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.”
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]
20
See Appendix, Letter to the Editor of the