On Friday, an AP news story mentioned that Vietanam and the United States will be working together to clean up the environmental damage left behind from the United State’s use of Agent Orange during the Vietnam War. Those areas in Vietanam that were used to store and mix the chemical herbicide are the focus of the clean up as they contain an unintended component of Agent Orange, dioxin, in concentrations 300 to 400 times the amount of international limits. It has taken this long after the Vietnam war for the United States to approach the matter of clean up, as it seems politics led to much debate about the health consequence of using Agent Orange as a war tactic. By using it as an herbicidal defoliate, the United States was able to expose the enemy hiding in the jungle, and destroy food sources for animals and peasants in these rural areas, thereby forcing the enemy to urban areas that were under increased United States control. Although a brilliant war tactic, the biological consequence appears to have been horrendous.
Agent Orange is the code name for the 50:50 mixture of two synthetic biological herbicides from the Monsanto and Dow chemical companies, 2,4 dichlorophenoxyacetic acid and 2, 4, 5 trichlorophenoxyacetic acid. These are considered synthetic organic herbicides as they are carbon based and very similar to auxins naturally produced in plants. Auxins, synthetic or natural, are characterized by an aromatic ring (ringed hydrocarbon with alternating double and single bonds) and a carboxylic functional group. The 2, 4, and 5 refer to the position of chlorines on the aromatic ring; remember each carbon is numbered. In small doses, these synthetic auxins are considered moderately toxic to humans, however the Agent Orange mixture was found to be contaminated with 2,3,7,8 tetrachlorodibenzodioxin, a extremely toxic byproduct of the synthesis of the other auxins. 2,3,7,8 tetrachlorodibenzodioxin is referred to simply as dioxin after the two oxygen bridges that join the chlorinated benzene rings. In addition to being a byproduct of synthetic organic herbicides, it is also found as a byproduct of the incineration of chlorine based substances such as PVC, and non combustion processes such as bleaching paper. Naturally, it can be produced from volcanoes and forest fires. Looking at the structure of dioxin, why is it lipophylic?
It is interesting to look at Agent Orange with regard to its intended consequence as well as its unintended consequences from the molecular to ecosystem level. In terms of intended consequence, how does a synthetic form of auxin promote defoliation? Auxin is a natural plant hormone scientifically shown to promote plant growth at plant meristems, as well as the growth of plant organs such as leaves and flowers, not defoliation. In general, how does the accumulation of additional auxin cause leaf abscission? On the molecular level, how does auxin promote growth? Hormones are either hydrophobic (not water soluble and typically lipophylic) or hydrophilic (water soluble)… how are auxins classified? Based on auxin’s nature in water, what is the signal transduction pathway? In other words, how does the production of auxin initiate the transcription of genes responsible for the growth of the plant? What is happening with Agent Orange in terms of the signal transduction pathway to cause leaf abscission?
The chemical nature of dioxin, also makes it biomagnify in animal tissues. What is biomagnification? What are reported potential consequences of the biomagnification of dioxin for consumers in top trophic levels?
On the molecular level, the mechanism of action that causes the array of birth defects, health issues, and cancers has been difficult to determine. Two studies in 1990 indicate that the actions of dioxin and dioxin-like chemicals are mediated by the aryl hydrocarbon receptor (AhR) (Safe, 1990), a transcription factor with a helix-loop-helix structure. Following ligand binding, the receptor-ligand complex is moved to the nucleus through AhR nuclear translocator where DNA binding occurs, resulting in transcriptional activation. Target genes include cytochrome P-450 and genes involved in cellular growth, differentiation, and inflammation (Whitlock, 1990). In addition to those ligands that normally bind with AhR, AhR also has an affinity for dioxin, causing unintended transcription of genes. What is a transcription factor? Why would the unintended activation of genes be detrimental? Has research since 1990 revealed specific mechanistic pathways, where dioxin has been directly shown to activate genes associated with a specific defect, health problem, or cancer?
Beyond the havoc caused on the molecular level in both plants and animals, the destruction of repeated spraying over a large area of Southern Vietnam obliterated forest ecosystems that housed an enormous biomass of plants of tremendous biodiversity, as well as the immense biodiversity of animals, including humans, that relied on the productivity, nutrient balance, hydrological regime, and enhanced soil stability the forest ecosystem provided. In his paper Agent Orange and Dioxin in Vietnam, 35 years later, presented at the Proceedings of the Paris Conference Senate, March, 11-12th, 2005, Vo Quy describes that with exposure to dioxin, leaves of hundreds of species of trees and plants, particularly large woody trees of the Dipterocarpaceae and Fabaceae within upper and dominant ecological layers, fell, resulting in the scarcity of the genetic pool of a number of ecologically and economically precious trees. Those species that were tolerant of dioxin, such as bamboo and some faster growing species, were able to invade and replace the indigenous species of woody trees with a secondary forest of less ecologic and economic value. A prolonged dry season has prevented natural regeneration of the forest, making artificial planting by the Vietnamese people essential. Despite these efforts satellite images taken before and after indicate that this effort is proceeding slowly, and in some areas are not being rehabilitated at all. The natural succession to grassland after the spraying in these cases is still being maintained by periodic fires of human origin. What is succession? Why would periodic fire limit natural ecologic succession of an ecosystem?
Where topography is steep, runoff has exasperated the problem by having produced changes in soil properties that come with the loss of top soil including lower organic matter, lower nitrogen content, less available phosphorus, and lower calcium, magnesium, and iron in the soil’s cation exchange complex. On the cellular level, how are the mentioned minerals used in plants? How does the cation exchange complex work?
It was thought that natural succcession would occur through normal slash-and-burn farming, followed by leaving the farmland, invasion of tall grass, bamboo, and wild bamboo, followed by fast-growing woody trees, followed by those trees of the climax tropical rainforest (including Dipterocarpaceae). Aside from farmers in some cases maintaining the grassland, elsewhere ecological conditions of these forest regions were destroyed and changed so completely by the spraying of dioxin and other chemicals, that natural succession has not been able to occur. Favorable soil, water, light, and temperature conditions were lost for the growth of forest trees. Saplings would die on the spot, and dispersal from unaffected forest areas was extremely limited due to distance. Additionally, competition from invasive grasses and bamboo made it difficult for any saplings to take hold naturally. Vo Quy mentions that the World Bank stated a generation after the war that “one of the least understood and potentially most detrimental aspects of the war is how the modification in species distribution that it caused may have permanently damaged the biodiversity of Viet Nam.” How do invasive species directly affect biodiversity? What is the difference between invasive species and those that comprised the original forest that enable them to thrive in conditions unsuitable to those that comprised the original forest?