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 --