Book Read Free

Waiting for an Army to Die

Page 15

by Fred A. Wilcox


  Another thing Codario would like to determine is how many of the veteran’s problems are due to the storage of TCDD in their fatty tissues because he believes it may be possible to flush these residues from the human body. But his efforts to test this theory have been hampered by the fact that the VA has done only a very limited fat biopsy study on Vietnam veterans, and when I spoke with him, he had already been waiting for nearly six months for the return of five biopsies.

  “I sent the five fat biopsies to Dr. Thomas Tiernan at the Brehm Laboratory at Wright State University because Dr. Tiernan had done research on dioxin for the government and he is considered an ‘independent’ researcher. He was involved in studying dioxin levels on the ship Vulcanus,[15] and seems to be an expert in the field.”

  Although dioxin can be stored in the human body for many years, standard laboratory tests, commonly used by the VA in its “Agent Orange examinations” fail to detect traces of dioxin in the blood, urine, or spinal fluid. “They take your blood and urine,” one veteran told me, “and when they don’t find dioxin in it—which they knew goddamn well they wouldn’t in the first place—they conclude that you’re clean, you weren’t exposed to Orange in Nam. Just more fun and games, because they know that TCDD is stored in the fatty tissues of the body. Their own research has shown that.”

  The research the veteran refers to is a “blind” study conducted by Dr. Michael Gross of the University of Nebraska, on contract to the Veterans Administration. In this study, thirty grams of fat were removed from twenty Vietnam veterans who believed they had been exposed to Agent Orange. An additional thirty grams were removed from ten veterans who presumably had no contact with Agent Orange and from three US Air Force officers who had done dioxin research. The samples were forwarded to Dr. Gross’s laboratory, where they were analyzed for residues of TCDD-dioxin. Two of the three men who had been described as heavily exposed had TCDD in their fatty tissues of approximately twenty-five to one hundred parts per trillion, while three of the five who were classified as receiving “light exposure” had concentrations of from five to seven parts per trillion. Ten out of the twenty Vietnam veterans had TCDD in their fatty tissues. Two of the control samples contained low levels of TCDD in the abdominal adipose ranging from five to six parts per trillion.1

  Called as an expert witness at the Environmental Protection Agency’s 2,4,5-T suspension hearings, Dr. Gross said: “It appears that Vietnam veterans heavily exposed to herbicide Orange will carry low levels of TCDD in their body fat. This conclusion is supported by the observation that two of the three most heavily exposed men have the highest levels detected in this blind study. It is extremely unlikely that this finding is a matter of chance or has occurred because of herbicides or other TCDD-related exposure in the United States. Furthermore, 50 percent of the veterans of Vietnam tested in this study exhibited low levels of TCDD in their abdominal fat whereas only 20 percent of the controls were found to be positive.

  “Additional support for this conclusion comes from the replicate analysis of the adipose samples from the ‘heavily exposed’ veterans, and from the validation analysis performed by Mr. Harless. We recognize the need for additional validation studies, and these are planned.

  “We propose that the results are relevant to the cancellation hearings. They constitute support for the concept that exposure to TCDD can lead to long-term storage in human fat tissues.”2

  Dr. Gross’s discoveries seem to have been received by the VA with the same amount of enthusiasm that the Atomic Energy Commission displayed when informed by John Gofman and other researchers that long-term exposure to low-level radiation could be dangerous, even deadly. In the two years following Dr. Gross’s testimony at the EPA hearings, the Veterans Administration conducted no further tests to determine the extent to which Vietnam veterans may have TCDD in their fatty tissues. However, the VA recently announced that it does intend to conduct further studies on the adipose tissue of veterans.

  Should he discover that the fatty tissue of veterans he has examined contain residues of TCDD, Codario will attempt to flush dioxin from their bodies with a drug used to treat victims of kepone poisoning. Kepone is an insecticide which, like dioxin, collects in the fatty tissues of the human body, producing numbness of the hands, headaches, personality changes, and other dioxin-like symptoms. Another similarity between kepone and dioxin is that it is eliminated in the bile fluid, passed into the intestine, and then reabsorbed in the body in what physicians call an enterohepatic cycle. At the University of Virginia, a researcher administering cholestyramine (a bile-salt binder commonly used to treat patients with elevated levels of cholesterol and, in some cases, jaundice) to workers who had high levels of kepone in their bodies discovered that within two months all of the workers showed dramatic improvements, and within one year seven of the twenty-two workers were totally kepone free. The results were published in The New England Journal of Medicine (1978, vol. 298) by Dr. Philip S. Guzelian et al., and Codario believes that Guzelain’s findings may be vital to physicians working with Vietnam veterans or victims of domestic herbicide spraying.

  “So if dioxin behaves similarly to kepone, and we have evidence that it does,” says Codario, “it would certainly be tempting to postulate that it could be eliminated from the body by the aid of cholestyramine. And so, once I get the fat biopsies back, I can start giving my patients this drug and doing follow-up examinations to measure for dioxin in their bowel movements. In that manner I can determine if TCDD is actually being washed from their bodies.”

  Ronald A. Codario seems to find nothing unusual about the fact that he is doing work that should have been done years ago by the Veterans Administration, or that, without a grant from any of the national health institutes or foundations, he has discovered a medical basis for proving that Vietnam veterans were exposed to Agent Orange and that their exposure is now crippling and killing them. As a specialist in internal medicine he could demand fifty dollars an hour for his advice, yet he donates twenty to thirty hours each week to people whom many Americans still prefer to use as scapegoats for the Vietnam War.

  Will the Veterans Administration listen to his theories, accept his statistics, and take action of behalf of Vietnam veterans? Codario thinks they will. He believes that the men and women who run the VA are honest people who are stifled by the inherent inefficiency of big government; moreover, he intensely dislikes what he calls “Monday morning quarterbacking,” and says that trying to place blame for what has happened to Vietnam veterans will only prolong their agony.

  “Look,” he says, shuffling a stack of papers on his desk, “it’s just too easy if you ask me to say, ‘Hey, Dow did this, and the VA did that.’ Sure, maybe there was conflict of interest back then, and we all know that somebody makes, or rather made, a lot of money from selling herbicides. But it’s just too easy, if you ask me, to look back fourteen years and place the blame. That just isn’t the thrust of my work. I’m just trying to show that these fellas have a problem, and I want to get them some help. And in getting help for them I want to say, ‘Hey, listen, these things have caused the problems.’ Let’s just make sure it doesn’t happen again because certainly the people that can help the veterans much quicker than I can are the federal government and the chemical companies. I think that where we have to exercise our diligence and care now is trying to make sure that mass herbicide spraying and pollution of the environment doesn’t continue to happen in the future.”

  Codario and I shake hands and he walks me to the waiting room, where his receptionist and an elderly black woman are watching television. I ask directions to the subway, explaining that on my way to his office I had gotten off at the wrong stop. Codario, the elderly woman, and the receptionist appear shocked that I would have taken the subway, and insist on calling a cab. During the drive to the train station, the cab driver chats pleasantly, weaving skillfully in and out of the rush-hour traffic and laughing happily at his own jokes. But I am mesmerized by the clicking meter and unable
to put out of my mind what Codario said as I was about to leave. The Green Beret, he told me, has continued to deteriorate. His liver and spleen are swollen, his arms and legs are often numb, and he has lost much of his coordination. Rising from a chair or sofa, he often falls down, walks into walls, stumbles about the room. He has episodes in which he goes blind for fifteen minutes, and has lost consciousness while driving, ramming into the car in front of him. Sometimes he “goes off” for a couple of days, flying into terrible rages, banging his hands through walls. X-rays have failed to determine why his urine is darkened and his head throbs and he has blood in his bowel movements.

  As I pay the driver and prepare to enter the station, I remember something else Codario told me about the first Vietnam veteran to enter his office complaining of “bizarre” and “exotic” symptoms. The man’s wife, said Codario, had given birth to a horribly deformed baby girl who died in the veteran’s arms.

  9. Humans, Rats, and Lesser Beings

  On one wall of the receptionist’s office at the Oregon Regional Primate Research Center in Portland a large female monkey and her baby snuggle beneath the caption LOVE US OR LOSE US. On the opposite wall a sullen great ape informs visitors that AROUND HERE WE CAN USE ALL THE SMILES WE CAN GET. After checking the appointment roster and handing me a name tag (NO ACCESS TO ANIMAL ROOMS), the receptionist suggests I wait in the center’s cafeteria. Fifteen minutes late Dr. Wilbur McNulty, whose research into the effects of TCDD-dioxin of rhesus monkeys has often been quoted by opponents of domestic herbicide use, appears. Thin and polite, he answers my questions with the cautious reserve of a scientist who has been drawn, somewhat against his will, into the controversy over dioxin.

  The Oregon Regional Primate Research Center, McNulty explains, is one of the seven primate centers established in the early sixties as scientific institutes under the assumption “that because primates are our nearest biological relatives they might in many cases be good or even superior models of handling diseases.” Because the supply of rhesus monkeys appeared to be inexhaustible, they were considered ideal for laboratory experiments, but in recent years an international controversy has developed over the capture and sale of this species of primate. After several decades the rhesus population has been so depleted that at least one Asian nation has placed a ban on their export.

  “But we don’t have to worry too much about all that,” McNulty explains with a touch of pride. “In fact, we now have over 2,500 primates living on the grounds of our center. And they live outdoors all the time all year round, and they seem to do quite well in this climate. We’re pretty self-sufficient, at least where the rhesus is concerned, and no longer depend on capture from the wild.”

  When he first began feeding a select group of rhesus monkeys minute quantities of TCDD-dioxin, McNulty was actually doing research into polychlorinated biphenyls (PCBs), which he describes as his first love. “Back some years ago, the thought was around that the toxicity of PCBs might not in fact be due to the PCBs themselves, but rather to a contaminant that was contained in the PCBs, something called polychlorinated dibenzofurans. But there really wasn’t any information available at that time on the relative potency of PCBs and/or the dibenzofurans. So, obviously, in order to investigate whether the toxicity of commercial PCBs might be due to contaminants, I had to know just what the potency of the contaminant might be. But the contaminants were not available; however, since the polychlorinated dibenzofurans are a very close relative of dioxin, which was indeed available, I started testing with a dioxin compound called TCDD. I wanted to see just what its relative potency might be, and as you can well guess, it was enormously more potent than PCBs, although qualitatively the diseases they cause are the same. On a per-weight basis dioxin is much, much stronger.”

  In the beginning McNulty placed what he thought were small quantities of dioxin in the food of his rhesus monkeys. “As fools rush in,” he admits, “the doses, in retrospect, were astronomical. They were in the parts per billion instead of parts per trillion range, which is more relevant when it comes to food. I think the first level I used was twenty parts per billion in the diet, and that killed a young male rhesus monkey in twelve days. This was an estimated total intake of well under ten micrograms (TCDD) per kilogram (body weight). A level of two parts per billion was lethal in seventy-six days. I discovered that monkeys are several times more sensitive to TCDD than mice, rats, rabbits, and dogs.”

  Dioxin turned out to be so toxic to his experimental animals that McNulty decided to suspend all research with TCDD until the primate center could construct a special building with carefully controlled access, assigning the care of his monkeys to only one or two well-trained people in an effort to minimize the risk of contaminating other areas of the center.

  “Dioxin,” says McNulty, “is the most toxic small man-made molecule we know of. It is less toxic on a per-gram basis than some biological toxins like botulin, but that’s a very huge molecule. So molecule for molecule dioxin is probably the leader of the pack.”[16]

  After consuming food containing minute amounts of TCDD, McNulty’s primates became very quiet, began losing weight, lost their appetite, grew progressively thinner and weaker, and then “just laid down and died.” Sometimes they would have episodes of retching and vomiting, but, says McNulty, “these were at the higher doses. At much, much lower doses a certain fraction of the animals remain well for one to three or four months, and then will suffer from an ailment characterized by failure of the elements of the bone marrow. They will have low white counts, very low platelet counts, so that they suffer from hemorrhages and infections and are essentially carried away by bone marrow failure.”[17]1

  Unlike Vietnam veterans who complained of fluctuations in weight patterns, gains as well as losses, the monkeys did not regain weight they lost. “They just go down,” says McNulty, “although I did have one animal who lost a lot of weight over a period of about three and a half months, without showing any of the other characteristic signs of toxic poisoning. And then she began to regain her weight and is still alive today, and appears to be quite well. But usually if they are sufficiently poisoned that they lose a significant amount of weight, they don’t recover from it. It simply goes on and they become worse and then they die.”

  Although TCDD, when given to rats and mice in minute doses, causes congenital abnormalities, including fetal deaths, cleft palate, and kidney abnormalities, McNulty’s research failed to indicate that TCDD acts as a teratogen in rhesus monkeys. McNulty did find, however, that TCDD is fetotoxic in rhesus monkeys. “The experiment,” says McNulty, “was designed to explore whether short-term exposure to dioxin, either in a single or a few closely spaced doses during that period in early pregnancy when the organs are forming, would result in malformations. At the highest dose it was very toxic to the mother, and since I wasn’t really interested in that, I did very little at that particular level. At the intermediate level there was a fairly high level of abortion, or loss of the fetus. But those which did not abort gave birth to normal offspring. We were unable to find any malformations. Also, at the level that TCDD caused a fair number of abortions there were some late toxicities and deaths among the mothers. But the number of animals was relatively small, and unlike experimenting with rats and mice, you can’t use the number you would like for statistical significance. Still, with the relatively small number of animals I used it seems extraordinarily likely that TCDD is toxic to the fetus, but I did not conclude that it causes malformations in the offspring of rhesus monkeys.”

  Fetotoxic effects, which means the ability of TCDD to destroy developing fetuses, have been observed in three different mouse strains, two rat strains, and one species of monkey. In a study by Dow Chemical, rats fed on nanogram (billionth of a gram) of TCDD per kilogram body weight per day exhibited increased stillbirth and shortened life spans for surviving pups. Skeletal birth defects have also been observed in four different mouse strains as well as other types of defects in rats when pregnant females a
re exposed to TCDD.2

  Dr. McNulty has not researched the possible mutagenic effects of TCDD on male monkeys because, he says, “there isn’t any reason to think it would be a good experiment. As you recall, I said there is no evidence that TCDD is a mutagen, and any reproductive failures in terms of abortions or malformations that are going to be transmitted through the father almost necessarily have to be due to the mutagenicity of his germ cells. So it’s not the kind of experiment that’s likely to get results. Now, I’m sure Vietnam veterans would raise the question: ‘How do you know if you haven’t done it?’ Well, with mature monkeys now running around a thousand dollars each, it becomes a matter of choosing experiments that one has some reason to assume will give one conclusive results. It’s always difficult to prove that something doesn’t exist. In other words, how many males would I have to expose and then breed with females before I could say with confidence that TCDD does not cause reproductive failures through the male? One sure wouldn’t be enough. Would ten be enough? Not likely. Would a hundred be enough? Well, maybe, but still a little bit doubtful. And that’s just an impossibly expensive experiment if you don’t have any good reason ahead of time to think that it’s going to pay off.”

 

‹ Prev