8/13/2019 The Terrible Legacy of Agent Orange and Dioxin

http://slidepdf.com/reader/full/the-terrible-legacy-of-agent-orange-and-dioxin 1/16

 Abou t Link s   Editorial advisory board   Contact us   Comments policy

Documents

Espanol

HOT TOPICS at Links

Multimedia

Pamphlets, book excerpts &dossiers

Past issues

Conferences and gatherings

Subscribe to Links

Join Links' Facebook group

Follo w Links on Twitter 

Links on your mobile phone

Education for Socialists mediaplayer 

Donate

 

Search

Click on Links masthead to clear previous query from search box

Home

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 wasmanufact ured by Monsanto Corporation and Dow Chemicals to use as a herbicide and def oliantin the Vietnam War. Agent Orange is the combination of the code names for Herbicide Orange(HO) and Agent LNX.

 At the famous Bat t le of Dien Bien Phu, Nort h Vietnamese General Giap and t he Viet Minh forces

 PDFmyURL.com

8/13/2019 The Terrible Legacy of Agent Orange and Dioxin

http://slidepdf.com/reader/full/the-terrible-legacy-of-agent-orange-and-dioxin 2/16

837 people like this. SignLikeLike

ReadGr siste

 totally defeated the French army on May 7, 1954, and the French garrison surrendered. At the1954 Geneva Conference, t he French negotiated a ceasef ire agreement with t he Viet Minh, andits leader Ho Chi Minh, and independence was granted to Cambodia, Laos and Vietnam.

Under t he agreement, Vietnam was t emporarily partitioned at the 17t h parallel and divided intoNorth Vietnam under the government of Ho Chi Minh and South Vietnam under the Catholicemperor 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 wouldeasily win the elections, decided to abort the process a nd appointed their puppet Ngo Dinh Diemas president of South Vietnam in a fraudulent 1955 plebiscite. So began the 20-year-long war 

with t he USA.The Viet Minh, known as the “Vietcong” in the West, built a trail, running from North Vietnam toSouth Vietnam t o supply the National Front f or t he Liberation of South Vietnam with armamentsand logistics. The t rail, mostly in Laos but also crossing into part s of Cambodia, was called t heHo Chi Minh trail by t he Yanks. According t o t he US Nat ional Security Agency, the t rail was “one of the great est achievements of military engineering of the 20th century”. Parts of what becamethe t rail had existed f or centuries as f ootpa ths, which facilitat ed t rade in the region. The areathrough which the syst em meandered was among t he most diff icult in South-East Asia: asparsely populated region of rugged mountains (1500–8000 f eet), t riple-canopy jungle anddense primeval rainforest s.

To stop the supply of weapons and national liberation fighters, the US military d ecided on astrat egy based on chemical warfare, to expose t he trail and dense f orest by dropping millions of 

tonnes of herbicides in the area and t hereby force t he Viet Minh into t he open. At f irst, USsoldiers at tempt ed t o blow up rice paddies and rice st ocks, 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 thepaddies: straight out chemical warfare. Another goal was t o induce t he peasants t o f lee to urbancentres, controlled by the US and South Vietnamese army, by dest roying t he ability of peasantsto support themselves in the countryside, and depriving the guerrillas of their rural support andfood supply. The chemical warfare was called “Operation Ranch Hand” and was operated from1961 to 1971. The first aerial spraying was ordered by US President John F. Kennedy.

The chemicals

The history of Agent Orange began in 1943 when botanist Arthur Galston b egan st udying agrowth plant hormone, a tri-iodobenzoic acid (benzene with t hree iodine atoms att ached to the

benzene ring) in an att empt to f orce soya beans to grow f aster. Galston found that excessiveuse of the comp ound caused cat astrophic def oliation. Galston was especially concerned aboutthe compound's side eff ects both t o humans and the environment.

However t here is an earlier history, which is rarely t old. 2,4 dichlorophenoxyacet ic acid, known as2,4-D was actually co-discovered independently in both the US and the UK in 1941. The twoteams involved were Templeman and Colleagues at ICI (USA) and Nutman and Collaborators atRothamsted Experimental Station in England. In both cases the researchers were part of aclandestine wartime eff ort by t heir governments t o create chemical warfare agents f or use inWWII. The new chemical's ability to kill weeds was entirely accidental and not the aim of theresearch 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 

 PDFmyURL.com

8/13/2019 The Terrible Legacy of Agent Orange and Dioxin

http://slidepdf.com/reader/full/the-terrible-legacy-of-agent-orange-and-dioxin 3/16

 

Recent

Mandela and neo-liberalism

1 day 4 hours ago

"insurrection" - a terminologicaldebate

1 day 10 ho urs ago

Dave Holmes’ article is

3 days 8 hours ago

Mandela an inspiration

3 days 11 hours ago

What a great tribute to a

4 days 1 hour ago

Nelson mandela

4 days 5 hours ago

Correction

5 days 19 hours ago

Move on?

the Geneva Convention and many other international treaties signed by both the USA and theUK. This meant t hat a p lausible cover st ory was needed to hide t he actual nature of anychemical warfa re research. For both the Allies and t he Nazis, the civilian label of “agriculturalresearch” was of ten used to conceal illegal and/or secret chemical warfare research.

In 1943, the US Department o f the Army contract ed t he University of Chicago t o st udy theeffects 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 st udies,arose the concept of using aerial applications of herbicides to de stroy enemy crops t o disruptthe food supply. In early 1945, the US army ran tests of various 2,4-D and 2,4,5-T mixtures at theBushnell Army Airfield in Florida. So the US army was we ll aware of dioxin´s dest ructive capacit yon foliage.

 PDFmyURL.com

8/13/2019 The Terrible Legacy of Agent Orange and Dioxin

http://slidepdf.com/reader/full/the-terrible-legacy-of-agent-orange-and-dioxin 4/16

6 days 14 hours ago

That is over and done with.

1 week 6 hours ago

Transitional demands not enough

1 week 2 days ago

Follow this blog

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 mixt ure of 50% 2,4-D and 50% of 2,4,5-T. The t richloro agent 2,4,5-T itself has low toxicity. However, the manufacturing process for 2,4,5-T contaminates this chemical withsignificant a mounts of 2,3,7,8-tet rachlorodibenzo- p-dioxin (TCDD) or often simply called dioxin. (Iuse TCDD and dioxin interchangeably). TCDD causes cancer and is a long-term persistentcontaminant in the environment , with horrendous consequences f or humans (Figure 3). It isTCDD, which is t he cause of most of the severe health problems for t he Vietnamese peop le, theUS, Australian Vietnam ve te rans and ot her allied personnel including from South Korea and t hePhilippines, who were exposed to Agent Orange and thus TCDD from 1961-1971. TCDD hasbeen described as perhaps the most toxic molecule ever synthesised by humans. The ot her chemicals used in the Vietnam War will also cause some diseases but it is dioxin that is the mostlethal. Agent Orange is not the same as dioxin but nevertheless contained very highconcentrations 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 ma nufact ure of 2,4,5-T, accidental overheating of the react ion mixture easily causes t heproduct t o condense into the t oxic product as a side reaction fo rming TCDD. With proper tempe rature control during production of 2,4,5-T, TCDD levels can be held t o about 0.005 ppm(parts per million). Before the TCDD risk was well understood, early production facilities atMonsanto lacked proper te mperature controls and individual batches t ested later were f ound t ohave as much as 60 ppm of TCDD or 12,000 times more concentrat ed with respect t o T CDD(http://en.wikipedia.org/wiki/2,4,5-T ). The 2008 US Vietnam report therefore proposed 366 kg of 

TCDD as a p lausible est imate of the t otal amount of TCDD applied in Vietnam during 1961 –1971.

In 1970, the United St ate s Department of Agriculture halted the use of 2,4,5-T on all food cropsexcep t rice, and in 1985 the US Environmental prot ect ion Agency (EPA) te rminated a ll remaininguses in the US of t his herbicide. The international trade in 2,4,5-T is restricted by the Rott erdamConvention.

United St ate s Air Force records show that at least 6542 spraying missions t ook place over thecourse of Operation Ranch Hand (Figure 4). By 1971, 12 % of the total area of South Vietnamhad been sprayed with def oliating chemicals, at an average concentration of 13 times t he

recommended USDA application rate for domest ic use. In South Vietnam alone, an estimated 10

 PDFmyURL.com

8/13/2019 The Terrible Legacy of Agent Orange and Dioxin

http://slidepdf.com/reader/full/the-terrible-legacy-of-agent-orange-and-dioxin 5/16

million hectares, of agricultural land was ultimately destroyed. In some areas TCDDconcentrat ions in soil and water were hundreds of times great er t han the levels considered"saf e" by the US EPA. Overall, more than 20% of South Vietnam's f orests were sprayed at leastonce over a nine-year period.

 PDFmyURL.com

8/13/2019 The Terrible Legacy of Agent Orange and Dioxin

http://slidepdf.com/reader/full/the-terrible-legacy-of-agent-orange-and-dioxin 6/16

Syndic

 

PDFmyURL.com

8/13/2019 The Terrible Legacy of Agent Orange and Dioxin

http://slidepdf.com/reader/full/the-terrible-legacy-of-agent-orange-and-dioxin 7/16

Figure 4: Extent of aerial spraying of South Vietnam with Agent Orange.

The Vietnamese government estimates 5 million people were killed with hundreds of thousandsstill missing and 500,000 children born with birth defects as a result of its use. There are alsoestimat es t hat up t o 5 million Vietnamese are st ill exposed directly t o Agent Orange. The RedCross of Vietnam est imates t hat up t o 1 million people are disabled or have health problems dueto Agent Orange.

Exposure to TCDD (dioxin)

There are t wo diff erent health eff ects that must be considered when dealing with dioxin. One isthe ef fect of direct exposure to t he individual and the second is the ef fect s on the germline of the individual, both mat ernal and pat ernal. The latt er is far worse as it signifies t here is apermanent eff ect on the human genome and all fut ure generations. This is one of the horrificlegacies 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 isthought t o occur primarily via the mouth, skin and lungs. Dioxins will enter the fo od chain mainly byoral ingestion of contaminated subst ances, through the water, vegeta tion and soil. So whereanimals are allowed t o graze, roam or scavenge in outside areas, the a nimals have a great er chance of becoming expose d t o dioxins from t he environment and ingest ing t he poison. This isquite unintuitive as f ree-range chickens, and free-roaming catt le are thought to be f ree of chemicals, suff ering much less t rauma, in the public mind.

The magnitude of contamination will depend on t he frequency of exposure to the animals andthe 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 benoted that climate change will influence the spread of dioxins into agricultural environment.

Due to f looding, contaminated sediment could be transported to areas that were previouslyclean (Chobtang et al .2011). Thus dioxins will accumulate in meat and meat product s, includingsheep, poult ry and pigs. Milk and milk products, hen eggs and egg product s are usually thesource of ingested dioxin. Contamination of the rivers and water supply as happened in Vietnamwill 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 manfound t hat 87% of the oral dose was absorbed. Dioxins are virtually permanently in theenvironment once formed, as it is a very stab le molecule and very diff icult t o break down. Thehalf-life of dioxin in humans is over 10 years, depending on the age, sex and exposureconcentration, 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. Aft er ingestion, TCDD associates p rimarily with t he lipoprotein f raction of the blood andlater partitions into the cellular membranes and tissues (Henderson and Patterson 1988). TCDDis distributed t o all compartment s of t he body; the amounts diff er from organ to organ, but moststudies indicate that the primary disposition of T CDD is in the liver and adipose tissues.

In a human volunteer, it was f ound t hat at 135 days aft er ingest ion, 90% of TCDD was in fat(Poiger and Schlatter 1986). Direct binding of TCDD to CYP1A2, the enzyme that can break itdown to a limited extent , is thought to result in sequestrat ion of T CDD in the liver and to inhibitits distribution to other tissues. This is a reaction of t he body to t ry and protect t he fet us againstTCDD-induced terat ogenesis (Dragin et al . 2006).

 PDFmyURL.com

8/13/2019 The Terrible Legacy of Agent Orange and Dioxin

http://slidepdf.com/reader/full/the-terrible-legacy-of-agent-orange-and-dioxin 8/16

Dioxin undergoes virtually no metabolism. Animals have evolved to eliminate most toxins by thedevelopment of enzymes in the liver that det oxify a spe cific toxin. Because dioxins are not f oundin nature, animals have not developed enzymes t o det oxify t his group of chemicals. Very smallamounts of dioxin are slowly excreted throughurine and faeces so t hat t he remaining ingesteddioxin remains in the body for d ecades. Faeces has been f ound t o 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 theamount of adipose tissue mass in the body. Relatively high exposures of TCDD af fect a variety

of organs and result in organ dysfunction and deat h. The specif ic organ dysfunction thatconstitutes the lethal event, however, is not known. A characteristic of TCDD exposure is awasting 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 andexcreted through breast milk. As a consequence of the environmental ubiquity of dioxins, allhumans have acquired some exposure to dioxins and this load is slowly increasing even now(White and Birnbaum 2009).

Health reports f rom the Australian Department of Veteran Aff airs

There were 60,000 Australian personnel involved in the Vietnam War, from 1962 to 1973, of which500 were killed in act ion and 3100 severely physically wounded. The Australian governmentcommissioned several reports on the health of Vietnam vet erans. The f irst was completed in1984, called t he Aust ralian Vet erans Health Study or AVH. A second study, called t he Vietnam

Veterans Mortality st udy was completed in 1997. The Australian Department of Vete rans Aff airsreleased a report in 2002 and concluded that the list of cancers that could have been caused byexposure to T CDD were as listed in Table 1. However the stat us of t his report is not clear as itstat es t hat some of these cancers are associat ed with smoking and alcohol, which was nottaken into account when estimating cancer incidence. The scientific report, mainly based onmortality rat es of Vietnam veterans compared with the civilian Australian population, was t hensent t o the Repatriation Commission and the final report given to t he minister of vet eran affa irsDanna Vale in 2002 (in Liberal Party Prime Minister Jo hn Howard’s g overnment ). The report canbe located athttp://www.dva.gov.au/aboutDVA/publications/health_research/vietnam_vets/vvdr/Documents/Dapsone_Report_Appendices.pdf.

 

Table 1. Diseases asso ciated with exposure to TCDD, estimated b ythe Australian Army

Specific conditions showing statistically significant increased riskassociated with Vietnam service in the Australian studies are:

 All cause mort ality (t ot al number o f dea ths relat ive t o t he t ot alpopulation)

Mortality from all neoplasms (cancers)

Mortality from lung, prostat e, t ongue, and ‘ot her’ digestive organ cancers

Mortality and morbidity from cirrhosis of the liver 

 PDFmyURL.com

8/13/2019 The Terrible Legacy of Agent Orange and Dioxin

http://slidepdf.com/reader/full/the-terrible-legacy-of-agent-orange-and-dioxin 9/16

8/13/2019 The Terrible Legacy of Agent Orange and Dioxin

http://slidepdf.com/reader/full/the-terrible-legacy-of-agent-orange-and-dioxin 10/16

nausea and vomiting. Some 90 men who were still alive say that of the 300 who were spraying,they are a ware of about 4 0 deat hs, many of whom were in their 30s when they died. Aboriginalwoman Lucy Marshall has been trying f or decades t o obt ain compensation for t he death of her son Cyril Hunter at 33 years of age as well as a younger son who died of cancer possibly f romthe cont aminated chemicals, brought home by Hunter. No safet y equipment was handed to themen, as t hey were t old t he spray was d rinkable. Another Aboriginal worker went blind. One of theworkers, Carl Drysdale, remembered that the d rums, which came f rom Singapore redirected fromVietnam, were labe lled 2,4,5-T, which most cert ainly would have had d ioxin as a contaminant. A2003 government inquiry recommended that 27 workers still alive be compensated but nothinghas 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 placesin the world and t he precautions t aken by governments t o cover t his up or underplay itssignificance. It should be noted that although some of the poisoning events refer t oPolychlorinated Biphenyls, a close relative of dioxin, these would also contain small amounts of TCDDs or dioxins (White a nd Birnbaum 2009).

The e arliest evidence of a human-made dioxin molecule comes from a German chemicalproduction 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 until1980s when a playground and school intended for children was to be built on the site where

the plant had st ood t hat t he extensive dioxin contamination of the soil was discovered(Balzar et al . 2007).

In 1947, X-disease was f irst reported in catt le. It caused a hyperkeratotic co ndition akin tochloracne with a thickening of the st ratum corneum, oft en associated with a qualitat iveabnormality of the keratin. It was later shown to have arisen due to exposure to dioxin-likecompounds. It could accumulate and f inally cause de at h in the a nimals (Engel and Bell1953).

 An explosion in a Monsant o chemical plant in Nitro , West Virginia, resulted in t he exposureof workers to 2,4,5-T contaminated with dioxin in 1949. Persistent chlorache was observedin the exposed workers. Later studies demonstrated an increase in all cancers combined, inthe most highly exposed workers (Suskind and Hertzberg 1984; Steenland et al. 1999).

On November 17, 1953, an uncontrolled decomposition reaction occurred in at richlorophenol (TCP) production unit owned by BASF AG and locat ed in Ludwigshafen,Germany. Byproducts t hat escaped f rom the damaged aut oclave contaminate d surfacesthroughout the immediate work area of the enclosed production building. Within days,workers who were engaged in clean-up eff orts d eveloped severe acne as well as ot her signs and sympt oms, and some were t aken into hospital. The agent most likely t o havecaused these responses was not identified until 1957 when high TCDD levels were found inthe b lood lipids. Employees were exposed to residues contaminated with TCDD during t heclean-up and repair activities t hat lasted for abo ut f our to f ive months, during incidentalmaintenance work in the building after completion of the restoration work, and finally duringdemolition of t he reactor port ion of t he building in 1968-69. Some 30 years lat er T CDD

 PDFmyURL.com

8/13/2019 The Terrible Legacy of Agent Orange and Dioxin

http://slidepdf.com/reader/full/the-terrible-legacy-of-agent-orange-and-dioxin 11/16

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, namedchick oedema disease in 1957 and was later found to be caused by contamination of feedsupplies by TCDD (Firestone 1973).

In 1968 in Kyushu, Japan, a rice bran oil company became conta minated with PCBs andpolychlorinated dibenzofurans, PCDFs. The contaminated oil was sold and f ed t o livestockand humans resulting in t he deat hs of hundreds of thousands of dead birds. This wascalled “Yusho” disease (lite rally 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 associat ed with impaired cognitive developmentand behavioural problems due to gestational exposure among the male children. (Guo et al.2004).

 An ent ire town in the USA was exposed to high levels o f dioxins when cont aminat ed wa st eoil was spread on a dirt road of Times Beach, Missouri, to control dust levels. BecauseTCDD was identified t hat year as a terat ogen, all the properties in Times Beach werebought out by the US EPA for a total of $32 million in 1983, the inhabitants relocated andthe town demolished. Some 265,000 tons of regional soil were incinerated (White andBirnbaum 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. Multiplespecies of birds, fish, reptiles and mammals have exhibited reproductive impairment,immunologic dysfunction, hyperplasia of the thyroid and adrenal glands, porphyria,congenital malf ormation, growth retardat ion amongst ot hers (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 fromhigh consumption of fish from polluted waterways (Wickizer 1981).

The most famous case occurred in Seveso, Italy, when an explosion occurred in 1976 at anItalian chemical plant producing 2,4,5 t richlorophenol, an inte rmediat e in 2,4,5-T synthesis.Because of t he nature of t he uncontrolled react ion that produced t he explosion, not onlyTCDD was released but the levels were far higher than the normal range of 1 ppm and

could have reached 100 ppm. Immediately af ter t he accident, t hose exposed had skinlesions consistent with chlorache. Later studies revealed that TCDD could increase the riskof many cancers, as well as diabetes, adverse cardiovascular ef fect and altered endocrineand 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 t hat t he eff ect of TCDDscan be passed on to the next generation. The sperm count in children exposed in Sevesohas been measured now that they are adults. Those children of an age bef ore pubertyhave shown a much lower sperm count as adults but t hose exposed at an age af ter puberty have higher sperm counts. So the eff ect of TCDDs depends not o nly on thedosage but also on the t iming of exposure.

 PDFmyURL.com

8/13/2019 The Terrible Legacy of Agent Orange and Dioxin

http://slidepdf.com/reader/full/the-terrible-legacy-of-agent-orange-and-dioxin 12/16

In 1981, a PCB dielectric f luid-filled t ransformer caught fire in the basement of theBinghamton Stat e of fice building in the stat e of New York. The f ire deposit ed an oily sootthroughout the 18-storey building with some levels measured as high as 1200 ppm of PCDDs and PCDFs. Millions of do llars were spent in cleaning the building and it was close dup for 13 years (O’Keefe et al. 1985).

 A massive die-of f event in t he Balt ic Sea o f 20,000 harbour seals occurred in 1988. Theunderlying cause of deat h was f ound t o be an infect ion with Phocine dist emper virus.However it is t hought t hat PCB exposure contributed t o t he viral infect ion and deat h due tohigh 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 poisonedwith very high levels of dioxin with a calculated body burden of 1.6 mg of TCDD, the highestlevel ever recorded. It was measured as 144,000 picograms TCDD/gm of blood fa t(Geusau et al. 2001).

In Belgium in 1999, an overwhelming percentage of national livestock were given PCB-contaminated f eed t hat 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 Vikto r 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 inSeptember 2004 with a serum dioxin level of over 6000 times the normal level. He washospitalised with acute pancreatitis, followed by chlorache and oedema, resulting in apockmarked face (Sorg et al . 2009). In 2012, Yushchenko st at ed he is st ill suf fering from theeff ects of dioxin poisoning.

Finally, in 2008, all Irish pork products were removed from supermarkets due to thecontamination of pigs resulting f rom ingestion of dioxin contaminated f eed supplies. Arepeat of the Belgian contamination, 10 years prior (White and Birnbaum 2009).

Nowadays human exposure to TCDDs mainly occurs through oral ingestion of food, whichcontains high levels of the toxins. Milk from cows, fish, which concentrate the dioxins through thecontaminated wat erways, eggs from hens and meat from g razing cows, pigs and chickens aremost affected.

Vietnam today

Vietnam and Laos are still the most af fect ed and devasta ted b y the dumping of 76 million litresof Agent Orange on their countries. Vietnamese women who are pregnant are still ingestingcontaminated eggs from chickens, milk from grazing cows, fish, ducks and snails grown inartificial or natural fish ponds where there are high levels of dioxins in the beds of the ponds andany meat from a nimals, grazing on contaminate d land. Vietnamese peasants a re extremely poor and have litt le option but to eat their own grown food . Even when the baby is born, the breastmilk will be highly contaminated with ingested dioxins and continues to contribute to the horrificbirth deformities.

 PDFmyURL.com

8/13/2019 The Terrible Legacy of Agent Orange and Dioxin

http://slidepdf.com/reader/full/the-terrible-legacy-of-agent-orange-and-dioxin 13/16

 PDFmyURL.com

8/13/2019 The Terrible Legacy of Agent Orange and Dioxin

http://slidepdf.com/reader/full/the-terrible-legacy-of-agent-orange-and-dioxin 14/16

Figure 5: The yellow markings indicate the Ho Chi Minh trail between Vietnam and Laos.

 About 28 of the f ormer US milit ary bases in South Vietnam where the herbicides were st ored andloaded onto airplanes still have high level of dioxins in the soil, posing a health threat to thesurrounding communities. Extensive testing for dioxin contamination has been conducted at theformer US airbases in Da Nang, Phu Cat and Bien Hoa. Some of the soil and sediment on thebases have extremely high levels of dioxin requiring remediation. The Da Nang Airbase has dioxincontamination up to 350 t imes higher than international recommendations for act ion. The $43million joint project with Vietnam is expected to be complet ed by 2016 on t he 19-hectarecontaminated sit e, now an act ive Vietnamese military base near Danang's commercial airport.Some 73,000 cubic metres of soil are to be heated t o a t emperature to break down dioxin.

Washington has been quibbling for years over the need for more scientific research to show thatthe herbicide caused health problems among the Vietnamese people. The US recognises that Agent Orange is the cause of the healt h problems of its own Viet nam ve terans while at the sametime arguing t hat it may not be t he cause of the same problems in Vietnam! The US is planning

to evaluate what's needed f or remediation at the f ormer 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 ref uses to compensate Vietnamese vict ims of chemicalwarfare because t o do so would mean admitt ing t hat t he US committ ed war crimes in Vietnam”,reported the August 17-23, 2012, Vietweek  publication. “This would open the door to lawsuits thatwould cost the government billions of dollars.” This late US promise of aid has been driven by theneed 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 inthe Vietnam War (which they call the American War) to dete ct the t oxic deposits where t hehighest levels of T CDDs are located and all possible aid to clean up the t oxic depositions of dioxin, whate ver that takes.

References

 Aoki Y. (2001) Polychlorinated biphenyls, polychlorinated dibenzo-p-dioxins, and polychlorinateddibenzofurans as endocrine disrupters--what we have learned from Yusho disease. Environ Res.86, 2-11.

Baccarelli A, Mocarelli P, Pat te rson DG, Bonzini M, Pesato ri AC, Caporaso N et al (2002)Immunologic eff ects of dioxin: new results f rom Seveso and compa rison with ot her studies.Environ Health Perspect 110, 1169-73 .

Balzar W, Gaus H-M, Gaus C, Weber R, Schmitt -Biegel B, Urban U. (2007) Remediat ion measuresin a residential area highly contaminated with PCDD/PCDF, arsenic and heavy met als as a result

 PDFmyURL.com

8/13/2019 The Terrible Legacy of Agent Orange and Dioxin

http://slidepdf.com/reader/full/the-terrible-legacy-of-agent-orange-and-dioxin 15/16

of industrial production in the early 19th century. Organohalogen Compounds 69 , 857-60.

Berta zzi PA, Zocchett i C, Guercilena S, Consonni D, Tironi A, Landi MT, et al (1997) Dioxinexposure and cancer risk: a 15-year mortality study af ter the "Seveso accident". Epidemiology 8,646-52.

Bertazzi PA, Consonni D, Bachetti S, Rubagotti M, Baccarelli A, Zocchetti C et al (2002) Healtheff ects of dioxin exposure: a 20 year mortality st udy. Am J Epidemiol 153, 1031-44.

Chobtang J, de Boer IJ, Hoogenbo RL, Haasnoot W, Kijlst ra A, Meerburg BG. (2011) The need andpotential of biosensors to detect dioxins and dioxin-like polychlorinated biphenyls along the milk,eggs and meat f ood chain. Sensors (Basel) 11, 11692-716.

Dragin N, Dalton TP, Miller ML, Shertzer HG, Nebert DW. (2006) For dioxin-induced birth def ect s,mouse or human CYP1A2 in mat ernal liver prot ect s whereas mouse CYP1A1 and CYP1B1 areinconsequential. J Biol Chem 281, 18591–600.

Engel RW, Bell WB. (1953) T he nature of X-disease in catt le. 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. Lawrencebasin. 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 HealthPerspect 109, 865-9.

Guo YL, Lambert GH, Hsu CC, Hsu MM. (2004) Yucheng: Health ef fe cts of prenatal exposure topolychlorinat ed biphenyls and d ibenzofurans. Int Arch Environ Health 77 , 153-8.

Henderson L, Patterson DJ. (1988) Distribution of 2,3,7,8-tetrachlorodibenzo-p-dioxin in humanwhole blood and its association with, and extractability from lipoproteins. Bull Environ ContaminToxicol 40, 604– 611.

Mocarelli P, Gerthoux PM, Pat terson DG, Milani S, Limonta G, Bert ona M et al. (2008) Dioxinexposure, from infancy t hrough puberty, produces endocrine disruption and aff ects humansemen quality. Environ Health Perspect 116, 70-7.

Mueller J, Gaus C, Bundred K, Alberts V, Moore MR, Horsley K. (2001) Co-dist illat ion of TCDD andother POPs during distillation of water: A potential source for exposure. OrganohalogenCompounds 52 , 243–246.

O’Keefe PW, Silkworth JB, Gierthy JF, Smith RM, De Caprio AP, Turner JN et al. (1985)  Chemicaland biological invest igat ions of a transf ormer accident at Binghamt on, NY. Environ HealthPerspect 60, 201-9.

Ott MG, Zober A (1996) Cause specific mortality and cancer incidence among employeesexposed t o 2,3,7,8-T CDD aft er a 1953 react or accident. Occup Environ Med 53, 606-12.

Poiger H, Schlatt er C. (1986) Pharmacokinetics o f 2,3,7,8-TCDD in man. Chemosphere 15, 1489 –94 .

Ross P, De Swart R, Addison R, van Loveren H, Vos J, Ost erhaus A. (1996) Contaminant-inducedimmunotoxicit y in harbour seals: wildlife at risk? Toxicology 112, 157-69.

 PDFmyURL.com

8/13/2019 The Terrible Legacy of Agent Orange and Dioxin

http://slidepdf.com/reader/full/the-terrible-legacy-of-agent-orange-and-dioxin 16/16

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 andmeasurement of TCDD met abolites. Lancet 374 (9696), 1179-85.

Steenland K, Piacitelli L, Deddens J, Fingerhut M, Chang LI. (1999) Cancer, heart disease, anddiabetes 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 overv iew of the ef fect s of dioxins and diox in-like compounds

on vertebrates, as documented in human and ecological epidemiology. J Environ Sci Health Pt CEnviron Carcinog Ecot oxicol Rev 27, 197-211.

Wickizer T M, Brilliant LB, Copeland R, Tilden R. (1981) Polychlorinated biphenyl contamination of 

nursing mothers' milk in Michigan. Am J Public Health 71, 132-7.

 Asi a   environment   US imperialism   Vietnam   Vietnam War 

 Ad d ne w co mme nt

Powered by Drupal  - Design by  Arti ne t

 PDFmyURL.com