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Politics : Foreign Policy Discussion Thread -- Ignore unavailable to you. Want to Upgrade?


To: zonder who wrote (4613)2/25/2003 10:52:00 AM
From: Neocon  Respond to of 15987
 
Presidential Advisory Committee on Gulf War Veterans Illnesses: Final Report



At the time of the Gulf War, the U.S. military believed Iraq had weapons that could deliver OP nerve agents, including sarin, soman, and VX, and mustard (blister) agents. Hence, U.S. forces were supplied with protective gear, detectors, and prophylactic drugs to protect against the known consequences of exposure.

Immediate signs and symptoms of nerve agent poisoning. OP nerve agents are designed to incapacitate and kill humans. Inhalation exposure to these agents leads to immediate effects, including miosis, runny nose, and increased salivation. Immediate effects following skin exposure include local sweating and muscle twitching. Eye exposure rapidly produces miosis, which often is associated with eye pain, headache, and blurred vision.264 In fact, miosis is the most sensitive and specific immediate response to acute poisoning in humans, and this reaction has served as the basis for establishing allowable occupational concentrations for CW nerve agents. Higher doses of these agents cause more severe effects, including convulsions, neuromuscular blockage, profuse airway obstruction and apnea-developing within one to two minutes of exposure.77 Death occurs due to respiratory paralysis. The effects of nerve agent poisoning (figure 4-1) are virtually identical to those of severe OP-pesticide poisoning.

Data on human effects of CW nerve agent poisoning derive largely from human experiments carried out by the U.S. Army from the 1940s to the 1960s. Table 4-2 illustrates the type of information on immediate poisoning effects from low-level exposures to the OP nerve agent sarin.

Immediate signs and symptoms of mustard agent poisoning. With mustard agents, poisoning symptoms are severe irritation and tissue damage to eyes, skin, and respiratory and gastrointestinal (GI) tracts. Usually the onset of symptoms is delayed for some hours after exposure.

One report of Iraqi use of mustard agent against Iranian troops in 1984 documented health effects in more than 5,000 Iranian casualties. Affected individuals had first to third degree burns over 20 to 70 percent of the total skin surface. Eye exposure caused tearing, severe conjunctivitis, and temporary loss of vision. Corneal abrasion was nearly always present, and photophobia and blurred vision developed in some cases. Upper airway involvement due to chemical burning of the throat led to pharyngitis and tracheobronchitis. These effects were quite severe, and this group suffered approximately 15 percent mortality. Those who survived the initial symptoms later experienced various GI complaints, including nausea, vomiting, and diarrhea. After five to seven days, hematologic problems were the greatest health threat to survivors.105

Long-term health effects of exposure to CW nerve agents. Two NRC reports addressed possible long-term morbidity and mortality in about 1,400 servicemen intentionally exposed to CW nerve agents in experiments conducted over a 20-year period ending in 1975. The possibilities of excess cancer risk and adverse mental, neurologic, hepatic, and reproductive effects were reviewed. Both NRC analyses concluded that no evidence exists that CW nerve agents cause long-term, adverse human health effects at the doses tested. The doses were nonlethal, but were high enough to cause clinical effects (such as miosis). NRC reported that both analyses had the power to detect any major health effects had they been present. A statistically significant increase in admissions to VA hospitals for malignant neoplasms was detected, with the caveat that admission numbers were small, showed no dose relationship, and no clustering of specific chemicals in relation to tumor site.174,175

Numerous studies in humans and animals report that survival from severe, immediate poisoning by OP nerve agents (including OP pesticides) can be associated with measurable, long-term neurological effects. One study of 77 industrial workers exposed to levels of sarin that caused immediate toxicity showed slight alterations in electroencephalograms (EEGs) one year after exposure. The study also reported, however, that trained experts could not distinguish an individual EEG from an exposed individual from an EEG of a person who had not been exposed, and that no clear relationship existed between alterations in EEG frequency spectrum and alterations in brain function.22 A 1975 review by Lohs of the effects of CW agents in humans similarly reported long-lasting effects following severe, immediate OP pesticide and CW agent poisoning.140

CW nerve agents do not show OPIDN toxicity as measured in EPA's standardized hen bioassay for evaluating OP pesticides, except with extremely high doses (10 to 100 times the lethal dose) where immediate and severe toxic effects, including death, are seen.117 Because OP CW nerve agents are chemically similar to OP pesticides and affect the same enzyme system in the body, similar long-term health effects would likely occur in the aftermath of immediate, severe poisoning with sarin, soman, or VX-i.e., the subtle, but measurable, neurophysiological and neuropsychological effects described earlier in this chapter. Again, these health effects did not occur in populations that had been exposed to subclinical amounts of OP pesticides. Current scientific evidence suggests that subclinical exposure to OP CW nerve agents does not result in long-term neurophysiological and neuropsychological health effects. Ongoing research at the Boston and Portland Environmental Hazards Research Centers is investigating the possibility of such effects in Gulf War veterans.

Long-term health effects of exposure to mustard agents. Based on epidemiologic research, humans exposed to mustard agent are at increased risk for lung cancer.98,287 Several other reviews of human exposure to mustard agent during World War I (WWI) and other wars also indicate veterans exposed to mustard agents during the Gulf War could experience other respiratory problems as well.98,287

During World War II (WWII), more than 60,000 U.S. service members were used as human test subjects and exposed to mustard agents, including at least 4,000 individuals exposed to high concentrations of these agents.98 An Institute of Medicine (IOM) review concluded that several specific chronic diseases are causally associated with mustard agent exposure. These include various respiratory cancers, skin cancer, chronic skin ulceration and scar formation, chronic respiratory disease including asthma, chronic bronchitis, emphysema, chronic eye diseases, and various psychological disorders including PTSD. IOM also found suggestive evidence (weaker than the associations for the conditions just mentioned) that exposure to mustard agent was associated with leukemia. Finally, IOM also analyzed two studies that examined the link between mustard and reproductive dysfunction, but determined that the database could not be used to make conclusions about human reproductive health effects.98





What do we conclude about the risks of CW agents to Gulf War veterans?

Current scientific literature indicates that when exposure to OP CW agents results in immediate and severe poisoning, long-term, subtle neuropsychological and neurophysiological effects could occur. Available scientific evidence does not indicate that such long-term effects occur in humans following low-level exposures, but the amount of data from either human or animal research on low-level exposures is minimal. Long-term effects in humans exposed to mustard agents include an elevated risk of lung cancer beginning decades after exposure. Based on available data, it is unlikely the health effects reported by Gulf War veterans today are the result of exposure to OP or mustard CW agents during the Gulf War. Ongoing or planned federally-funded studies focused specifically on low-level exposures and delayed neurotoxicity of CW agents should elucidate gaps in knowledge and eliminate uncertainty and/or identify new directions for research.

pbs.org



To: zonder who wrote (4613)2/25/2003 10:56:04 AM
From: Neocon  Read Replies (2) | Respond to of 15987
 
An interview Dr. Philip Landrigan, a member of the PAC and of the American Legion committeed studying Gulf War syndrome

Q: What special problems did you face in this case?

A: Well, the diseases, of course, are variable. There are certain symptoms that a lot of people have, but the actual manifestations of disease are different in different people. By itself, that didn't bother me, because the mindset that I had as I approached this problem was to think of it as really a very complicated problem in--in occupational medicine. Frequently in a big workplace, there will be different groups of people that have different exposures and suffer different diseases as a result of those exposures. And that was the mindset I brought to this task. I reckoned that the way to go at it was to look for different diseases, look for different exposures, and try to establish relationships between the two.




Q: In the beginning, in some of the Congressional hearings, in the media, there were a large number of quite acute things being mentioned--as well as what we now come to associate with Gulf War illnesses--things including arthritis, Lou Gehrig's disease, birth defects, and so forth.

A: Those were never big issues. There were reports of a particular birth defect called Goldenhar syndrome, but some good, competent investigations of that syndrome were done early by groups like the Centers for Disease Control, and the evidence that there was excess Goldenhar syndrome among the children of the vets simply did not sustain close scrutiny.

Q: So this didn't look like it had acute disease outcomes, in the sense that, say, Legionnaire's disease or AIDS did?

A: There were a few cases of acute disease in the vets, that were quite clearly associated with service in the Gulf. There have been some 30 or 40 cases of the parasitic disease leishmaniasis. There have been a few cases of malaria. There have been a certain number of veterans who are known to have come home with fragments of depleted uranium embedded in their bodies. Those are real events, and they clearly related to service in the Gulf. But I think they're different from the chronic sort of illness that continues to plague some number of the veterans who are now 7 years post-service.

Q: Now, we're talking about a group of people, quite a large group, 700,000--

A: 700,000 total, of whom 100,000 and some still complain of various degrees of symptoms.

Q: So from your point of view in terms of analyzing this, you'd have to get some idea of what the prevalence of disease was in a group of 700,000. Because that's a concept that it's difficult for people to understand, that you would expect a certain amount of illness of all kinds.

A: Oh yes. And in a population of 700,000, there would inevitably be a certain amount of illness, whether these folks had gone to war or not. There'd be cases of diabetes; there'd be cases of cancer; there'd be cases of neurologic disease and other chronic ailments. So the real question is whether the group of veterans who served in the Gulf have more cases of these diseases than other people of the same age, the same station in life, who did not go to the Gulf.

Q: And pretty soon, you say, you got to the stage where the things which seemed to be showing up perhaps at a higher frequency were not things like Lou Gehrig's disease, arthritis, or birth defects, but a cluster of chronic symptoms.

A: That's absolutely right. A cluster of symptoms, including joint pain, muscle pain, fatigue, headaches, gastrointestinal complaints.

Q: Now are these symptoms common in the normal population?

A: Oh yes, of course. I think everyday experience tells us that they're common.

Q: So given your background in occupational medicine, was it perfectly reasonable, from your mindset, that a heterogeneous mix of these kinds of things could be caused by something in the Gulf environment?

A: A priori, that was true. Yes.

Q: Let's go through some of the candidates, then. The oil fires. This was something that was considered early on.

A: Yes. And the concern there was that oil fires contain soot and--and particles that would be toxic upon inhalation, and the principal concern was that they would produce bronchitis and respiratory irritation.

Q: So why didn't that pan out?

A: For two reasons. First of all, because there just didn't seem to be an excess of respiratory complaints among the veterans who had returned from the Gulf. There may have been some small groups who did, but across the board, there were not. And then secondly, measurements that were made of smoke and soot particles in the air did not find very high levels.

Q: So the conclusion is, that's not a very likely--

A: Not a major contributor. Yeah.

Q: Depleted uranium?

A: Depleted uranium is well known to be toxic to the kidneys. Studies in industrial groups have shown this very clearly. And there may yet be some cases of chronic kidney disease develop among those vets who've come back with uranium particles in their bodies. It's a chronic disease, sometimes takes many years to evolve.

Q: Would this explain the cluster of symptoms?

A: I don't think so. The reason I say that is that the number of vets who have been documented to have fragments of depleted uranium is, at most, a couple of hundred, and using strict criteria, fewer than that. It just doesn't account numerically for the thousands of people who complain of symptoms.

Q: Now, another thing that was suggested, which seems to get round the exposure problem, are the sort of vaccines, jabs, and medicines distributed to the troops, because some of them were quite widely given. Therefore you get to hundreds of thousands, possibly. What about those?

A: Well, it's certainly an intriguing notion that the vaccines could have caused symptoms, or that combinations of vaccines and antidotes, such as the PB antidote that was given for the poison war gases, could cause symptoms. The problem is that none of the research undertaken so far establishes any of those connections. I'm very pleased that the research is continuing. Something may yet come to light. But I've not seen any plausible basis so far for linking the vaccines with disease.

Q: So this falls on the basis of what? Biological plausibility?

A: It falls down on the basis first that there's no empirical evidence, and second, biologic plausibility.

Q: Now, a lot of pesticides and insecticides were used. And particularly in Britain, there's been something that's [had] political force. What about these?

A: Well, pesticides are certainly toxic chemicals. And in some of the studies in this country as well, it's been reported that some of the veterans wore dog flea collars in the desert, either around their necks or on their wrists and ankles, to keep down bug infestations. And there's no question that DEET, which is the pesticide that's in those flea collars, is a neurotoxin. We've seen cases of neurotoxicity in people like park rangers in the Everglades, who slathered themselves with DEET every day for a whole season. So it's not impossible to think that there may have been a few cases, even a few hundred cases, of overdose of pesticides among the veterans. I wouldn't be a bit surprised if there were a few cases, in there. But again, I just can't imagine that thousands of people had the kinds of heavy exposure to pesticides that would be required to produce the overall pattern of illness that we're seeing here.

Q: Is there also a dogma in toxicology that you could have some chronic symptoms if you'd had an acute effect, but not otherwise? Can you address that one, that issue?

A: Yes. In some cases, when a person has been heavily poisoned with a pesticide, there are residual toxic effects, even after they have recovered from the acute poisoning. It's much more a gray area, though, to know whether low dose exposure to a pesticide, exposure that produces no symptoms acutely-- it's really not known whether such low dose exposure produces chronic effects. One of the questions that we posed to the VA, one of the challenges that we made to the VA, is that they institute research to look at the chronic consequences of low dose exposure to pesticides. We really need to know that. It's a gap in the knowledge.

Q: Now, all of those risk factors we've mentioned, we have some familiarity with: pesticides, oil, so forth. Chemical weapons are quite exotic to us, and they've had a lot of influence in this debate. And there have been stories I've heard about veterans seeing dead animals with dead flies on them, and assuming these are chemical weapons. What's sort of unreasonable about that?

A: Well, most of the chemical weapons of concern in the Gulf theater are, in fact, chemical first cousins to the major class of pesticides in use in this country, the organophosphates. The CW agents, like sarin, are simply hopped up cousins of malathion, is what they are. So we understand very well the toxicology of those chemicals. We know how to measure them. We know what physiologic effects they produce. So I don't know about the dead animals. Ican't comment on that. But the real issue here, with regard to the chemical warfare agents, is whether low dose exposure to these agents--for example, in areas around Khamisiyah-- Did low dose exposure to these agents produce chronic, low grade symptoms in the veterans?

At the present time, there is no body of medical evidence to say that low dose exposure to chemical warfare agents produces chronic symptoms. On the other hand, there's a real dearth of information in that area. And it's for that reason that the committee has made the recommendation to the VA that they conduct research into the chronic, low dose effects of exposure to chemical warfare agents. And we're all gratified that the VA has accepted that challenge, and they're going forward with the research.

Q: Let me ask you about the work by Dr. Haley that was published in the Journal of the American Medical Association recently, this year. This was a sort of complicated sort of set of papers and articles, and proponents of a chemical etiology for Gulf War illnesses have made a lot of this heavily publicized. Can you talk from a scientific point of view, about some of the shortcomings of the paper as have been discussed in the JAMA?

A: Yes, you probably are aware that I did an editorial on it.

Q: Yes.

Q: I think that there are several very fundamental problems with the Haley papers. The first is what epidemiologists call selection bias. He studied a battalion of Seabees, naval construction battalion. Of that battalion, he succeeded in bringing only 41 percent of the men in for examinations. That's a very low participation rate for this kind of a study. And when the participation is so low as that, such a low rate immediately raises the question: What about the other 60 percent? Why did only 40 percent come in? Were they sicker? How were they different from the 60 percent who didn't come? Such a low participation rate suggests to me that the people who came in were somehow atypical of the rest of the group, not representative of them. And what that means, in turn, is that it becomes very difficult to generalize to the whole population of 700,000 Gulf War veterans the findings of this small and highly selected group.

Second problem with the Haley study was, the detailed neurological exams were done on only 23 or 24 of the men whom he studied. So now we're looking at just a tiny subset within an already small selected population, and the results are further skewed. I just find it impossible to know how examinations on 23 men can be projected to a population of 700,000. There's also a technical concern that some of the tests that were used to assess neurologic function were less than--than state of the art.

And then finally, and a very fundamental concern, is that Dr. Haley and his colleagues simply have no independent objective information on the exposures that these veterans suffered. The only information that they have on exposure is information that the veterans themselves gave by questionnaire. There's no external verification.

Q: So he asked the veterans whether they thought they were exposed?

A: He asked them whether they thought they were exposed to a series of chemicals, and he had a checklist: pesticides, chemical warfare agents, smoke, and so on. And they replied.

Q: Is this usual?

A: No. Usually in epidemiologic studies of chemical exposure, we expend an enormous effort on trying objectively, independently to verify exposure. For example, in workplace settings we bring in engineers to make air measurements. In acute industrial accidents like Chernobyl of Bopal, engineers rush to the scene and try to reconstruct exposure after the fact, from objective data.

Q: What kind of impression do you think the media have left the public with?

A: I think many of the public today believe that illness in the Gulf War veterans was caused by chemicals, and that the federal government has been suppressing this information. And the real truth is, we don't know what's causing the illness in the Gulf War veterans. We certainly have not identified a chemical that's causing it. Our best guess is that most of the illness is caused by psychologic stress.

Q: Why has that message been so hard to get over, to sell?

A: I think a lot of it just reflects the American psyche, that too many of us think that to suffer stress is to admit weakness. That's not the case at all. I mean, war is hell. People that go to war are heroes, and they suffer enormously. It's not surprising that when they come home, they have symptoms. It's not necessary to invoke chemical exposure. If there is chemical exposure, we need to know it; we need to study it; we need to prevent it. But we don't need to invoke chemicals to account for the great majority of illness in the veterans who served in the Gulf.

Q: Is there anything else you want to add, concerning your experience on the PAC?

A: Just one final point. You asked about the importance of scientific overview of the research endeavor. The absolute bedrock of good science is peer review, peer review in which panels of independent scientists with no stake in an issue review proposed research and make a decision to fund or not to fund a particular research project.

As a practicing scientist, I'm very disturbed to learn that some research has recently been funded by the Department of Defense, using a channel that totally bypassed and indeed overrode peer review. I think that that's a serious mistake. It sends a terrible message to the scientific community, because it tells people in the scientific community that good science is not rewarded; what will be rewarded is loud voice and good politics.

pbs.org