But not all scientists would agree with McNulty’s conclusions regarding the mutagenicity of TCDD. In their paper “The Mutagenicity of Dioxin and Its Effects on Reproduction among Exposed War Veterans,” Vietnamese doctors Ton That Tung, Ton Duc Lang, and Do Duc Van suggest that scientists should at least consider the possibility that TCDD might act as a human mutagen. Comparing birth defects among children born to North Vietnamese soldiers who had served in the South to those among children of soldiers who remained in the North, and noting that “none of the wives of exposed or non-exposed veterans received any exposure themselves,” the doctors wrote:
The congenital malformations are of many types, with an increased frequency of anencephaly in the children of former soldiers… In spite of the limitations of the available data, it is striking to compare the absence of anencephaly among the births in the unexposed civilian population to the seven cases among the births to former soldiers. The excessive incidence of congenital malformations in the children of soldiers exposed to dioxin were discovered by interviewing each couple. In relation to national and international norms, the incidence of neural tube malformations is particularly elevated.
Likewise, the rate of abortion, premature births, and sterility is significantly higher in the group of exposed veterans from the South. Moreover, the number of molar pregnancies[18] in Hanoi seems abnormally high; the Institute for Mothers and Children (The National Ob-Gyn Institute) has just reported the hospitalization of nineteen cases of molar pregnancies or chorioepitheliomas, of which nine were diagnosed in woman married to former soldiers from the South.
A plausible explanation for the association established between exposure to dioxin and excessive congenital malformations in first-generation offspring is that exposure may affect the father’s genetic material. This association calls for a vigorous epidemiological study taking into account the various factors which could interfere with reproduction. It also indicates that a cytologic and biological study of sperm of both man and animal exposed to dioxin should be carried out.”
A scientific paper by David Kriebel, published by the Center for the Biology of Natural Systems, Washington University, also gives a number of reasons for considering the possibility that TCDD might act as a human mutagen.
RATS ARE NOT PEOPLE: WHAT DOES ALL THIS MEAN FOR US?
Two points must be made about the significance of the experimental animal data to human health. First, bacteria, rats and people have very few things in common. But one of those few is a genetic code made of deoxyribonucleic acid (DNA). If TCDD can damage DNA in salmonella, and lacking evidence to the contrary, we must assume it can damage it in humans as well. Second, chemicals known to harm humans (benzene, vinyl chloride, cigarette smoke, to name a few) via mutational damage almost invariably do it to other organisms as well. With only one exception (arsenic) all the known human carcinogens cause cancer in laboratory animals as well.
TCDD—A HUMAN MUTAGEN
Scattered evidence supports what experimental studies suggest—that TCDD is probably a human mutagen. There is often conflicting data, and room for different interpretations; however, there is much more evidence now that there was two years ago, and this trend will probably continue. Chromosome damage has been reported in Hungarian workers exposed to TCDD in a chemical plant, and in Vietnamese civilians sprayed with the herbicide Agent Orange, which contained TCDD in small amounts (parts per million).
BIRTH DEFECTS FROM AGENT ORANGE?
Could the exposure of veterans to Agent Orange in Vietnam over ten years ago cause birth defects in their children born today? There is no direct proof, but a mechanism capable of causing this effect certainly exists. If TCDD is a human mutagen, and if it causes mutations in male germ cells, then children born of men exposed at any time in their life could develop abnormally. At least three other environmental pollutants have been shown to cause birth defects or other reproductive problems; most likely via mutations in male germ cells.4
Neither Dr. Tung and his associates nor Kriebel argue that there is indisputable proof that TCDD is a human mutagen, but both papers suggest that the possible mutagenicity of TCDD should be examined further. Dr. Steven D. Stellman, assistant vice president for epidemiology, American Cancer Society, has also suggested that scientists continue research into the mutagenicity of TCDD. Testifying before the Subcommittee on Medical Facilities and Benefits of the Veterans’ Affairs Committee, Stellman said that it is conceivable, though not provable at this time, that Vietnam veterans exposed to Agent Orange may have increased the odds of their children would be born with defects. Stellman and his wife had been coding and analyzing some of the thousands of questionnaires sent out to Vietnam veterans by Citizen Soldier, a veterans’ organization headquartered in New York. Although, they found some of the exposure histories to be “unreliable,” Stellman felt that “the next best thing to an exposure history may be an exposure marker.[19] Since we asked about skin effects in four different ways, we compared the association of one particular heath outcome—namely, the presence of any birth defect in a child born after the father’s return from Vietnam—with the presence or absence of this exposure marker. Odds ratios ranged from 1.3 to 1.8… Continuing this line of inquiry, we also found a quantitative association between the number of gastrointestinal complaints reported, and the likelihood of fathering a child with a birth defect. Taken literally, this could mean that men having the stated skin conditions were 30 to 80 percent more likely to father children with birth defects. However, without more objective clinical evaluation of the men and their children, I would caution a more conservative interpretation, and simply state that the results are highly suggestive of a possible effect, and that they should be confirmed by new studies in which the subjects are selected on a random basis rather than on their own initiative.”5
“The problem,” Dr. McNulty explains, “is that there are enormous differences in the reactions of species to TCDD. The hamster, for example, will take a dose five thousand times as large as a guinea pig, and the hamster excretes TCDD quite rapidly. Other animals will store TCDD in their fat tissues, but the problem with doing a half-life study of this stored dioxin is that you’ve got to give just enough TCDD that you won’t kill or seriously damage the animal. And there are various estimates of what it costs to measure the dioxin in one piece of tissue, and most of them run to the order of two to five thousand dollars per sample. So we’re talking dollars again like we were with the monkeys. When people ask why these things haven’t been done, why they haven’t been measured, the answer, at least one of the basic answers, is money.”
Dr. McNulty apologizes for a persistent cough, pauses while I examine my notes, and appears not to notice as a woman enters the office rather brusquely, lays a manila folder on his desk, and leaves. But when I ask whether the primate center has done any research into the carcinogenicity of TCDD in rhesus monkeys, he replies with the convivial irritation one might expect from a congressman asked once too often about his voting record.
“No, neither I nor anyone else has, or probably ever will, for several reasons. In general the latency period for induction of cancer into an animal is correlated with the life span of the animal. So one can get skin cancers in mice by painting them with polyaromatic hydrocarbons for just a matter of weeks or months, but then a mouse only lives for about a year and a half. Some years ago a researcher here was trying to reproduce these sorts of things in monkeys by painting them with polyaromatic hydrocarbons and exposing them to ultraviolet light. And he finally pretty much gave up. But several years later the animals were still around and did begin to show up with skin cancers. So it just isn’t practical, at least in the research environment today, to conduct an experiment that would go on for twenty or even forty years, particularly when there is no evidence that TCDD is carcinogenic in animals or humans.”
Observing my surprise, McNulty points to a large file drawer and declares: “It’s all there, and it’s all, or at least 90 percent of it, negative.”<
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But McNulty’s insistence that TCDD has not proven to be carcinogenic in laboratory animals or humans only demonstrates, once again, that scientists disagree on just how much and exactly what kind of damage TCDD does to living organisms. For example, Dr. Samuel S. Epstein, a human and experimental pathologist and toxicologist who has devoted the past thirty years to the study of the hazardous effects of chemicals and chemical pollutants believes that “TCDD is the most potent known carcinogen.” An expert on the delayed and chronic toxic effects—most notably cancer, reproductive, and genetic—of chemicals and chemical pollutants, including pesticides and herbicides, Epstein testified before the House Subcommittee on Medical Facilities and Benefits of the Committee on Veterans’ Affairs that
In tests with small groups of rats over a dose range from 1 ppt (0.0003 ug/kg) to 1000 ppb (500 ug/kg), all animals receiving doses in excess of 500 ppt died within 95 weeks. TCDD induced a wide range of malignant tumors in doses as low as 5 ppt (Van Miller et al., 1977). These included squamous carcinomas of the lung, cholangiosarcoma of the liver, and malignant histiocytomas at 1 and 5 ppb levels, and carcinomas of the ear duct, kidney and skin, malignant histiocytomas and testicular tumors at the 5 ppt dose. In more large-scale carcinogenicity tests by Dow Chemical, which are generally confirmatory on the Van Miller studies, TCDD was administered orally to rats at levels of 0.001, 0.01 and 0.1 ug/kg (Kociba et al., 1978). Carcinomas of the liver, lung, palate and tongue were induced at the highest dose levels, neoplastic liver nodules at the intermediate dose level, and toxic liver effects at the lowest dose level tested.6
Contradicting the VA’s contention that there is no evidence that TCDD is harmful to humans, Dr. Epstein told the subcommittee about a study of forestry, paper pulp, and sawmill workers in northern Sweden who were exposed primarily to 2,4,5-T and 2,4-D. The study concluded that the risk for soft tissue sarcomas in the Swedish workers was five times greater than in those not exposed to these herbicides.7 A “statistically significant excess of stomach cancer” was also found in Swedish railroad workers exposed to phenoxyacetic acids and amitrole over a ten-year period,8 and a study conducted in southern Sweden found “statistically significant excess risks for soft-tissue sarcomas.”9 In the follow-up of the 1953 Ludwigshafen (West Germany) accident in a TCP plant, a seven-fold excess in stomach cancer over expected rates was noted.10
Among Vietnam veterans, Epstein testified, “the incidence of testicular cancer appears high, even allowing for selection bias. In one group of about 5,000 plaintiffs, approximately 200 testicular cancers, mainly seminomas, have been recognized. There are also suggestions of an increased incidence of lymphomas and leukemias.” When Dr. Epstein described the “symptomatology” of TCDD in human beings, which he said is “well recognized in the clinical and toxicological literature,” he might very well have been a Vietnam veteran talking about some of the problems he had experienced since returning from Asia. TCDD, said Epstein, “is a potent multi-system toxic agent producing a panoply of a wide range of acute and delayed effects, many of which can progress to the chronic. Recognized clinical symptoms include asthenia, muscular weakness, pains in limbs and joints, insomnia, photosensitivity, nausea, vomiting and diarrhea. Recognized signs include abnormalities in liver function, porphyria, peripheral neuropathy, elevated blood triglycerides and cholesterol, and psychological and personality changes… This disease complex is generally consistent with that recognized in preliminary surveys of Vietnam veterans, although no large-scale analysis has yet been published.”[20]
What Epstein did not tell the subcommittee is that thousands of Vietnam veterans have been complaining of these very symptoms for a number of years, only to be given a Rorschach or Minnesota Multiple Personality Inventory (MMPI) test by VA hospital staff and sent home—or, all too often, to the psychiatric ward with a prescription for uppers or downers. Unfortunately Valium and Thorazine have not proven very effective in arresting liver cancer, and Gelusil (an antacid) seems not to have acted as an antidote to the destructive effects of TCDD on the stomachs, colons, livers, and even prostrate glands of many young veterans.
Although many studies have shown that TCDD is carcinogenic in laboratory animals and there is now suggestive evidence that “exposure to phenoxy acids and chlorophenols might constitute a risk factor in the development of soft-tissue sarcomas,”11 the VA has failed to conduct a national outreach program that might determine just how many Vietnam veterans are ill, have died, or may be dying from various types of cancer. With over a quarter million employees and a yearly budget of approximately $24 billion, the VA’s failure to do cohort studies, says Victor Yannacone, is based not on scientific caution but on a singular lack of compassion.
“I can go to my terminal in my little country law office in Patchogue,” says Yannacone, “and I can sit there and I can ask my relatively inexpensive computer to tell me the names and addresses of every veteran with testicular cancer. That is not terribly hard. I can tell the computer to tell me who had testicular cancer and the birth defects, and who was a Marine, and who served in a particular place during the month of January or February of 1968… It takes two minutes and forty-five seconds to get the answer.
“Why hasn’t the government done this kind of study? Because, quite simply, they don’t really think the veterans are that important; the Vietnam veteran is an expendable commodity to the US government.”
Yannacone, whose first brief against the manufacturers of Agent Orange was 184 pages long and contained “every piece of scientific data that was then known about dioxin or phenoxy herbicides,” believes that many veterans have already died from the “wasting effects” observed in rhesus monkeys by Dr. Wilbur McNulty and researcher Dr. James Allen. “People under the age of thirty-five don’t waste away and die with an autopsy report that says the veteran looked considerably older than his stated age of thirty-two years. He looks like a ninety-six-year-old mummy fresh out of the tomb. There isn’t a single piece of measureable fat on his skeleton. Now, that is ten years after his tour in Vietnam. What does that mean? It means somehow the amount that was loaded in his fat was mobilized and eventually killed him, and it killed him as if he had an acute dose years before. It just took ten years instead of ten days.”
Since 1949 there have been a number of accidents involving the release of dioxin at industrial plants throughout the world, the best known of which occurred at the ICMESA plant in Seveso, Italy, on July 10, 1976. The ICMESA plant was producing 2,4,5-trichlorophenol, and the accident took place in a chemical reactor. The explosion blew a safety disk out of the reactor, sending the bubbling brew up a venting pipe into the atmosphere, where it formed first a plume, then a cloud that eventually settled over a seven hundred-acre area where five thousand people lived and worked. Soon animals began to sicken and die, and those who were exposed to the dioxin-laden cloud suffered symptoms similar to those Vietnamese peasants had complained of following a defoliation raid; bouts of diarrhea, excruciating headaches, stomach cramps, dizziness, and sleeplessness.
During his tenure as VA chief, Max Cleland would on occasion draw Seveso from his grab bag of justifications for the VA’s recalcitrance on disability payments to Vietnam veterans who had been exposed to Agent Orange. Seveso, according to Cleland, only demonstrated that human beings can be exposed to dioxin without suffering demonstrably calamitous effects. This argument is fallacious for at least two reasons: First, because Vietnam veterans, unlike the victims of industrial accidents, were exposed to toxic herbicides over a twelve-month period and their exposure involved what scientists call “multiple routes”—which means that they drank water and ate food contaminated with dioxin, inhaled smoke from brush that had been sprayed with herbicides containing dioxin, swam in water polluted with dioxin, waded through brush coated with toxic sprays, and wore clothing for days, even weeks, which in some cases had been liberally doused with herbicides. Second, the accident at Seveso did have some very serious health effects on the residents of that community. In
The Pendulum and the Toxic Cloud: The Course of Dioxin Contamination, Thomas Whiteside, who visited Seveso soon after the accident and again two years later, describes the aftermath of the explosion at the ICMESA plant.
Bird life appeared to have been devastated; fields, gardens, and orchards were littered with the carcasses of swallows, martins, warblers, and goldfinches, and also with those of thousands of rats, mice, and moles. Both brown field rabbits and white rabbits that residents of the area had been raising for food had been dying by the hundreds, and chickens by the thousands. Cats that survived were meowing piteously; dogs, which are known to be comparatively resistant to dioxin poisoning, looked sickly, and their behavior was reported to be nervous and aggressive.
…Inside Zone A [the zone closest to the reactor], the scene was desolate indeed, inhabited only by occasional hooded figures encased in impermeable white decontamination suits and boots and wearing face masks; scientists monitoring soil samples and veterinarians collecting dead animals in plastic bags. From time to time, shots could be heard as dying animals were put out of their misery and those still capable of moving were killed to prevent them from traveling out of the contaminated zone. Toxicological analysis demonstrated beyond doubt that most of the animals found dead had died from dioxin poisoning, and post-mortem examination showed extensive liver damage.12
Returning to Seveso two years later, Whiteside interviewed four doctors at Desio Hospital about their impressions of the effects of dioxin on the population. After explaining to Whiteside that they had requested qualified epidemiologists be sent to the area but “nobody has been sent so far,” the doctors said that, because of the lack of information on abortion rates prior to the accident, it was difficult to determine just how many spontaneous abortions had occurred since the accident. “Many spontaneous abortions had undoubtedly not been recorded as such, or perhaps even noticed by mothers if they occurred early in pregnancy,” the physicians said. They also told Whiteside about a small herd of cows fed grass grown in fields near the ICMESA factory. Thirteen of the cows had experienced spontaneous abortions, and out of three calves that were born only one survived more than a short time after birth. Because of the considerable amount of organic damage that had been observed in animals (dioxin had been discovered even in the livers of animals that had been considered healthy), the doctors felt it would make sense to assume that human beings would also have been affected by TCDD. In a study group of residents living outside Zone A, as well as some living in the upper half of Zone A, 35 percent of those examined had enlarged livers, said the doctors.13
Waiting for an Army to Die Page 16
