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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
manuf act ured by Monsant o Corporat ion and Dow Chemicals t o use as a herbicide and def oliant
in t he Viet nam War. Agent Orange is t he combinat ion of t he code names f or Herbicide Orange
(HO) and Agent LNX.
At t he f amous Bat t le of Dien Bien Phu, Nort h Viet namese General Giap and t he Viet Minh f orces
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At t he f amous Bat t le of Dien Bien Phu, Nort h Viet namese General Giap and t he Viet Minh f orces
t ot ally def eat ed t he French army on May 7, 1954, and t he French garrison surrendered. At t he
1954 Geneva Conf erence, t he French negot iat ed a ceasef ire agreement wit h t he Viet Minh, and
it s leader Ho Chi Minh, and independence was grant ed t o Cambodia, Laos and Viet nam.
Under t he agreement , Viet nam was t emporarily part it ioned at t he 17t h parallel and divided int o
Nort h Viet nam under t he government of Ho Chi Minh and Sout h Viet nam under t he Cat holic
emperor Bao Dai. Elect ions were t o be held t hroughout Viet nam in July 1956 t o unif y Viet nam.
The US government didnt agree wit h t he Geneva Accords and, realising t hat Ho Chi Minh would
easily win t he elect ions, decided t o abort t he process and appoint ed t heir puppet Ngo Dinh Diem
as president of Sout h Viet nam in a f raudulent 1955 plebiscit e. So began t he 20-year-long war
wit h t he USA.
The Viet Minh, known as t he Viet cong in t he West , built a t rail, running f rom Nort h Viet nam t o
Sout h Viet nam t o supply t he Nat ional Front f or t he Liberat ion of Sout h Viet nam wit h armament s
and logist ics. The t rail, most ly in Laos but also crossing int o part s of Cambodia, was called t he
Ho Chi Minh t rail by t he Yanks. According t o t he US Nat ional Securit y Agency, t he t rail was one of
t he great est achievement s of milit ary engineering of t he 20t h cent ury. Part s of what became
t he t rail had exist ed f or cent uries as f oot pat hs, which f acilit at ed t rade in t he region. The area
t hrough which t he syst em meandered was among t he most dif f icult in Sout h-East Asia: a
sparsely populat ed region of rugged mount ains (15008000 f eet ), t riple-canopy jungle and
dense primeval rainf orest s.
To st op t he supply of weapons and nat ional liberat ion f ight ers, t he US milit ary decided on a
st rat egy based on chemical warf are, t o expose t he t rail and dense f orest by dropping millions of
t onnes of herbicides in t he area and t hereby f orce t he Viet Minh int o t he open. At f irst , US
soldiers at t empt ed t o blow up rice paddies and rice st ocks, using hand grenades. But grains of
rice were f ar more durable, and were not easily dest royed. Every grain t hat survived was a seed,
t o be collect ed and plant ed again. So t he US Army went t o an opt ion t hat would kill of f t he
paddies: st raight out chemical warf are. Anot her goal was t o induce t he peasant s t o f lee t o urban
cent res, cont rolled by t he US and Sout h Viet namese army, by dest roying t he abilit y of peasant s
t o support t hemselves in t he count ryside, and depriving t he guerrillas of t heir rural support and
f ood supply. The chemical warf are was called Operat ion Ranch Hand and was operat ed f rom
1961 t o 1971. The f irst aerial spraying was ordered by US President John F. Kennedy.
The chemicals
The hist ory of Agent Orange began in 1943 when bot anist Art hur Galst on began st udying a
growt h plant hormone, a t ri-iodobenzoic acid (benzene wit h t hree iodine at oms at t ached t o t he
benzene ring) in an at t empt t o f orce soya beans t o grow f ast er. Galst on f ound t hat excessive
use of t he compound caused cat ast rophic def oliat ion. Galst on was especially concerned about
t he compound's side ef f ect s bot h t o humans and t he environment .
However t here is an earlier hist ory, which is rarely t old. 2,4 dichlorophenoxyacet ic acid, known as
2,4-D was act ually co-discovered independent ly in bot h t he US and t he UK in 1941. The t wo
t eams involved were Templeman and Colleagues at ICI (USA) and Nut man and Collaborat ors at
Rot hamst ed Experiment al St at ion in England. In bot h cases t he researchers were part of a
clandest ine wart ime ef f ort by t heir government s t o creat e chemical warf are agent s f or use in
WWII. The new chemical's abilit y t o kill weeds was ent irely accident al and not t he aim of t he
research in eit her count ry. Due t o int ernat ional legal reasons, research of t his sort was never
done openly. Research, product ion and use of chemical warf are agent s were illegal act ions under
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t he Geneva Convent ion and many ot her int ernat ional t reat ies signed by bot h t he USA and t he
UK. This meant t hat a plausible cover st ory was needed t o hide t he act ual nat ure of any
chemical warf are research. For bot h t he Allies and t he Nazis, t he civilian label of agricult ural
research was of t en used t o conceal illegal and/or secret chemical warf are research.
In 1943, t he US Depart ment of t he Army cont ract ed t he Universit y of Chicago t o st udy t he
ef f ect s of 2,4 dichlorophenoxyacet ic acid, known as 2,4-D, and 2,4,5-t richlorophenoxyacet ic acid
(2,4,5-T) on cereal grains (including rice) and broadleaf crops (Figure 2). From t hese st udies,
arose t he concept of using aerial applicat ions of herbicides t o dest roy enemy crops t o disrupt
t he f ood supply. In early 1945, t he US army ran t est s of various 2,4-D and 2,4,5-T mixt ures at t he
Bushnell Army Airf ield in Florida. So t he US army was well aware of dioxins dest ruct ive capacit y
on f oliage.
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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 it self
has low t oxicit y. However, t he manuf act uring process f or 2,4,5-T cont aminat es t his chemical wit h
signif icant amount s of 2,3,7,8-t et rachlorodibenzo-p-dioxin (TCDD) or of t en simply called dioxin. (I
use TCDD and dioxin int erchangeably). TCDD causes cancer and is a long-t erm persist ent
cont aminant in t he environment , wit h horrendous consequences f or humans (Figure 3). It is
TCDD, which is t he cause of most of t he severe healt h problems f or t he Viet namese people, t he
US, Aust ralian Viet nam vet erans and ot her allied personnel including f rom Sout h Korea and t he
Philippines, who were exposed t o Agent Orange and t hus TCDD f rom 1961-1971. TCDD has
been described as perhaps t he most t oxic molecule ever synt hesised by humans. The ot her
chemicals used in t he Viet nam War will also cause some diseases but it is dioxin t hat is t he most
let hal. Agent Orange is not t he same as dioxin but nevert heless cont ained very high
concent rat ions of dioxin. Int ernal memoranda revealed t hat Monsant o (t he manuf act urer of
2,4,5-T) had inf ormed t he US government in 1952 t hat it s 2,4,5-T was cont aminat ed wit h dioxin.
Figure 3: Figure 3: Chemical structure of 2,3,7,8 tetrachlorodibenzo-p-dioxin or TCDD.
In t he manuf act ure of 2,4,5-T, accident al overheat ing of t he react ion mixt ure easily causes t he
product t o condense int o t he t oxic product as a side react ion f orming TCDD. Wit h proper
t emperat ure cont rol during product ion of 2,4,5-T, TCDD levels can be held t o about 0.005 ppm
(part s per million). Bef ore t he TCDD risk was well underst ood, early product ion f acilit ies at
Monsant o lacked proper t emperat ure cont rols and individual bat ches t est ed lat er were f ound t o
have as much as 60 ppm of TCDD or 12,000 t imes more concent rat ed wit h respect t o TCDD
(ht t p://en.wikipedia.org/wiki/2,4,5-T). The 2008 US Viet nam report t heref ore proposed 366 kg of
TCDD as a plausible est imat e of t he t ot al amount of TCDD applied in Viet nam during 1961
1971.
In 1970, t he Unit ed St at es Depart ment of Agricult ure halt ed t he use of 2,4,5-T on all f ood crops
except rice, and in 1985 t he US Environment al prot ect ion Agency (EPA) t erminat ed all remaining
uses in t he US of t his herbicide. The int ernat ional t rade in 2,4,5-T is rest rict ed by t he Rot t erdam
Convent ion.
Unit ed St at es Air Force records show t hat at least 6542 spraying missions t ook place over t he
course of Operat ion Ranch Hand (Figure 4). By 1971, 12 % of t he t ot al area of Sout h Viet nam
had been sprayed wit h def oliat ing chemicals, at an average concent rat ion of 13 t imes t he
recommended USDA applicat ion rat e f or domest ic use.

In Sout h Viet nam alone, an est imat ed 10
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million hect ares, of agricult ural land was ult imat ely dest royed. In some areas TCDD
concent rat ions in soil and wat er were hundreds of t imes great er t han t he levels considered
"saf e" by t he US EPA. Overall, more t han 20% of Sout h Viet nam's f orest s were sprayed at least
once over a nine-year period.
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S y n d i c a t e
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Figure 4: Extent of aerial spraying of South Vietnam with Agent Orange.
The Viet namese government est imat es 5 million people were killed wit h hundreds of t housands
st ill missing and 500,000 children born wit h birt h def ect s as a result of it s use. There are also
est imat es t hat up t o 5 million Viet namese are st ill exposed direct ly t o Agent Orange. The Red
Cross of Viet nam est imat es t hat up t o 1 million people are disabled or have healt h problems due
t o Agent Orange.
Exposure to TCDD (dioxin)
There are t wo dif f erent healt h ef f ect s t hat must be considered when dealing wit h dioxin. One is
t he ef f ect of direct exposure t o t he individual and t he second is t he ef f ect s on t he germline of
t he individual, bot h mat ernal and pat ernal. The lat t er is f ar worse as it signif ies t here is a
permanent ef f ect on t he human genome and all f ut ure generat ions. This is one of t he horrif ic
legacies of dioxin, only now being underst ood. (It will be dealt wit h in a lat er art icle).
TCDD is absorbed int o t he body rapidly, but is eliminat ed slowly. Exposure of humans t o TCDD is
t hought t o occur primarily via t he mout h, skin and lungs. Dioxins will ent er t he f ood chain mainly by
oral ingest ion of cont aminat ed subst ances, t hrough t he wat er, veget at ion and soil. So where
animals are allowed t o graze, roam or scavenge in out side areas, t he animals have a great er
chance of becoming exposed t o dioxins f rom t he environment and ingest ing t he poison. This is
quit e unint uit ive as f ree-range chickens, and f ree-roaming cat t le are t hought t o be f ree of
chemicals, suf f ering much less t rauma, in t he public mind.
The magnit ude of cont aminat ion will depend on t he f requency of exposure t o t he animals and
t he levels of cont aminant s. St udies have shown t hat roughage in general cont ain higher levels of
dioxins t han commercial compound f eed, at least in West ern count ries. In addit ion, it should be
not ed t hat climat e change will inf luence t he spread of dioxins int o agricult ural environment .
Due t o f looding, cont aminat ed sediment could be t ransport ed t o areas t hat were previously
clean (Chobt ang et al .2011). Thus dioxins will accumulat e in meat and meat product s, including
sheep, poult ry and pigs. Milk and milk product s, hen eggs and egg product s are usually t he
source of ingest ed dioxin. Cont aminat ion of t he rivers and wat er supply as happened in Viet nam
will of course result in accumulat ion in all f ish product s.
Dioxins are f at soluble and virt ually insoluble in wat er. A st udy perf ormed in a 42-year-old man
f ound t hat 87% of t he oral dose was absorbed. Dioxins are virt ually permanent ly in t he
environment once f ormed, as it is a very st able molecule and very dif f icult t o break down. The
half -lif e of dioxin in humans is over 10 years, depending on t he age, sex and exposure
concent rat ion, i.e., it t akes 10 years t o remove 50% of t he dioxin in t he body, once it is absorbed
(Sorg et al . 2009). Dioxins accumulat e in t he lipids, especially t he liver and f at deposit s of
humans. Af t er ingest ion, TCDD associat es primarily wit h t he lipoprot ein f ract ion of t he blood and
lat er part it ions int o t he cellular membranes and t issues (Henderson and Pat t erson 1988). TCDD
is dist ribut ed t o all compart ment s of t he body; t he amount s dif f er f rom organ t o organ, but most
st udies indicat e t hat t he primary disposit ion of TCDD is in t he liver and adipose t issues.
In a human volunt eer, it was f ound t hat at 135 days af t er ingest ion, 90% of TCDD was in f at
(Poiger and Schlat t er 1986). Direct binding of TCDD t o CYP1A2, t he enzyme t hat can break it
down t o a limit ed ext ent , is t hought t o result in sequest rat ion of TCDD in t he liver and t o inhibit
it s dist ribut ion t o ot her t issues. This is a react ion of t he body t o t ry and prot ect t he f et us against
TCDD-induced t erat ogenesis (Dragin et al . 2006).
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Dioxin undergoes virt ually no met abolism. Animals have evolved t o eliminat e most t oxins by t he
development of enzymes in t he liver t hat det oxif y a specif ic t oxin. Because dioxins are not f ound
in nat ure, animals have not developed enzymes t o det oxif y t his group of chemicals. Very small
amount s of dioxin are slowly excret ed t hroughurine and f aeces so t hat t he remaining ingest ed
dioxin remains in t he body f or decades. Faeces has been f ound t o be t he main rout e of
eliminat ion, wit h 60% of t he TCDD eliminat ed unchanged, wit h t he rest being minor amount s of
hydroxylat ed dioxins.
Finally, t he eliminat ion rat e of TCDD, in part icular af t er low exposures, depends heavily on t he
amount of adipose t issue mass in t he body. Relat ively high exposures of TCDD af f ect a variet y
of organs and result in organ dysf unct ion and deat h. The specif ic organ dysf unct ion t hat
const it ut es t he let hal event , however, is not known. A charact erist ic of TCDD exposure is a
wast ing syndrome wit h loss of adipose and muscle t issues and severe weight loss. A major
source of human exposure is t hrough breast milk, as t he dioxin load in t he body is mobilised and
excret ed t hrough breast milk. As a consequence of t he environment al ubiquit y of dioxins, all
humans have acquired some exposure t o dioxins and t his load is slowly increasing even now
(Whit e and Birnbaum 2009).
Health reports f rom the Australian Department of Veteran Af f airs
There were 60,000 Aust ralian personnel involved in t he Viet nam War, f rom 1962 t o 1973, of which
500 were killed in act ion and 3100 severely physically wounded. The Aust ralian government
commissioned several report s on t he healt h of Viet nam vet erans. The f irst was complet ed in
1984, called t he Aust ralian Vet erans Healt h St udy or AVH. A second st udy, called t he Viet nam
Vet erans Mort alit y st udy was complet ed in 1997. The Aust ralian Depart ment of Vet erans Af f airs
released a report in 2002 and concluded t hat t he list of cancers t hat could have been caused by
exposure t o TCDD were as list ed in Table 1. However t he st at us of t his report is not clear as it
st at es t hat some of t hese cancers are associat ed wit h smoking and alcohol, which was not
t aken int o account when est imat ing cancer incidence. The scient if ic report , mainly based on
mort alit y rat es of Viet nam vet erans compared wit h t he civilian Aust ralian populat ion, was t hen
sent t o t he Repat riat ion Commission and t he f inal report given t o t he minist er of vet eran af f airs
Danna Vale in 2002 (in Liberal Part y Prime Minist er John Howards government ). The report can
be locat ed at
ht t p://www.dva.gov.au/about DVA/publicat ions/healt h_research/viet nam_vet s/vvdr/Document s/Dapsone_Report _Appendices.pdf .

Table 1. Diseases associated with exposure to TCDD, estimated by
the Australian Army
Specif ic condit ions showing st at ist ically signif icant increased risk
associat ed wit h Viet nam service in t he Aust ralian st udies are:
All cause mort alit y (t ot al number of deat hs relat ive t o t he t ot al
populat ion)
Mort alit y f rom all neoplasms (cancers)
Mort alit y f rom lung, prost at e, t ongue, and ot her digest ive organ cancers
Mort alit y and morbidit y f rom cirrhosis of t he liver
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Mort alit y f rom ischaemic heart disease
Suicide
Brain t umours
Mot or neurone disease
Non-Hodgkins lymphoma

The Aust ralian Navy was f ound t o have t he highest mort alit y, even t hough personnel may not
have spent much t ime on land. There is no explanat ion f or t his in t he Aust ralian report . However
t his can be underst ood by t he f act t hat navy vessels collect ed drinking wat er as close t o shore
as possible t o minimise salt cont ent . This wat er was t hen dist illed, wit hout t he realisat ion t hat
dioxin would co-dist il wit h t he st eam.
An Aust ralian research st udy f ocused on t he evaporat ive dist illat ion process t hat was used t o
produce pot able wat er on board ship f rom surrounding est uarine wat ers. Vessels wit h such
dist illat ion processes t hat t raveled near land or even at some dist ance f rom river delt as would
periodically collect wat er t hat cont ained dioxin. The st udy f ound t hat co-dist illat ion of dioxins
was observable in all experiment s conduct ed and t hat dist illat ion increased t he concent rat ion of
dioxins in t he dist illat e compared wit h t he concent rat ion in t he source wat er (Mueller et al . 2001).
On t he basis of t hat st udy and ot her evidence, t he Aust ralian Depart ment of Vet erans Af f airs
det ermined t hat Royal Aust ralian Navy personnel, who served of f shore, were exposed t o dioxins.
These experiment s were repeat ed by t he US scient ist s and t hese f indings were conf irmed.
Cont aminant s wit h low wat er solubilit y would evaporat e f rom wat er and t hat t he dist illat ion
process would enhance t he process by adding heat and reducing t he pressure. No
measurement s of dioxin concent rat ions in sea wat er were collect ed during t he Viet nam conf lict ,
so it is not possible t o ascert ain t he ext ent t o which drinking wat er on Aust ralian vessels may
have been cont aminat ed t hrough dist illat ion processes. Thus, t he US 2008 report st at ed t hat a
presumpt ion of exposure of milit ary personnel serving on t hose vessels is not unreasonable. This
result is not recorded in t he 2010 US VAO updat e.
There is anot her worrying Aust ralian connect ion, report ed by Aust ralian Greens part y senat or Lee
Rhiannon. Jean Williams, a researcher who received t he Order of Aust ralia medal f or her research
on t he ef f ect s of chemicals on Aust ralian war vet erans, f ound t hat cancer rat es in Innisf ail,
Queensland, were 10 t imes higher t han t he st at e average. This was linked t o secret t est ing of
Agent Orange by Aust ralian milit ary scient ist s during t he Viet nam War. Williams based her
allegat ions on Aust ralian government report s f ound in t he Aust ralian War Memorial museum
archives. A f ormer soldier, Ted Boswort h, backed up t he claims, saying t hat he had been involved
in t he secret t est ing. The Queensland healt h depart ment claimed t hat cancer rat es in Innisf ail
were not higher t han t hose in ot her part s of t he st at e. This denial is similar t o t hat of t he US and
Aust ralian government s when lobbied t o t ake responsibilit y f or t he damage and deat hs caused
by Agent Orange (ht t p://lee-rhiannon.greensmps.org.au/cont ent /speeches/speech-agent -orange).
There is evidence t hat Agent Orange was used t hroughout t he Kimberley region in West ern
Aust ralia f rom t he 1970s unt il as lat e as t he 1980s, using many Aboriginal workers employed by
t he Aboriginal Prot ect ion Board (a misnomer). Many of t hose who were working became sick wit h
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nausea and vomit ing. Some 90 men who were st ill alive say t hat of t he 300 who were spraying,
t hey are aware of about 40 deat hs, many of whom were in t heir 30s when t hey died. Aboriginal
woman Lucy Marshall has been t rying f or decades t o obt ain compensat ion f or t he deat h of her
son Cyril Hunt er at 33 years of age as well as a younger son who died of cancer possibly f rom
t he cont aminat ed chemicals, brought home by Hunt er. No saf et y equipment was handed t o t he
men, as t hey were t old t he spray was drinkable. Anot her Aboriginal worker went blind. One of t he
workers, Carl Drysdale, remembered t hat t he drums, which came f rom Singapore redirect ed f rom
Viet nam, were labelled 2,4,5-T, which most cert ainly would have had dioxin as a cont aminant . A
2003 government inquiry recommended t hat 27 workers st ill alive be compensat ed but not hing
has happened. The empt y 2,4,5-T drums remain in t he Derby t ip (ht t p://t hest ringer.com.au/agent -
orange-used-as-a-herbicide-t hroughout -t he-kimberley/ - .UaRc4iv8_bo).
History of poisonings by dioxins
There is a hist ory of accident al poisoning by dioxins in bot h animals and humans in many places
in t he world and t he precaut ions t aken by government s t o cover t his up or underplay it s
signif icance. It should be not ed t hat alt hough some of t he poisoning event s ref er t o
Polychlorinat ed Biphenyls, a close relat ive of dioxin, t hese would also cont ain small amount s of
TCDDs or dioxins (Whit e and Birnbaum 2009).
The earliest evidence of a human-made dioxin molecule comes f rom a German chemical
product ion plant in Lampert heim in Sout h Hesse t hat was making sodium carbonat e
(washing soda or soda ash) and in t he process generat ed dioxin in 1827. It was not unt il
1980s when a playground and school int ended f or children was t o be built on t he sit e where
t he plant had st ood t hat t he ext ensive dioxin cont aminat ion of t he soil was discovered
(Balzar et al . 2007).
In 1947, X-disease was f irst report ed in cat t le. It caused a hyperkerat ot ic condit ion akin t o
chloracne wit h a t hickening of t he st rat um corneum, of t en associat ed wit h a qualit at ive
abnormalit y of t he kerat in. It was lat er shown t o have arisen due t o exposure t o dioxin-like
compounds. It could accumulat e and f inally cause deat h in t he animals (Engel and Bell
1953).
An explosion in a Monsant o chemical plant in Nit ro, West Virginia, result ed in t he exposure
of workers t o 2,4,5-T cont aminat ed wit h dioxin in 1949. Persist ent chlorache was observed
in t he exposed workers. Lat er st udies demonst rat ed an increase in all cancers combined, in
t he most highly exposed workers (Suskind and Hert zberg 1984; St eenland et al. 1999).
On November 17, 1953, an uncont rolled decomposit ion react ion occurred in a
t richlorophenol (TCP) product ion unit owned by BASF AG and locat ed in Ludwigshaf en,
Germany. Byproduct s t hat escaped f rom t he damaged aut oclave cont aminat ed surf aces
t hroughout t he immediat e work area of t he enclosed product ion building. Wit hin days,
workers who were engaged in clean-up ef f ort s developed severe acne as well as ot her
signs and sympt oms, and some were t aken int o hospit al. The agent most likely t o have
caused t hese responses was not ident if ied unt il 1957 when high TCDD levels were f ound in
t he blood lipids. Employees were exposed t o residues cont aminat ed wit h TCDD during t he
clean-up and repair act ivit ies t hat last ed f or about f our t o f ive mont hs, during incident al
maint enance work in t he building af t er complet ion of t he rest orat ion work, and f inally during
demolit ion of t he react or port ion of t he building in 1968-69. Some 30 years lat er TCDD
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could st ill be det ect ed in t he survivors. Workers died f rom lung cancer, st omach cancer, liver
cancer and cardiovascular disease (Ot t and Zober 1996)
The deat h of huge numbers of commercially raised chickens in t he US occurred, named
chick oedema disease in 1957 and was lat er f ound t o be caused by cont aminat ion of f eed
supplies by TCDD (Firest one 1973).
In 1968 in Kyushu, Japan, a rice bran oil company became cont aminat ed wit h PCBs and
polychlorinat ed dibenzof urans, PCDFs. The cont aminat ed oil was sold and f ed t o livest ock
and humans result ing in t he deat hs of hundreds of t housands of dead birds. This was
called Yusho disease (lit erally meaning oil) (Aoki 2001).
This was repeat ed in Taiwan in 1979 but was ref erred t o as Yucheng (again meaning oil)
disease. This episode was more clearly associat ed wit h impaired cognit ive development
and behavioural problems due t o gest at ional exposure among t he male children. (Guo et al.
2004).
An ent ire t own in t he USA was exposed t o high levels of dioxins when cont aminat ed wast e
oil was spread on a dirt road of Times Beach, Missouri, t o cont rol dust levels. Because
TCDD was ident if ied t hat year as a t erat ogen, all t he propert ies in Times Beach were
bought out by t he US EPA f or a t ot al of $32 million in 1983, t he inhabit ant s relocat ed and
t he t own demolished. Some 265,000 t ons of regional soil were incinerat ed (Whit e and
Birnbaum 2009).
The Great Lakes region of US and Canada saw t he great ly diminished reproduct ion among
t rout and mink, which has persist ed t o t his day, due t o dioxin cont aminat ion. Mult iple
species of birds, f ish, rept iles and mammals have exhibit ed reproduct ive impairment ,
immunologic dysf unct ion, hyperplasia of t he t hyroid and adrenal glands, porphyria,
congenit al malf ormat ion, growt h ret ardat ion amongst ot hers (Fox, 2001).
In t he lat e 1970s, nursing mot hers across Michigan had t heir breast milk assessed f or
cont aminat ion and levels of PCBs were f ound t o be as high as 5100 ppm, result ing f rom
high consumpt ion of f ish f rom pollut ed wat erways (Wickizer 1981).
The most f amous case occurred in Seveso, It aly, when an explosion occurred in 1976 at an
It alian chemical plant producing 2,4,5 t richlorophenol, an int ermediat e in 2,4,5-T synt hesis.
Because of t he nat ure of t he uncont rolled react ion t hat produced t he explosion, not only
TCDD was released but t he levels were f ar higher t han t he normal range of 1 ppm and
could have reached 100 ppm. Immediat ely af t er t he accident , t hose exposed had skin
lesions consist ent wit h chlorache. Lat er st udies revealed t hat TCDD could increase t he risk
of many cancers, as well as diabet es, adverse cardiovascular ef f ect and alt ered endocrine
and immune f unct ion and early deat h (Bert azzi et al. 1997; Bert azzi et al. 2002; Baccarelli et
al. 2002; Mocarelli et al. 2008). It is t his case t hat has indicat ed t hat t he ef f ect of TCDDs
can be passed on t o t he next generat ion. The sperm count in children exposed in Seveso
has been measured now t hat t hey are adult s. Those children of an age bef ore pubert y
have shown a much lower sperm count as adult s but t hose exposed at an age af t er
pubert y have higher sperm count s. So t he ef f ect of TCDDs depends not only on t he
dosage but also on t he t iming of exposure.
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In 1981, a PCB dielect ric f luid-f illed t ransf ormer caught f ire in t he basement of t he
Binghamt on St at e of f ice building in t he st at e of New York. The f ire deposit ed an oily soot
t hroughout t he 18-st orey building wit h some levels measured as high as 1200 ppm of
PCDDs and PCDFs. Millions of dollars were spent in cleaning t he building and it was closed
up f or 13 years (OKeef e et al. 1985).
A massive die-of f event in t he Balt ic Sea of 20,000 harbour seals occurred in 1988. The
underlying cause of deat h was f ound t o be an inf ect ion wit h Phocine dist emper virus.
However it is t hought t hat PCB exposure cont ribut ed t o t he viral inf ect ion and deat h due t o
high levels of PCBs in t he f ish eat en by t he seals. PCBs and PCDD are known
immunosuppressant s (Ross et al. 1996).
In Vienna in 1997, f ive people working as secret aries in a t ext ile inst it ut e were poisoned
wit h very high levels of dioxin wit h a calculat ed body burden of 1.6 mg of TCDD, t he highest
level ever recorded. It was measured as 144,000 picograms TCDD/gm of blood f at
(Geusau et al. 2001).
In Belgium in 1999, an overwhelming percent age of nat ional livest ock were given PCB-
cont aminat ed f eed t hat result ed in an int ernat ional recall of all product s cont aining meat or
dairy f rom t he af f ect ed animal, even including Belgian chocolat e. However it is not clear
how t he chocolat e was cont aminat ed (Whit e and Birnbaum 2009).
Some people would remember t he dioxin poisoning of Vikt or Yushchenko in 2004.
Yushchenko was t he candidat e and lat er president of t he Ukraine f rom 2005-10. He was
int ent ionally poisoned t o weaken his polit ical inf luence and t o remove him as a candidat e in
Sept ember 2004 wit h a serum dioxin level of over 6000 t imes t he normal level. He was
hospit alised wit h acut e pancreat it is, f ollowed by chlorache and oedema, result ing in a
pockmarked f ace (Sorg et al . 2009). In 2012, Yushchenko st at ed he is st ill suf f ering f rom t he
ef f ect s of dioxin poisoning.
Finally, in 2008, all Irish pork product s were removed f rom supermarket s due t o t he
cont aminat ion of pigs result ing f rom ingest ion of dioxin cont aminat ed f eed supplies. A
repeat of t he Belgian cont aminat ion, 10 years prior (Whit e and Birnbaum 2009).
Nowadays human exposure t o TCDDs mainly occurs t hrough oral ingest ion of f ood, which
cont ains high levels of t he t oxins. Milk f rom cows, f ish, which concent rat e t he dioxins t hrough t he
cont aminat ed wat erways, eggs f rom hens and meat f rom grazing cows, pigs and chickens are
most af f ect ed.
Vietnam today
Viet nam and Laos are st ill t he most af f ect ed and devast at ed by t he dumping of 76 million lit res
of Agent Orange on t heir count ries. Viet namese women who are pregnant are st ill ingest ing
cont aminat ed eggs f rom chickens, milk f rom grazing cows, f ish, ducks and snails grown in
art if icial or nat ural f ish ponds where t here are high levels of dioxins in t he beds of t he ponds and
any meat f rom animals, grazing on cont aminat ed land. Viet namese peasant s are ext remely poor
and have lit t le opt ion but t o eat t heir own grown f ood. Even when t he baby is born, t he breast
milk will be highly cont aminat ed wit h ingest ed dioxins and cont inues t o cont ribut e t o t he horrif ic
birt h def ormit ies.
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Figure 5: The yellow markings indicate the Ho Chi Minh trail between Vietnam and Laos.
About 28 of t he f ormer US milit ary bases in Sout h Viet nam where t he herbicides were st ored and
loaded ont o airplanes st ill have high level of dioxins in t he soil, posing a healt h t hreat t o t he
surrounding communit ies. Ext ensive t est ing f or dioxin cont aminat ion has been conduct ed at t he
f ormer US airbases in Da Nang, Phu Cat and Bien Hoa. Some of t he soil and sediment on t he
bases have ext remely high levels of dioxin requiring remediat ion. The Da Nang Airbase has dioxin
cont aminat ion up t o 350 t imes higher t han int ernat ional recommendat ions f or act ion. The $43
million joint project wit h Viet nam is expect ed t o be complet ed by 2016 on t he 19-hect are
cont aminat ed sit e, now an act ive Viet namese milit ary base near Danang's commercial airport .
Some 73,000 cubic met res of soil are t o be heat ed t o a t emperat ure t o break down dioxin.
Washingt on has been quibbling f or years over t he need f or more scient if ic research t o show t hat
t he herbicide caused healt h problems among t he Viet namese people. The US recognises t hat
Agent Orange is t he cause of t he healt h problems of it s own Viet nam vet erans while at t he same
t ime arguing t hat it may not be t he cause of t he same problems in Viet nam! The US is planning
t o evaluat e what 's needed f or remediat ion at t he f ormer Bien Hoa air base in sout hern Viet nam,
anot her Agent Orange hot spot .
However t he clean-up in Da Nang does not ref lect a change in US policy on Agent Orange.
Nevert heless, t he US government ref uses t o compensat e Viet namese vict ims of chemical
warf are because t o do so would mean admit t ing t hat t he US commit t ed war crimes in Viet nam,
report ed t he August 17-23, 2012, Vietweek publicat ion. This would open t he door t o lawsuit s t hat
would cost t he government billions of dollars. This lat e US promise of aid has been driven by t he
need f or t he US t o count er t he inf luence of China in t he region.
Viet nam must be given f inancial and t echnical support by all t he allied government s who f ought in
t he Viet nam War (which t hey call t he American War) t o det ect t he t oxic deposit s where t he
highest levels of TCDDs are locat ed and all possible aid t o clean up t he t oxic deposit ions of
dioxin, what ever t hat t akes.
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Asi a envi ronment US i mperi al i sm Vi etnam Vi etnam War
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