Agent Orange
Background
Agent Orange was one of a suite of six color-coded chemical herbicides developed by the United States government which was used from 1961 to 1970 in the Vietnam War by U.S. military forces to defoliate the dense jungle vegetation of South Vietnam. Additionally, out of the six colors Agent Orange use accounted for up to sixty percent of all total herbicides used until the White House Science Advisory Committee announced in 1969 that Agent Orange use posed detrimental risks to humans and should be stopped, with complete termination of use occurring in April of 1970. The widespread dispersion was aimed at both the triple canopy forests and local crops and farmland in an effort to reduce food sources and hiding places available to the Vietnamese resistance forces, the Viet Cong. The destruction that resulted from the use of Agent Orange caused acute adverse side effects in Vietnamese citizens and American soldiers alike due to dioxin exposure, a pollutant and chemical by-product of Agent Orange known to cause cancers, diabetes and serious birth defects. Between 2.4 to 4.5 million Vietnamese citizens and around 3 million U.S. soldiers were severely affected or lost their lives due to dioxin exposure. Such high numbers can be attributed to the fact that Agent Orange was sprayed at almost twenty times the recommended concentration that was determined lethal to plants. Although this allowed the military to gain short-term victories, the high concentration and prolonged use created health issues that proliferated into subsequent Vietnamese and American generations, as well as several long-lasting, negative socioeconomic and environmental impacts on Vietnamese land and citizens that have persisted to this day.
Mechanism
The original chemical composition of Agent Orange was created by combining two herbicides, known as 2,4-Dichlorophenoxyacetic acid (2,4-D), and 2,4,5-Trichlorophenoxyacetic acid (2,4,5-T), both of which are only effective during short periods of time due to their relatively short half-lives. However, 2,3,7,8-Tetrachlorodibenzodioxin (TCDD) more commonly referred to as simply dioxin, is often formed as a chemical side-product from the process of both organic synthesis and the burning of organic materials. TCDD is the most toxic member of the dioxin family and in years prior to its acknowledged presence in Agent Orange it was labeled as a powerful environmental pollutant. In the case of the combination of 2,4-D and 2,4,5,-T, TCDD was created and detectable but its presence was dismissed for almost a decade, allowing for such a high degree of usage.
In contaminated individuals, TCDD targets the arylhydrocarbon receptor (AhR), a transcription factor involved in the regulation of gene expression in fatty acid metabolism, cell cycle regulation, and immune response. TCDD disrupts the normal function of this receptor by directly binding to it, resulting in either an increase or decrease in each type of gene expression. Normal activation of AhR is seen as an adaptive mechanism that is beneficial to organisms in the breakdown of harmful and potentially carcinogenic materials, but overstimulation and activation, as is the case with TCDD, can trigger the premature breakdown of normal, essential chemicals within the body, resulting in systemic damage. The degree to which TCDD promotes mutation also suggests that it may be linked to oncogene expression, via either direct or indirect mechanisms. In 2007 researchers were able to pinpoint the actual target of TCDD, the mitochondria, and were able to better understand the way that it promotes tumor progression and metastasis. It was discovered that in the presence of high TCDD concentrations, the chemical causes the mitochondria to undergo a phenomenon known as mitochondria-to-nucleus stress signaling. The signaling is normally generated by AhR activation, but is commandeered by TCDD in TCDD-induced signaling which occurs through increasing calcium concentrations within cells and causing the subsequent activation of calcium responsive factors which trigger a signal cascade that inactivates P53, the gene responsible for apoptosis. This allows for uncontrollable cellular proliferation and the maintenance of tumor metastasis.
In contaminated individuals, TCDD targets the arylhydrocarbon receptor (AhR), a transcription factor involved in the regulation of gene expression in fatty acid metabolism, cell cycle regulation, and immune response. TCDD disrupts the normal function of this receptor by directly binding to it, resulting in either an increase or decrease in each type of gene expression. Normal activation of AhR is seen as an adaptive mechanism that is beneficial to organisms in the breakdown of harmful and potentially carcinogenic materials, but overstimulation and activation, as is the case with TCDD, can trigger the premature breakdown of normal, essential chemicals within the body, resulting in systemic damage. The degree to which TCDD promotes mutation also suggests that it may be linked to oncogene expression, via either direct or indirect mechanisms. In 2007 researchers were able to pinpoint the actual target of TCDD, the mitochondria, and were able to better understand the way that it promotes tumor progression and metastasis. It was discovered that in the presence of high TCDD concentrations, the chemical causes the mitochondria to undergo a phenomenon known as mitochondria-to-nucleus stress signaling. The signaling is normally generated by AhR activation, but is commandeered by TCDD in TCDD-induced signaling which occurs through increasing calcium concentrations within cells and causing the subsequent activation of calcium responsive factors which trigger a signal cascade that inactivates P53, the gene responsible for apoptosis. This allows for uncontrollable cellular proliferation and the maintenance of tumor metastasis.
Methods of Dissemination
Aerial
Ground
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Pollutant Mechanisms
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- Sprayed mechanically by United States Soldiers by hand
- Carried in backpacks fitted with spray equipment
- Trucks fitted with spray equipment
Exposure
Agent Orange's toxic contaminant, dioxin, is known to be absorbable into the body through inhalation, ingestion, skin contact, or eye contact with direct skin contact or ingestion being the most common forms of exposure. Barrels of TCDD that were dumped in mass quantities after the termination of use in 1969 caused the pollutant to seep into the soil and contaminate whole ecosystems, with concentrations rising as progression up the food chain occurred. Subsequently, immediate effects received little notoriety. It was not until the long-term effects were observed that the White House Science Advisory Committee issued the statement suggesting the termination of use in 1969.
Symptoms
Gastrointestinal
Psychiatric Effects
Endocrine
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Genitourinary
Cardiovascular
Metabolic
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Neurological
Family
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Preventative Measures and Treatments
The use of Agent Orange along with the five other color-coded herbicides was originally intended to rapidly defoliate the jungle and farmland used by the Viet Cong. Although previously acknowledged as a persistent pollutant, the effects of dioxin on humans was not well known, nor was it investigated once its presence was confirmed in Agent Orange. Therefore, when birth defects, carcinogenic developments, and chronic illnesses began to arise and proliferate quickly throughout a very large population of both American and Vietnamese individuals which all linked back to Agent Orange exposure, no antidotes existed, nor was there time to develop treatments since much of the damage had already been done. To date, no specific treatments exist to reverse the damaging effects of Agent Orange and TCDD and although experimental measures to accelerate the transformation and excretion of TCDD are being investigated, only preventative measures and precautions have been established as guides for individuals living in contaminated areas to aid in the reduction of overall exposure. Additionally, due to the high percentage of U.S. veterans that returned home and experienced adverse long-term side effects, chiefly the development of certain cancers, the U.S. Department of Veterans Affairs compiled a list of diseases attributed to Agent Orange exposure and the qualifications that must be met in order to receive benefits which address those illnesses.
Preventative Guidelines
- Avoid contact with contaminated soils located near waste sites
- Children should avoid:
- Eating dirt
- Putting toys that have been in the dirt in their mouths
- Putting hands in their mouth after having played with anything that has come into contact with soil which has been deemed likely to be contaminated
- Avoid recreational smoking or alcohol consumption
- Dietary restrictions:
- Avoid fish that have been caught in areas known to have high Agent Orange exposure levels
- Avoid food sources of any kind from known contaminated sites
- Wash and peel fruits and vegetables obtained from contaminated areas
- Do not stop breastfeeding even if suspect contamination
Vietnam Veteran Diseases Associated with Dioxin Exposure
- AL Amyloidosis:
A rare disease caused when an abnormal protein, amyloid, enters tissues or organs - Chronic B-cell Leukemias:
A type of cancer which affects white blood cells - Chloracne (or similar acneform disease):
A skin condition that occurs soon after exposure to chemicals and looks like common forms of acne seen in teenagers. Under VA's rating regulations, it must be at least 10 percent disabling within one year of exposure to herbicides. - Diabetes Mellitus Type 2:
A disease characterized by high blood sugar levels resulting from the body’s inability to respond properly to the hormone insulin - Hodgkin's Disease:
A malignant lymphoma (cancer) characterized by progressive enlargement of the lymph nodes, liver, and spleen, and by progressive anemia - Ischemic Heart Disease:
A disease characterized by a reduced supply of blood to the heart, that leads to chest pain - Multiple Myeloma:
A cancer of plasma cells, a type of white blood cell in bone marrow - Non-Hodgkin's Lymphoma:
A group of cancers that affect the lymph glands and other lymphatic tissue - Parkinson's Disease:
A progressive disorder of the nervous system that affects muscle movement - Peripheral Neuropathy, Early-Onset:
A nervous system condition that causes numbness, tingling, and motor weakness. Under VA's rating regulations, it must be at least 10 percent disabling within one year of herbicide exposure. - Porphyria Cutanea Tarda:
A disorder characterized by liver dysfunction and by thinning and blistering of the skin in sun-exposed areas. Under VA's rating regulations, it must be at least 10 percent disabling within one year of exposure to herbicides. - Prostate Cancer:
Cancer of the prostate; one of the most common cancers among men - Respiratory Cancers (includes lung cancer):
Cancers of the lung, larynx, trachea, and bronchus - Soft Tissue Sarcomas (other than osteosarcoma, chondrosarcoma, Kaposi's sarcoma, or mesothelioma):
A group of different types of cancers in body tissues such as muscle, fat, blood and lymph vessels, and connective tissues
Long-Term Effects
The long term effects of the widespread use of this herbicide are still present to date in both Vietnamese citizens and American Vietnam Veteran populations. The prevalence of birth defects in children born to Vietnamese women who were directly exposed to high concentrations of TCDD are thought to be present in over 150,000 children born during or after the Vietnam war. Additionally, the high rate of cancers and systemic multi-system effects caused by the disruptive mechanism affecting normal cell replication TCDD causes has heavily impacted the ability of Vietnam veterans to resume a life after the war. Both serve as a reminder of the mass devastation to Vietnamese citizen health, environment, and economic livelihood experienced and the terrible consequences that arise with the use of chemical warfare.