Donate to Links
Click on Links masthead to clear previous query from search box
- AWP on Lal Shehbaz Qalandar shrine terrorist attack
2 days 15 hours ago
- US Intervention
5 days 23 hours ago
- Patrick Bond writes, "Trump
3 weeks 2 days ago
- Women's March 2017: The Birth of a New Women's Movement?
3 weeks 4 days ago
- This article is not very complete
3 weeks 4 days ago
3 weeks 5 days ago
- United States: The Rise of Trumpism
4 weeks 5 days ago
- Join the petition campaign
4 weeks 6 days ago
- Pakistan: Protests to continue if activists are not released
5 weeks 2 days ago
- Wallerstein's view on a possible US-Russia deal against China
5 weeks 2 days ago
The terrible legacy of Agent Orange and dioxin
US wages chemical warfare on Vietnam.
By Coral Wynter
December 16, 2013 -- Links International Journal of Socialist Renewal -- Agent Orange was manufactured by Monsanto Corporation and Dow Chemicals to use as a herbicide and defoliant in the Vietnam War. Agent Orange is the combination of the code names for Herbicide Orange (HO) and Agent LNX.
At the famous Battle of Dien Bien Phu, North Vietnamese General Giap and the Viet Minh forces totally defeated the French army on May 7, 1954, and the French garrison surrendered. At the 1954 Geneva Conference, the French negotiated a ceasefire agreement with the Viet Minh, and its leader Ho Chi Minh, and independence was granted to Cambodia, Laos and Vietnam.
Under the agreement, Vietnam was temporarily partitioned at the 17th parallel and divided into North Vietnam under the government of Ho Chi Minh and South Vietnam under the Catholic emperor Bao Dai. Elections were to be held throughout Vietnam in July 1956 to unify Vietnam. The US government didn’t agree with the Geneva Accords and, realising that Ho Chi Minh would easily win the elections, decided to abort the process and appointed their puppet Ngo Dinh Diem as president of South Vietnam in a fraudulent 1955 plebiscite. So began the 20-year-long war with the USA.
The Viet Minh, known as the “Vietcong” in the West, built a trail, running from North Vietnam to South Vietnam to supply the National Front for the Liberation of South Vietnam with armaments and logistics. The trail, mostly in Laos but also crossing into parts of Cambodia, was called the Ho Chi Minh trail by the Yanks. According to the US National Security Agency, the trail was “one of the greatest achievements of military engineering of the 20th century”. Parts of what became the trail had existed for centuries as footpaths, which facilitated trade in the region. The area through which the system meandered was among the most difficult in South-East Asia: a sparsely populated region of rugged mountains (1500–8000 feet), triple-canopy jungle and dense primeval rainforests.
To stop the supply of weapons and national liberation fighters, the US military decided on a strategy based on chemical warfare, to expose the trail and dense forest by dropping millions of tonnes of herbicides in the area and thereby force the Viet Minh into the open. At first, US soldiers attempted to blow up rice paddies and rice stocks, using hand grenades. But grains of rice were far more durable, and were not easily destroyed. Every grain that survived was a seed, to be collected and planted again. So the US Army went to an option that would kill off the paddies: straight out chemical warfare. Another goal was to induce the peasants to flee to urban centres, controlled by the US and South Vietnamese army, by destroying the ability of peasants to support themselves in the countryside, and depriving the guerrillas of their rural support and food supply. The chemical warfare was called “Operation Ranch Hand” and was operated from 1961 to 1971. The first aerial spraying was ordered by US President John F. Kennedy.
The history of Agent Orange began in 1943 when botanist Arthur Galston began studying a growth plant hormone, a tri-iodobenzoic acid (benzene with three iodine atoms attached to the benzene ring) in an attempt to force soya beans to grow faster. Galston found that excessive use of the compound caused catastrophic defoliation. Galston was especially concerned about the compound's side effects both to humans and the environment.However there is an earlier history, which is rarely told. 2,4 dichlorophenoxyacetic acid, known as 2,4-D was actually co-discovered independently in both the US and the UK in 1941. The two teams involved were Templeman and Colleagues at ICI (USA) and Nutman and Collaborators at Rothamsted Experimental Station in England. In both cases the researchers were part of a clandestine wartime effort by their governments to create chemical warfare agents for use in WWII. The new chemical's ability to kill weeds was entirely accidental and not the aim of the research in either country. Due to international legal reasons, research of this sort was never done openly. Research, production and use of chemical warfare agents were illegal actions under the Geneva Convention and many other international treaties signed by both the USA and the UK. This meant that a plausible cover story was needed to hide the actual nature of any chemical warfare research. For both the Allies and the Nazis, the civilian label of “agricultural research” was often used to conceal illegal and/or secret chemical warfare research.
In 1943, the US Department of the Army contracted the University of Chicago to study the effects of 2,4 dichlorophenoxyacetic acid, known as 2,4-D, and 2,4,5-trichlorophenoxyacetic acid (2,4,5-T) on cereal grains (including rice) and broadleaf crops (Figure 2). From these studies, arose the concept of using aerial applications of herbicides to destroy enemy crops to disrupt the food supply. In early 1945, the US army ran tests of various 2,4-D and 2,4,5-T mixtures at the Bushnell Army Airfield in Florida. So the US army was well aware of dioxin´s destructive capacity on foliage.
Figure 2: A) Chemical structure of 2,4-Dichlorophenoxy acetic acid (2,4-D) and B) 2,4,5-Trichorophenoxy acetic acid (2,4,5-T).
Agent Orange was a mixture of 50% 2,4-D and 50% of 2,4,5-T. The trichloro agent 2,4,5-T itself has low toxicity. However, the manufacturing process for 2,4,5-T contaminates this chemical with significant amounts of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) or often simply called dioxin. (I use TCDD and dioxin interchangeably). TCDD causes cancer and is a long-term persistent contaminant in the environment, with horrendous consequences for humans (Figure 3). It is TCDD, which is the cause of most of the severe health problems for the Vietnamese people, the US, Australian Vietnam veterans and other allied personnel including from South Korea and the Philippines, who were exposed to Agent Orange and thus TCDD from 1961-1971. TCDD has been described as perhaps the most toxic molecule ever synthesised by humans. The other chemicals used in the Vietnam War will also cause some diseases but it is dioxin that is the most lethal. Agent Orange is not the same as dioxin but nevertheless contained very high concentrations of dioxin. Internal memoranda revealed that Monsanto (the manufacturer of 2,4,5-T) had informed the US government in 1952 that its 2,4,5-T was contaminated with dioxin.
Figure 3: Figure 3: Chemical structure of 2,3,7,8 tetrachlorodibenzo-p-dioxin or TCDD.
In the manufacture of 2,4,5-T, accidental overheating of the reaction mixture easily causes the product to condense into the toxic product as a side reaction forming TCDD. With proper temperature control during production of 2,4,5-T, TCDD levels can be held to about 0.005 ppm (parts per million). Before the TCDD risk was well understood, early production facilities at Monsanto lacked proper temperature controls and individual batches tested later were found to have as much as 60 ppm of TCDD or 12,000 times more concentrated with respect to TCDD (http://en.wikipedia.org/wiki/2,4,5-T). The 2008 US Vietnam report therefore proposed 366 kg of TCDD as a plausible estimate of the total amount of TCDD applied in Vietnam during 1961–1971.
In 1970, the United States Department of Agriculture halted the use of 2,4,5-T on all food crops except rice, and in 1985 the US Environmental protection Agency (EPA) terminated all remaining uses in the US of this herbicide. The international trade in 2,4,5-T is restricted by the Rotterdam Convention.
United States Air Force records show that at least 6542 spraying missions took place over the course of Operation Ranch Hand (Figure 4). By 1971, 12 % of the total area of South Vietnam had been sprayed with defoliating chemicals, at an average concentration of 13 times the recommended USDA application rate for domestic use. In South Vietnam alone, an estimated 10 million hectares, of agricultural land was ultimately destroyed. In some areas TCDD concentrations in soil and water were hundreds of times greater than the levels considered "safe" by the US EPA. Overall, more than 20% of South Vietnam's forests were sprayed at least once over a nine-year period.
Figure 4: Extent of aerial spraying of South Vietnam with Agent Orange.
The Vietnamese government estimates 5 million people were killed with hundreds of thousands still missing and 500,000 children born with birth defects as a result of its use. There are also estimates that up to 5 million Vietnamese are still exposed directly to Agent Orange. The Red Cross of Vietnam estimates that up to 1 million people are disabled or have health problems due to Agent Orange.
Exposure to TCDD (dioxin)
There are two different health effects that must be considered when dealing with dioxin. One is the effect of direct exposure to the individual and the second is the effects on the germline of the individual, both maternal and paternal. The latter is far worse as it signifies there is a permanent effect on the human genome and all future generations. This is one of the horrific legacies of dioxin, only now being understood. (It will be dealt with in a later article).
TCDD is absorbed into the body rapidly, but is eliminated slowly. Exposure of humans to TCDD is thought to occur primarily via the mouth, skin and lungs. Dioxins will enter the food chain mainly by oral ingestion of contaminated substances, through the water, vegetation and soil. So where animals are allowed to graze, roam or scavenge in outside areas, the animals have a greater chance of becoming exposed to dioxins from the environment and ingesting the poison. This is quite unintuitive as free-range chickens, and free-roaming cattle are thought to be free of chemicals, suffering much less trauma, in the public mind.
The magnitude of contamination will depend on the frequency of exposure to the animals and the levels of contaminants. Studies have shown that roughage in general contain higher levels of dioxins than commercial compound feed, at least in Western countries. In addition, it should be noted that climate change will influence the spread of dioxins into agricultural environment.
Due to flooding, contaminated sediment could be transported to areas that were previously clean (Chobtang et al.2011). Thus dioxins will accumulate in meat and meat products, including sheep, poultry and pigs. Milk and milk products, hen eggs and egg products are usually the source of ingested dioxin. Contamination of the rivers and water supply as happened in Vietnam will of course result in accumulation in all fish products.
Dioxins are fat soluble and virtually insoluble in water. A study performed in a 42-year-old man found that 87% of the oral dose was absorbed. Dioxins are virtually permanently in the environment once formed, as it is a very stable molecule and very difficult to break down. The half-life of dioxin in humans is over 10 years, depending on the age, sex and exposure concentration, i.e., it takes 10 years to remove 50% of the dioxin in the body, once it is absorbed (Sorg et al. 2009). Dioxins accumulate in the lipids, especially the liver and fat deposits of humans. After ingestion, TCDD associates primarily with the lipoprotein fraction of the blood and later partitions into the cellular membranes and tissues (Henderson and Patterson 1988). TCDD is distributed to all compartments of the body; the amounts differ from organ to organ, but most studies indicate that the primary disposition of TCDD is in the liver and adipose tissues.
In a human volunteer, it was found that at 135 days after ingestion, 90% of TCDD was in fat (Poiger and Schlatter 1986). Direct binding of TCDD to CYP1A2, the enzyme that can break it down to a limited extent, is thought to result in sequestration of TCDD in the liver and to inhibit its distribution to other tissues. This is a reaction of the body to try and protect the fetus against TCDD-induced teratogenesis (Dragin et al. 2006).
Dioxin undergoes virtually no metabolism. Animals have evolved to eliminate most toxins by the development of enzymes in the liver that detoxify a specific toxin. Because dioxins are not found in nature, animals have not developed enzymes to detoxify this group of chemicals. Very small amounts of dioxin are slowly excreted throughurine and faeces so that the remaining ingested dioxin remains in the body for decades. Faeces has been found to be the main route of elimination, with 60% of the TCDD eliminated unchanged, with the rest being minor amounts of hydroxylated dioxins.
Finally, the elimination rate of TCDD, in particular after low exposures, depends heavily on the amount of adipose tissue mass in the body. Relatively high exposures of TCDD affect a variety of organs and result in organ dysfunction and death. The specific organ dysfunction that constitutes the lethal event, however, is not known. A characteristic of TCDD exposure is a wasting syndrome with loss of adipose and muscle tissues and severe weight loss. A major source of human exposure is through breast milk, as the dioxin load in the body is mobilised and excreted through breast milk. As a consequence of the environmental ubiquity of dioxins, all humans have acquired some exposure to dioxins and this load is slowly increasing even now (White and Birnbaum 2009).
Health reports from the Australian Department of Veteran Affairs
There were 60,000 Australian personnel involved in the Vietnam War, from 1962 to 1973, of which 500 were killed in action and 3100 severely physically wounded. The Australian government commissioned several reports on the health of Vietnam veterans. The first was completed in 1984, called the Australian Veterans Health Study or AVH. A second study, called the Vietnam Veterans Mortality study was completed in 1997. The Australian Department of Veterans Affairs released a report in 2002 and concluded that the list of cancers that could have been caused by exposure to TCDD were as listed in Table 1. However the status of this report is not clear as it states that some of these cancers are associated with smoking and alcohol, which was not taken into account when estimating cancer incidence. The scientific report, mainly based on mortality rates of Vietnam veterans compared with the civilian Australian population, was then sent to the Repatriation Commission and the final report given to the minister of veteran affairs Danna Vale in 2002 (in Liberal Party Prime Minister John Howard’s government). The report can be located at http://www.dva.gov.au/aboutDVA/publications/health_research/vietnam_vets/vvdr/Documents/Dapsone_Report_Appendices.pdf.
Table 1. Diseases associated with exposure to TCDD, estimated by the Australian Army
Specific conditions showing statistically significant increased risk associated with Vietnam service in the Australian studies are:
All cause mortality (total number of deaths relative to the total population)
Mortality from all neoplasms (cancers)
Mortality from lung, prostate, tongue, and ‘other’ digestive organ cancers
Mortality and morbidity from cirrhosis of the liver
Mortality from ischaemic heart disease
Motor neurone disease
The Australian Navy was found to have the highest mortality, even though personnel may not have spent much time on land. There is no explanation for this in the Australian report. However this can be understood by the fact that navy vessels collected drinking water as close to shore as possible to minimise salt content. This water was then distilled, without the realisation that dioxin would co-distil with the steam.
An Australian research study focused on the evaporative distillation process that was used to produce potable water on board ship from surrounding estuarine waters. Vessels with such distillation processes that traveled near land or even at some distance from river deltas would periodically collect water that contained dioxin. The study found that co-distillation of dioxins was observable in all experiments conducted and that distillation increased the concentration of dioxins in the distillate compared with the concentration in the source water (Mueller et al. 2001). On the basis of that study and other evidence, the Australian Department of Veterans Affairs determined that Royal Australian Navy personnel, who served offshore, were exposed to dioxins.
These experiments were repeated by the US scientists and these findings were confirmed. Contaminants with low water solubility would evaporate from water and that the distillation process would enhance the process by adding heat and reducing the pressure. No measurements of dioxin concentrations in sea water were collected during the Vietnam conflict, so it is not possible to ascertain the extent to which drinking water on Australian vessels may have been contaminated through distillation processes. Thus, the US 2008 report stated that a presumption of exposure of military personnel serving on those vessels is not unreasonable. This result is not recorded in the 2010 US VAO update.
There is another worrying Australian connection, reported by Australian Greens party senator Lee Rhiannon. Jean Williams, a researcher who received the Order of Australia medal for her research on the effects of chemicals on Australian war veterans, found that cancer rates in Innisfail, Queensland, were 10 times higher than the state average. This was linked to secret testing of Agent Orange by Australian military scientists during the Vietnam War. Williams based her allegations on Australian government reports found in the Australian War Memorial museum archives. A former soldier, Ted Bosworth, backed up the claims, saying that he had been involved in the secret testing. The Queensland health department claimed that cancer rates in Innisfail were not higher than those in other parts of the state. This denial is similar to that of the US and Australian governments when lobbied to take responsibility for the damage and deaths caused by Agent Orange (http://lee-rhiannon.greensmps.org.au/content/speeches/speech-agent-orange).
There is evidence that Agent Orange was used throughout the Kimberley region in Western Australia from the 1970s until as late as the 1980s, using many Aboriginal workers employed by the Aboriginal Protection Board (a misnomer). Many of those who were working became sick with nausea and vomiting. Some 90 men who were still alive say that of the 300 who were spraying, they are aware of about 40 deaths, many of whom were in their 30s when they died. Aboriginal woman Lucy Marshall has been trying for decades to obtain compensation for the death of her son Cyril Hunter at 33 years of age as well as a younger son who died of cancer possibly from the contaminated chemicals, brought home by Hunter. No safety equipment was handed to the men, as they were told the spray was drinkable. Another Aboriginal worker went blind. One of the workers, Carl Drysdale, remembered that the drums, which came from Singapore redirected from Vietnam, were labelled 2,4,5-T, which most certainly would have had dioxin as a contaminant. A 2003 government inquiry recommended that 27 workers still alive be compensated but nothing has happened. The empty 2,4,5-T drums remain in the Derby tip (http://thestringer.com.au/agent-orange-used-as-a-herbicide-throughout-the-kimberley/ - .UaRc4iv8_bo).
History of poisonings by dioxins
There is a history of accidental poisoning by dioxins in both animals and humans in many places in the world and the precautions taken by governments to cover this up or underplay its significance. It should be noted that although some of the poisoning events refer to Polychlorinated Biphenyls, a close relative of dioxin, these would also contain small amounts of TCDDs or dioxins (White and Birnbaum 2009).
- The earliest evidence of a human-made dioxin molecule comes from a German chemical production plant in Lampertheim in South Hesse that was making sodium carbonate (washing soda or soda ash) and in the process generated dioxin in 1827. It was not until 1980s when a playground and school intended for children was to be built on the site where the plant had stood that the extensive dioxin contamination of the soil was discovered (Balzar et al. 2007).
- In 1947, X-disease was first reported in cattle. It caused a hyperkeratotic condition akin to chloracne with a thickening of the stratum corneum, often associated with a qualitative abnormality of the keratin. It was later shown to have arisen due to exposure to dioxin-like compounds. It could accumulate and finally cause death in the animals (Engel and Bell 1953).
- An explosion in a Monsanto chemical plant in Nitro, West Virginia, resulted in the exposure of workers to 2,4,5-T contaminated with dioxin in 1949. Persistent chlorache was observed in the exposed workers. Later studies demonstrated an increase in all cancers combined, in the most highly exposed workers (Suskind and Hertzberg 1984; Steenland et al. 1999).
- On November 17, 1953, an uncontrolled decomposition reaction occurred in a trichlorophenol (TCP) production unit owned by BASF AG and located in Ludwigshafen, Germany. Byproducts that escaped from the damaged autoclave contaminated surfaces throughout the immediate work area of the enclosed production building. Within days, workers who were engaged in clean-up efforts developed severe acne as well as other signs and symptoms, and some were taken into hospital. The agent most likely to have caused these responses was not identified until 1957 when high TCDD levels were found in the blood lipids. Employees were exposed to residues contaminated with TCDD during the clean-up and repair activities that lasted for about four to five months, during incidental maintenance work in the building after completion of the restoration work, and finally during demolition of the reactor portion of the building in 1968-69. Some 30 years later TCDD could still be detected in the survivors. Workers died from lung cancer, stomach cancer, liver cancer and cardiovascular disease (Ott and Zober 1996)
- The death of huge numbers of commercially raised chickens in the US occurred, named chick oedema disease in 1957 and was later found to be caused by contamination of feed supplies by TCDD (Firestone 1973).
- In 1968 in Kyushu, Japan, a rice bran oil company became contaminated with PCBs and polychlorinated dibenzofurans, PCDFs. The contaminated oil was sold and fed to livestock and humans resulting in the deaths of hundreds of thousands of dead birds. This was called “Yusho” disease (literally meaning oil) (Aoki 2001).
- This was repeated in Taiwan in 1979 but was referred to as “Yucheng” (again meaning oil) disease. This episode was more clearly associated with impaired cognitive development and behavioural problems due to gestational exposure among the male children. (Guo et al. 2004).
- An entire town in the USA was exposed to high levels of dioxins when contaminated waste oil was spread on a dirt road of Times Beach, Missouri, to control dust levels. Because TCDD was identified that year as a teratogen, all the properties in Times Beach were bought out by the US EPA for a total of $32 million in 1983, the inhabitants relocated and the town demolished. Some 265,000 tons of regional soil were incinerated (White and Birnbaum 2009).
- The Great Lakes region of US and Canada saw the greatly diminished reproduction among trout and mink, which has persisted to this day, due to dioxin contamination. Multiple species of birds, fish, reptiles and mammals have exhibited reproductive impairment, immunologic dysfunction, hyperplasia of the thyroid and adrenal glands, porphyria, congenital malformation, growth retardation amongst others (Fox, 2001).
- In the late 1970s, nursing mothers across Michigan had their breast milk assessed for contamination and levels of PCBs were found to be as high as 5100 ppm, resulting from high consumption of fish from polluted waterways (Wickizer 1981).
- The most famous case occurred in Seveso, Italy, when an explosion occurred in 1976 at an Italian chemical plant producing 2,4,5 trichlorophenol, an intermediate in 2,4,5-T synthesis. Because of the nature of the uncontrolled reaction that produced the explosion, not only TCDD was released but the levels were far higher than the normal range of 1 ppm and could have reached 100 ppm. Immediately after the accident, those exposed had skin lesions consistent with chlorache. Later studies revealed that TCDD could increase the risk of many cancers, as well as diabetes, adverse cardiovascular effect and altered endocrine and immune function and early death (Bertazzi et al. 1997; Bertazzi et al. 2002; Baccarelli et al. 2002; Mocarelli et al. 2008). It is this case that has indicated that the effect of TCDDs can be passed on to the next generation. The sperm count in children exposed in Seveso has been measured now that they are adults. Those children of an age before puberty have shown a much lower sperm count as adults but those exposed at an age after puberty have higher sperm counts. So the effect of TCDDs depends not only on the dosage but also on the timing of exposure.
- In 1981, a PCB dielectric fluid-filled transformer caught fire in the basement of the Binghamton State office building in the state of New York. The fire deposited an oily soot throughout the 18-storey building with some levels measured as high as 1200 ppm of PCDDs and PCDFs. Millions of dollars were spent in cleaning the building and it was closed up for 13 years (O’Keefe et al. 1985).
- A massive die-off event in the Baltic Sea of 20,000 harbour seals occurred in 1988. The underlying cause of death was found to be an infection with Phocine distemper virus. However it is thought that PCB exposure contributed to the viral infection and death due to high levels of PCBs in the fish eaten by the seals. PCBs and PCDD are known immunosuppressants (Ross et al. 1996).
- In Vienna in 1997, five people working as secretaries in a textile institute were poisoned with very high levels of dioxin with a calculated body burden of 1.6 mg of TCDD, the highest level ever recorded. It was measured as 144,000 picograms TCDD/gm of blood fat (Geusau et al. 2001).
- In Belgium in 1999, an overwhelming percentage of national livestock were given PCB-contaminated feed that resulted in an international recall of all products containing meat or dairy from the affected animal, even including Belgian chocolate. However it is not clear how the chocolate was contaminated (White and Birnbaum 2009).
- Some people would remember the dioxin poisoning of Viktor Yushchenko in 2004. Yushchenko was the candidate and later president of the Ukraine from 2005-10. He was intentionally poisoned to weaken his political influence and to remove him as a candidate in September 2004 with a serum dioxin level of over 6000 times the normal level. He was hospitalised with acute pancreatitis, followed by chlorache and oedema, resulting in a pockmarked face (Sorg et al. 2009). In 2012, Yushchenko stated he is still suffering from the effects of dioxin poisoning.
- Finally, in 2008, all Irish pork products were removed from supermarkets due to the contamination of pigs resulting from ingestion of dioxin contaminated feed supplies. A repeat of the Belgian contamination, 10 years prior (White and Birnbaum 2009).
Nowadays human exposure to TCDDs mainly occurs through oral ingestion of food, which contains high levels of the toxins. Milk from cows, fish, which concentrate the dioxins through the contaminated waterways, eggs from hens and meat from grazing cows, pigs and chickens are most affected.
Vietnam and Laos are still the most affected and devastated by the dumping of 76 million litres of Agent Orange on their countries. Vietnamese women who are pregnant are still ingesting contaminated eggs from chickens, milk from grazing cows, fish, ducks and snails grown in artificial or natural fish ponds where there are high levels of dioxins in the beds of the ponds and any meat from animals, grazing on contaminated land. Vietnamese peasants are extremely poor and have little option but to eat their own grown food. Even when the baby is born, the breast milk will be highly contaminated with ingested dioxins and continues to contribute to the horrific birth deformities.
Figure 5: The yellow markings indicate the Ho Chi Minh trail between Vietnam and Laos.
About 28 of the former US military bases in South Vietnam where the herbicides were stored and loaded onto airplanes still have high level of dioxins in the soil, posing a health threat to the surrounding communities. Extensive testing for dioxin contamination has been conducted at the former US airbases in Da Nang, Phu Cat and Bien Hoa. Some of the soil and sediment on the bases have extremely high levels of dioxin requiring remediation. The Da Nang Airbase has dioxin contamination up to 350 times higher than international recommendations for action. The $43 million joint project with Vietnam is expected to be completed by 2016 on the 19-hectare contaminated site, now an active Vietnamese military base near Danang's commercial airport. Some 73,000 cubic metres of soil are to be heated to a temperature to break down dioxin.
Washington has been quibbling for years over the need for more scientific research to show that the herbicide caused health problems among the Vietnamese people. The US recognises that Agent Orange is the cause of the health problems of its own Vietnam veterans while at the same time arguing that it may not be the cause of the same problems in Vietnam! The US is planning to evaluate what's needed for remediation at the former Bien Hoa air base in southern Vietnam, another Agent Orange hotspot.
However the clean-up in Da Nang does not reflect a change in US policy on Agent Orange. “Nevertheless, the US government refuses to compensate Vietnamese victims of chemical warfare because to do so would mean admitting that the US committed war crimes in Vietnam”, reported the August 17-23, 2012, Vietweek publication. “This would open the door to lawsuits that would cost the government billions of dollars.” This late US promise of aid has been driven by the need for the US to counter the influence of China in the region.
Vietnam must be given financial and technical support by all the allied governments who fought in the Vietnam War (which they call the American War) to detect the toxic deposits where the highest levels of TCDDs are located and all possible aid to clean up the toxic depositions of dioxin, whatever that takes.
Baccarelli A, Mocarelli P, Patterson DG, Bonzini M, Pesatori AC, Caporaso N et al (2002) Immunologic effects of dioxin: new results from Seveso and comparison with other studies. Environ Health Perspect 110, 1169-73.
Balzar W, Gaus H-M, Gaus C, Weber R, Schmitt-Biegel B, Urban U. (2007) Remediation measures in a residential area highly contaminated with PCDD/PCDF, arsenic and heavy metals as a result of industrial production in the early 19th century. Organohalogen Compounds 69, 857-60.
Bertazzi PA, Zocchetti C, Guercilena S, Consonni D, Tironi A, Landi MT, et al (1997) Dioxin exposure and cancer risk: a 15-year mortality study after the "Seveso accident". Epidemiology 8, 646-52.
Bertazzi PA, Consonni D, Bachetti S, Rubagotti M, Baccarelli A, Zocchetti C et al (2002) Health effects of dioxin exposure: a 20 year mortality study. Am J Epidemiol 153, 1031-44.
Chobtang J, de Boer IJ, Hoogenbo RL, Haasnoot W, Kijlstra A, Meerburg BG. (2011) The need and potential of biosensors to detect dioxins and dioxin-like polychlorinated biphenyls along the milk, eggs and meat food chain. Sensors (Basel) 11, 11692-716.
Dragin N, Dalton TP, Miller ML, Shertzer HG, Nebert DW. (2006) For dioxin-induced birth defects, mouse or human CYP1A2 in maternal liver protects whereas mouse CYP1A1 and CYP1B1 are inconsequential. J Biol Chem 281, 18591–600.
Engel RW, Bell WB. (1953) The nature of X-disease in cattle. Nutr Rev 11, 97-9.
Firestone D. (1973) Etiology of chick edema disease. Environ Health Perspect 5, 59-66.
Fox GA. (2001) Wildlife as sentinels of human health effects in the Great Lakes-St. Lawrence basin. Environ Health Perspect 109, Suppl 6, 853-61
Geusau A, Abraham K, Geissler K, Sator MO, Stingl G, Tschahler E. (2001) Severe 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) intoxication: clinical and laboratory effects. Environ Health Perspect 109, 865-9.
Guo YL, Lambert GH, Hsu CC, Hsu MM. (2004) Yucheng: Health effects of prenatal exposure to polychlorinated biphenyls and dibenzofurans. Int Arch Environ Health 77, 153-8.
Henderson L, Patterson DJ. (1988) Distribution of 2,3,7,8-tetrachlorodibenzo-p-dioxin in human whole blood and its association with, and extractability from lipoproteins. Bull Environ Contamin Toxicol 40, 604–611.
Mocarelli P, Gerthoux PM, Patterson DG, Milani S, Limonta G, Bertona M et al. (2008) Dioxin exposure, from infancy through puberty, produces endocrine disruption and affects human semen quality. Environ Health Perspect 116, 70-7.
Mueller J, Gaus C, Bundred K, Alberts V, Moore MR, Horsley K. (2001) Co-distillation of TCDD and other POPs during distillation of water: A potential source for exposure. Organohalogen Compounds 52, 243–246.
O’Keefe PW, Silkworth JB, Gierthy JF, Smith RM, De Caprio AP, Turner JN et al. (1985) Chemical and biological investigations of a transformer accident at Binghamton, NY. Environ Health Perspect 60, 201-9.
Ott MG, Zober A (1996) Cause specific mortality and cancer incidence among employees exposed to 2,3,7,8-TCDD after a 1953 reactor accident. Occup Environ Med 53, 606-12.
Poiger H, Schlatter C. (1986) Pharmacokinetics of 2,3,7,8-TCDD in man. Chemosphere 15, 1489–94.
Ross P, De Swart R, Addison R, van Loveren H, Vos J, Osterhaus A. (1996) Contaminant-induced immunotoxicity in harbour seals: wildlife at risk? Toxicology 112, 157-69.
Sorg O, Zennegg M, Schmid P, Fedosyuk R, Valikhnovskyi R, Gaide O et al. (2009) 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) poisoning in Victor Yushchenko: identification and measurement of TCDD metabolites. Lancet 374 (9696), 1179-85.
Steenland K, Piacitelli L, Deddens J, Fingerhut M, Chang LI. (1999) Cancer, heart disease, and diabetes in workers exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin. J. Natl. Cancer Inst. 91, 779-86.
Suskind RR, Hertzberg VS. (1984) Human health effects of 2,4,5-T and its toxic contaminants. JAMA 251, 2372-80.
White SS, Birnbaum LS. (2009) An overview of the effects of dioxins and dioxin-like compounds on vertebrates, as documented in human and ecological epidemiology. J Environ Sci Health Pt C Environ Carcinog Ecotoxicol Rev 27, 197-211.