[Also see: Recent Dioxin Contamination From Agent Orange in Residents of a Southern Vietnam City JOEM May01]
Michael Gochfeld, MD, PhD
In the late 1960s, the US military conducted one of the largest ecological experiments of all time – defoliation of the Vietnamese countryside by chemical and physical means. Massive amounts of chemical herbicides were applied to forests and fields, and huge "Rome Plows" cleared large areas of vegetation. Other military activities, such as bombing, also contributed to this assault, leaving behind a pockmarked landscape of water-filled craters, ideal for breeding mosquitoes. Although the long-term ecological consequences were predicted by the mid-1970s, [1-4] large-scale studies of the impact have been slow in accumulating. [5] Of all the effects, none has been as well studied as the dioxin exposure to humans attributable to the herbicide mixture known as Agent Orange.
I had the dubious privilege of serving as a pediatrician and provincial public health advisor in Vietnam* during a period of massive herbicide use. The information made available to physicians (and probably to sprayers) was scanty, but we knew that some highly toxic materials were being used to "deny cover." Some other chemicals were used to prevent rice crops from ripening, and at a briefing I learned that the farmers would not know what had happened until almost harvest time. Ironically, Agent Orange was considered one of the less toxic herbicides to humans because its ingredients, 2,4-diphenoxyacetic acid and 2,4,5-triphenoxyacetic acid (popularly known as 2,4-D and 2,4,5-T), were commonly used home and garden herbicides. Subsequent studies provide evidence that these compounds may not be as innocuous as thought, but most attention has focused on the dioxin content of Agent Orange, which reached the part per million level in some batches.
Dr Schecter, often in conjunction with colleagues in Vietnam, has been indefatigable in pursuing an understanding of the human consequences of dioxin exposure.[6,7} Although there are many congeners among the polychlorinated dibenzo-dioxins, only one, the 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD), occurred as a contaminant in Agent Orange. This was a consequence of the unique condensation reaction between two molecules of 2,4,5-trichlorophenol, used to synthesize 2,4,5-T. It is a sad irony that TCDD happens to be the most toxic of the dioxins. Although many chlorinated dioxins occur in the environment, mainly because of combustion of chlorine-containing materials, the structural relationship of 2,3,7,8-TCDD to other compounds (eg, 2,4,5-trichlorophenol) allows it to serve as a marker of Agent Orange occurrence and exposure. We were able to exploit this feature in our study of Vietnam veterans [8] because, of the 13 dioxin and furan congeners we analyzed, it was only the 2,3,7,8-TCDD levels that were elevated in the veterans who served in Vietnam, compared with their "era" counterparts who served at the same time but did not go to Vietnam.
In this issue, Schecter et al likewise exploit the unique property of 2,3,7,8-TCDD as an indication that residents around Bien Hoa air base, where a very large Agent Orange spill occurred 30 years ago, are still being exposed to the residual dioxin from contamination that occurred a long time ago. The authors contrast this with data from other parts of South Vietnam. Although they found elevated levels of 2,3,7,8-TCDD in blood and human milk in the early 1970s, representing exposure that occurred in South Vietnam during the period of herbicide use (1961 to 1971), levels generally declined over the subsequent 25 years, representing the gradual elimination of 2,3,7,8-TCDD, which is known to have a long half-life in the body. By contrast, today the Bien Hoa population shows very high levels, indicative of recent exposure unrelated to the applications that occurred during the war.
Human and environmental samples from North Vietnam generally do not show elevated TCDD levels. Because that area was not subject to defoliation, very little dioxin exposure would have occurred there; indeed, the average level of 2 ppt TCDD in blood is about half that found in industrial countries. [8,9] There was also a positive control, in that persons born or migrating into the contaminated Bien Hoa area after spraying had ceased had levels comparable with those of people who had been exposed to the spraying.
This article illustrates the value of a specific biomarker (namely, the 2,3,7,8 congener), for if only total dioxin had been analyzed, the signal would have been obliterated by the relatively higher amounts of the octa-chloro-dioxin resulting from other anthropogenic activities, such as incineration. It also demonstrates the long persistence of chlorinated organic compounds in soil.
TCDD levels in soils around Bien Hoa included a sample in the 1-ppm range, about 1000 times above the US soil cleanup level of 1 ppb. I agree with the authors that the ongoing exposure of all segments of the population is most likely due to food-chain contamination. Nevertheless, if high levels of TCDD are in the upper layers of soil, where they can be contacted directly, then this pathway should not be ignored. Indeed, in most risk assessments for soil contamination, the "driver" or major pathway contributing to elevated risk is the ingestion of contaminated soil by toddlers. Farmers, too, come into direct contact with soil and may inadvertently ingest significant quantities, particularly for a contaminant for which toxic levels are in the sub-ppb range.
The existence of this currently exposed population testifies to the problem of dioxin exposure among the Vietnamese. Although some American personnel had fairly high occupational exposure, it was recognized that many Vietnamese people had high exposure resulting from long-term exposure through multiple pathways – both direct and indirect. We are right to have focused concern on Americans but wrong to ignore the plight of the Vietnamese on whom the massive amounts of chemicals were bestowed. Moreover, although wishful thinkers might have assumed that the problem would go away over time, the data presented in this article indicate that for some populations the exposure continues.
It is hoped that this is a highly localized problem in Vietnam; fortunately, there are probably few populations anywhere else that currently have comparable levels of exposure. Thus this episode provides an opportunity to improve our understanding of both the biology of TCDD exposure and its consequences, while at the same time performing a service to the exposed individuals by monitoring them for adverse effects and providing them information on health maintenance and nutrition. It is also a unique opportunity to study in detail the environmental fate and movement of TCDD. Further monitoring could provide invaluable information on the long-term consequences of elevated exposure, particularly in a population whose levels are on an order of magnitude above background yet are below levels documented to cause overt harm.
The authors identify the need to substitute clean food for contaminated, and this is probably the easiest step for the government to take. At this point, no government intervention seems to be under way, nor has there been even the approval to undertake a comprehensive exposure study, either around Bien Hoa or in other areas where large concentrations of herbicides were used or stored.
It also would be desirable to interdict exposure pathways in other ways and to remove the contamination when feasible. In the United States, a typical remedial investigation for a hazardous waste site includes dozens of sample locations, numerous analyses, and high costs. It will not be easy for the government of Vietnam to afford such an extensive survey. Yet to decide whether "cleanup" of the contaminated soil and sediment is warranted, the government will need good data on the spatial distribution pattern of contamination, both over the area and by its depth profile. Given the high cost of dioxin analysis, adequate characterization for cleanup will be very challenging and costly. It may be reasonable to remove superficial topsoil; however, eliminating contamination, restoring land to productivity, and managing contaminated sediment is much more difficult. Sampling fish of various species, sizes, and sub-locations within a lake would clarify whether there are safe options for fish consumption from the lake or whether fishing should be banned for the time being.
Most puzzling to me, particularly given the long and successful cooperation between Dr Schecter and Vietnamese scientists, was the restriction imposed by the government on removal of specimens for analysis. Even though fish were collected for analysis, the researchers were not allowed to transport them to an analytic facility. Political issues in and between both Vietnam and the United States will continue to interfere with adequate scientific investigation and appropriate public health interventions. One can only hope that governments will see fit to separate the scientific from the political long enough to allow health researchers to address ongoing environmental health problems.
*The Americanized spelling of Viet Nam.
References:
1.
Tschirley FH. Defoliation in Vietnam. Science. 1969;163:779-786.
2. Orians
GH, Pfeiffer EW. Ecological effects of the war in Vietnam. Science.
1970;168:544-554.
3. Neilands
JB, Orians GH, Pfeiffer EW, Vennema A, Westing AH. Harvest of Death: Chemical
Warfare in Vietnam and Cambodia. New York: Free Press; 1972.
4. Gochfeld
M. The other victims of the Vietnam war. BioScience. 1975;25:540-541.
5. Westing
AH, ed. Herbicides in War. The Long Term Ecological and Human Consequences.
London: Taylor and Francis; 1984.
6. Schecter
AJ, Tong HY, Monson SJ, Goss ML. Levels of 2,3,7,8-TCDD in silt samples
collected between 1985-86 from rivers in the North and South of Vietnam. Chemosphere.
1989;19:547-550.
7. Schecter
AJM, Dai LC, Thuy LTB, et al. Agent Orange and the Vietnamese: the persistence
of elevated dioxin levels in human tissues. Am J Public Health.
1995;85:516-522.
8. Kahn
PC, Gochfeld M, Nyugen M, Hansson M, Rappe C, Velez H. Dioxins and dibenzofurans
in blood and adipose tissue of Agent Orange-exposed Vietnam veterans and matched
controls. JAMA. 1988;259:1661-1667.
9. Fingerhut
MA, Halperin WE, Marlow DA, et al. Cancer mortality in workers exposed to
2,3,7,8-tetrachlorodibenzo-p-dioxin. N Engl J Med. 1991;324:212-218.
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