincing.


Q: Now to generalize from the few Seabees you studied to the tens of thousands of vets who have registered with symptoms you have to overcome a problem, don't you: for 80.000 vets to be suffering from organophosphate (OP) induced neuropathy there has to be sufficient quantities of OP in the field.


A: Quantities of what?


Q: Organophosphates.


A: Right.


Q: Right. Now the pesticides that were used out there are the ones that you buy in hardware stores. They are the ones which we use here. As for the chemical weapons, How do you get exposure a little bit of exposure to so many Gulf War troops scattered all over the Gulf--a huge area--without anybody having an acute attack? That seems to me a very telling argument against chemical weapons.


A: No. Absolutely not. The hypothesis put forward is that many of these, that not nobody was exposed to levels of any of these organophosphates that, by themselves, would produce acute symptoms. Let me start over. Our theory is that people were exposed to residue low levels of these that would not have injured them, would not have produced acute symptoms, and we know that is true. Nobody was overcome by organophosphates, and so to posit that there were very high levels would make no sense.


Q: But how do you distribute over a large area --


A: It's a problem of, -- it's a good point. -- Take for example the use of pesticides. We know that there were several uses of pesticides. And because the military was very rightly concerned with protecting the troops from insects, because they had -- carry lethal diseases. So therefore they very carefully sprayed the camps with chlorpheriphos, with Dosman(ph) which is a pesticide which we have fought with here in Dallas county and many other counties in the city -- in the state and in the nation. They're in common practice. But low levels get around, everyone is exposed-- many people are exposed to low levels, particularly people who are outside at night, would be exposed to high levels, but not enough to injure anyone by itself. However, that is a little bit of pesticide exposure. You wouldn't expect anybody to be injured by that by itself. People put on DEET. After putting on 10% DEET, an insect repellent, typical OFF or also using Avon Skin So Soft, obvious get no DEET? However, a number of the troops were using the military issue that was 75% DEET and ethanol, thought to be harmless. But now we know that, by itself, will not injure an adult, but it will get high blood levels. Also, the people who were taking perlostigmine, thought(?) they were taking a dose that was know wouldn't hurt people, because we give 10 times that much to patients with thyastin nergravis so nobody should have been injured by perlistigmine by itself.


The theory we raised though is-- What if you are exposed to three innocent levels that won't produce acute symptoms, but if all three of those chemicals, or two of them, we've the symptoms? Moreover, you put each of those chemicals in groups of animals and they didn't injure the animals. The animals had no symptoms. But when you put in the animals two of those, they got brain damage. (reference to AbuDhonia study)


Q: So let's move on to the group you did the neurological testing on. Now this was a subset of the original --


A: That's correct --


Q: This is the 23 worst cases.


A: No. To determine whether these clustered syndromes were actually due to a neurological condition or not, we selected 23 of the veterans with the syndromes who were the most typical of those with the syndromes and then 20 controls who were not ill.


Now what do I mean by most typical and this gets in, unfortunately, into the math, but I will go ahead and do it. In the factor analysis for each of the syndromes you get what's called a factor score. It's a score that goes from minus-one to plus-one with a variance of one, okay, a standard deviation of one and the ones that are the highest on that scale are not the most severely ill -- and this has been misunderstood by some of the critics, these are the ones who are the most typical of syndrome 1 or syndrome 2. They're most like syndrome 2. And so we picked the ones who are highest on the scale because they were most typical of the syndrome. It says nothing about the severity of their illness, only about how typical they are of this cluster you see. So that's what we picked. Then we brought them in and showed in fact that they had more severe brain dysfunction than the controls.



Q: Now when neurologists tested these selected 23 individuals that you found, they couldn't find anything abnormal. Right?


A: That's correct. Right.


Q: And if you took the group of 23 as a whole, the results of these tests were not that different from normative data, but were different from a control group.


A: That's correct. By -- the answer to that is, you have to ask what is normative data. What is normative data? Normative data is a control group, but it's a control group of a cross-section of the population. So it's a very general control group and they set the normal limits against that control group very broadly -- in order to detect tumors, strokes, multiple sclerosis and very obvious, very dramatic neurological damage or neurological diseases you see because that's why these tests were invented, to detect tumors, strokes and multiple sclerosis, similar things.


They were not developed to detect neuro toxicity because neuro toxicity has very subtle differences from controls because, think about this, a tumor would take a big bite out of your side of your brain or a stroke would damage a large part and so therefore every part of your body that's controlled by that part of your brain would just stop functioning and so these tests would be very abnormal and that's why they set the control -- the normal limits to be very broad so that only people with those things stick out. See? Well, that's not applicable in neurotoxicity because in neurotoxicity the damage is a random neuron here and a random axon there throughout the nervous system -- or throughout certain parts of the nervous system and so no test is going to be dramatically abnormal. So if you set up confident -- if you use c- normal limits that only detect very dramatic things, you gotta conclude there's nothing here and that's the that's the problem we're facing in trying to diagnose this in the usual medical setting. See, we're applying normal limits that were set for more -- much more dramatic diseases. So, how do you solve that problem? What you do is you have to establish much tighter normal limits in people -- in controls that are exactly like the cases.


So what we do instead of picking the general population to set our normal limits as has been done for the tests in general, we pick a control group that are the same age, sex, race and even educational level to the cases, fairly similar people who even do the same jobs, they're in the same military unit, then ... do the tests at the same time and the variance you see in that normal control group is the normal limits --




Q: Tell me how you got involved with this issue.


A: I'm an epidemiologist. I spent 10 years at the CDC. Been here on the faculty now for almost 15 years. I was busily working on a number of epidemiologic projects including hepatitis C and some other fascinating new epidemics.


And one day we got a call from Ross Perot who lives here in Dallas and he came by the University here and said "I've been travelling around as usual talking to veterans groups and lately I've been getting an experience that is unusual. Groups of veterans will come up after one of my talks or will come and visit me here at my office and their wives or their company commanders will point to this fellow and say 'Look, before the war this guy was a strong, tough, can do person, and now look at this poor fellow, how sick he is and this change right after the war. And no-one's doing anything about it and they're telling him it's due to stress and he -- that just isn't in character for this fellow' and he says this has been happening all over. I don't know if this is real, but if it is, we need to -- we need an independent study and if you guys at this university will enter into such a study I will be happy to help defray the costs."


So we went into a 50/50 partnership where we provided the faculty time for nothing, and he chipped in and covered the out-of-pocket expenses. We started the study and actually I was very skeptical of this idea. I thought this was stress too. And I was collaborating with a toxicologist who had an inkling this might be a toxic problem, so we had that hypothesis --


Q: As an epidemiologist you know that these kinds of anecdotal pieces of evidence, they sound compelling but they often don't pan out.


A: Yes. Very frequently an epidemiologist is confronted with people who think they've been involved in an epidemic. Two or three cases of Hodgkin's disease at a high school reunion for example, and people say That's just too coincidental. But in fact most of these turn out to be not epidemics, just natural occurrences, things that would have occurred anyway, and that's what we thought the Gulf War Syndrome was, just illnesses that would have occurred. So we went into it really to disprove the syndrome. But then as we actually started studying it, at each stage the data just shouted out to us that this looked real.




Q: As an epidemiological problem this is really very hard isn't it ? You don't have a clear case definition for Gulf War Syndrome even today, you have dozens of possible risk factors and you don't have any good way of assessing which vets were exposed to which risk factors, and how big were the exposures they received. So what made you think this was an attackable problem?


A: Very good question. This is clearly the most complex epidemic investigation, epidemic problem that I've seen in my career, and I think it's the hottest thing that's happened in this half of the century. The reason for it is, not what you saw -- not the issues of risk factors and measurement of risk factors, that's not the problem.


The problem is the definition of the disease. Most diseases, Legionnaires' Disease, Toxic Shock Syndrome, AIDS, the big classic epidemics so far in recent time, the disease has been obvious and so you talk to half a dozen people who have it, and you write down a case definition and you study a population and divide them into the ones who meet the case definition, the cases, and those who don't, the controls, and you're off doing the study. You give the cases a questionnaire to have them write down what their exposures have been, for example in AIDS they would write down, they would tell you about their sexual behaviors; Legionnaires' Disease they would tell you about where they were in the Stratford Hotel in Philadelphia, and you gather self-reported risk factors.


In an epidemic investigation you almost then find the cause because an epidemic is unique in that the effects, the degree of association of risk factors with the disease is so strong that even with self-reported risk factors, you always find it. So the problem here is not measurement of risk factors, you can do that with self reports very satisfactorily. The problem was the case definition. All through 1994 and up through 1996 really nobody else would sit down and write down a case definition.


So what we did, we did a survey in order to devise a case definition from the data. We, in fact let me step back, when we teach the students about epidemiology there is a little saying, we say The first thing you do in an epidemic investigation is you examine half a dozen of the cases in an epidemic and then you write down a case definition. And if you can't do that then you devise a case definition because failure to develop a case definition means that you are doomed, you are -- it's a foregone conclusion that you will not find anything in an epidemic. That's just the way it is.


And so it was quite feasible to sit down and write down eight or ten symptoms that many of these people had in common, and so this is a case definition. Let's do a provisional study to see if that pays off. Well, nobody did that. Everybody said Well, these symptoms we've seen before and therefore we're reluctant to write down a case definition.... Now the reason I think they were reluctant to write down a case definition is to write down a case definition may have a political implication and that it may indicate that somebody has accepted this as a disease and to do that would have all kinds of political ramifications, so it was never done, and that's why the investigation never went forward.




Q: The other thing which has been voiced by your critics in the pages of JAMA is they say you used the wrong neurological tests for your hypothesis. The wrong tests for OPIDN

A: Yes. Some critics have suggested that the neurological tests we used were not the ones that they would prefer for this Organophosphate Induced Delayed Neuropathy. Unfortunately that comment comes from misunderstanding of the spectrum of the Organophosphate Induced Syndromes. The assumed is that the only type of illness you get from organophosphates is a severe neuro -- peripheral neuropathy. That is dysfunction or malfunction of the nerves in the arms and the legs. In fact, the truth about OPIDN, or organophosphate induced delayed neuropathy, is there's a spectrum from, if you take a very big dose of poisoning of one of these compounds, all at once in one dose, typically about 10 days later you get paralysis of the -- tingling or paralysis in the arms and legs, but over a year or so that tends to go away, leaving, in its place, severe dysfunction, or mild dysfunction of the spinal chord and the lower bone stem. So, critics say, Well you should have done studies of the peripheral neuropathy. Well, see, we were studying this 3 and 4 years later. After which you would have expected the peripheral neuropathy to have resolved and gone away leaving only the bone stem and the spinal chord. So why did we do studies of the peripheral neuropathy when in fact all we would predict that only the brain stem damage would be left. So see it reflects just a misunderstanding of the progression of this illness.



Q: But I thought that there was no evidence of large doses, acute symptoms in the field, or any of these typical --


A: I didn't make myself clear. If you're exposed only to small doses, for example a pesticide sprayer gets exposed, they don't have peripheral neuropathies. And our critics were saying, You should have tested for peripheral neuropathies. People who were exposed to small doses over periods of time and in combinations, they only get central problems. In fact they are often mistaken for psychiatric disorders, depression, schizophrenia, and so forth. So, Why did you test for peripheral neuropathy, when small doses should produce central problems. Central nervous system problems? The criticism doesn't make any sense based on what we know about the disease and what we expect occurred in the Gulf. Low doses, combinations, perhaps over a period of time, only cognitive, possibly psychiatric type changes in the brain, and very few symptoms related to neuropathy, why did we want to test for neuropathy and not test for central nervous system findings?


Q: I think that's a confusion. The hypothesis you're testing for is organophosphate induced delayed polyneuropathy, right?


A: Right, and organophosphate induced delayed polyneuropathy has a spectrum of symptoms. With a one time large dose you expect peripheral neuropathy. With repetitive small doses and combinations of things you expect central nervous things to -- abnormalities to predominate. We proposed that it was small doses over a short -- over a period of time and perhaps in combinations that would produce central neuropathic findings, the symptoms that the veterans have are of the central nervous system nature and we did tests, neurological tests to brain stem and central nervous system and spinal chord disorders. Our critics have said, You should have tested for peripheral nerve disorders. But that only occurs when you have severe one-time exposures, and even gets well after a year or two, and this was three or four years later, so it doesn't make any sense at all to test only for peripheral neuropathy and to avoid testing for central neuropathy as our critics have suggested. What we did was exactly what you would want to do.


Q: The other thing the critics say is that you have these 23 patients, which are then divided between three.


A: Right, the syndromes, right.


Q: Fairly small numbers, and then you run a lot of tests on them and therefore you run into the what is sometimes called the Texas Sharpshooter Problem, or the multiple comparison problem. How do you answer that? Don't you, in these things, have to be really specific up front about your hypothesis? Otherwise you're bound to find some sort of match.


A: Right. The Texas sharpshooter problem is a very good criticism. We anticipated it and in the articles we answered that criticism. We did an analysis of the number of tests that we performed on the 23 cases and 23 controls. We analyzed all of the total numbers of tests we did, how many showed that the ones with the syndromes may have merely been the controls. And, vice versa, how many of the tests came out the other way. The controls more sick than the cases. And then we did a statistical test on that to see if that difference of that pattern could have occurred by chance. And you know what the probability of that could have occurred be the sharpshooter effect? Less than one in 10,000.


Q: What do you say to the argument of the scientific panels that stress is a likely exacerbating factor for the symptoms--much more likely in fact than low levels of chemicals.


A: Right. Some of the critics have said that the Gulf War veterans' physical symptoms that they're having are due to stress. Now what does that argument really entail? The only illness we know of in the list of medical diseases and psychiatric diseases, that's caused by stress, is post traumatic stress disorder.


Listen, I've been in stressful conditions for three and a half years doing study and I don't have post traumatic stress disorder, and I don't have physiological affects. -- Business executives are all the time under stress. People who are forced to be on welfare or on -- have terrible stress. And no-one's ever connected these types of stresses to the types of symptoms these Gulf War veterans are having. That's just completely specious.


Q: People have fund the notion of chemical weapons terribly exciting. Much more exciting that DEET or other pesticides, right? But you are saying, am I getting you right? Your theory doesn't need chemical weapons?


A: Our findings show that our first syndrome, syndrome one, is associated with what appears to be pesticide exposure. Syndrome three is associated very strongly with DEET and pyridigstigmine bromide exposure, and probably a synergistic effect of the two. Our syndrome two, which is the most severe, most of the veterans who have it, unemployable very very handicapped with these neurological, very severe neurological deficits. This was most strongly associated with risk factors that strongly suggest low level chemical nerve agent exposure and toxicity from peritostigmine and a synergistic effect between the two. Does our theory need chemical weapon exposure to explain it? I don't think theories need anything. I think the problem is, that's what the risk factors suggest.


Others will, hopefully, duplicate this study and see that they find the same effect. We're going to do the same study in a large representative sample of veterans, and maybe we won't find the same thing the next time. That's certainly possible. Then we would have to adjust to that and our theories would have to change. But right now, on the table, that's one of the risk factors that -- and there's no counter evidence in veterans, epidemiologic evidence, that would suggest that's not right. It's just there's no other evidence. No-one else has done a study.


Q: I want to come back to the exposure question. For chemical agents to explain Gulf War illnesses, there has to be exposure that gets to masses of US troops all over the Gulf. Even if the doses are very very small, there still has to be a way to distribute it very widely. I mean the chemicals have got to come from somewhere. Now one popular theory is aerial bombings. But UNSCOM (the UN special commission on chemical and biological weapons who have been to all of Sadam's bunkers to find and destroy the weapons) told me that in their view allied bombings destroyed hardly any of Sadam's chemical weapons duing the war. And I pressed them on this, I said, "do you mean that Saddam, ended the war with about the same amount of chemical weapons than he started" -- they said, "Yes. A very small fraction was destroyed".


Now, I have problem from just the point of view of basic physics of how you get this stuff to so many troops if not much of it was blown up. Isn't that a problem that has to be addressed...you can't just say, Oh the epidemiology says otherwise.


A: I'm just an epidemiologist. I'm not qualified to talk about aerial bombing and intelligence information and so forth. That's so far out of my area I just couldn't comment on it.


Q: So-- it doesn't follow that there was any widespread chemical exposure from what you've found, from chemical weapons?


A: Our evidence pretty strongly suggests that chemical weapon, the perception of chemical weapon exposure and interaction, synergistic interaction with pyridigstigmine bromide is a serious risk factor that needs to be explored. Whether there were actual exposures on the battlefield, the evaluation of all the evidence, the political evidence and the intelligence evidence is just so far beyond my expertise I really just couldn't comment on it.


Q: But isn't that the point. There's a difference between perception of a toxic exposure and the toxic exposure?


A: We have a very high relative risk, which is a number indicating how strong the association is, with the perception of chemical exposure, synergistic effect with pyridigstigmine bromide which is a very dramatic finding epidemiologically. How that squares with intelligence information is somebody else's call.


Q: But perception of a toxic exposure is not the same as actual toxic exposure. Correct?


A: That's correct. Yes. But what you do have to worry is the plausibility of an eye witness testimony versus the plausibility of intelligence information, and again, that's just out of my area of expertise.


Q: To establish the ideas we've been talking about, you have to convince your scientific colleagues, it's not a question of being popular with veterans or with politicians. You have to establish in the scientific community. Is that going to be a hard job?


A: No. Very easy. That's the easiest part of the job. Where they, scientists, become convinced is, they read scientific papers and they go to scientific meetings and hear scientific presentations given on those data. And that's it. And then they form their opinions, or they don't.

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Note: Dr. Haley's 1997 articles in Journal of the American Medical Association can be accessed at JAMA's web site. Haley's articles elicited many letters in JAMA criticizing his studies. For example, read Dr. Philip J. Landrigan's editorial "Illness in Gulf War Veterans" Access this by going to JAMA's web site . Type in Landrigan's name and title of his editorial on the search page.