Agent Orange was a herbicide or defoliant, which was used in Vietnam to

kill unwanted plant life and to remove leaves from trees which otherwise

provided cover for the enemy. Agent Orange was a mixture of chemicals

containing equal amounts of the two active ingredients, 2,4-D and 2,4,5-T.

The name, Agent Orange,  came from the orange stripe on the 55-gallon

drums in which it was stored. Other herbicides, including Agent White and

Agent Blue, were also used in Vietnam to a much lesser extent.


Why are Vietnam veterans concerned about Agent Orange?


In the 1970 some veterans became concerned that exposure to Agent Orange

might cause delayed health effects. One of the chemicals (2,4,5-T) in

Agent Orange contained minute traces of 2,3,7,8-tetrachlorodibenzo-p-di-oxin

(also known as TCDD or dioxin), which has caused a variety of illnesses

in laboratory animals.  More recent studies have suggested that the chemical

may be related to a number of malignancies and other disorders.


When and where was Agent Orange used in Vietnam?


Fifteen different herbicides were shipped to and used in Vietnam between

January 1962 and September 1971. Agent Orange accounted for over 80 per-cent

of the herbicides sprayed in Vietnam. Agent Orange was used between

January 1965 and April 1970. Herbicides other than Agent Orange were used

in Vietnam prior to 1965, but to a very limited extent. The total area

sprayed with herbicides between 1962 and 1965 was small, less than 7 per-cent

of the total acreage sprayed during the Vietnam conflict. Rapid

increases in the annual number of acres sprayed occurred from 1962 to 1967.

The number of acres sprayed reached a maximum in 1967, leveled off slightly

in 1968 and 1969, and declined rapidly in 1970 prior to the termination of

spraying in 1971. During this time more than 20 million gallons of herbicides

were sprayed over 6 million acres, some of which were sprayed more

than once. More than 3.5 million acres of South Vietnam   approximately 8.5

percent of the country   were sprayed one or more times. Spraying occurred

in all 4 military zones of Vietnam


 After spray Agent Orange, a few days pass, remain as is gaunt branch

 and leaves of grass abandons gone some where.

  After spray Agent Orange and a few days pass, remain as is gaunt branch

 and leaves of grass abandons gone some where.




Dioxin Mean

Name used by the U.S. military for a 50:50 mixture of the herbicides 2,4-D and 2,4,5-T.  

Large quantities were sprayed in Vietnam to defoliate trees that might hide the enemy. Fears that agent orange can cause human illness stem from the presence in it of a contaminant called TCDD (short for 2,3,7,8-tetrachlorodibenzo-p-dioxin). TCDD is only one of a family of substances called dioxins, but it is the one that has gained the greatest notoriety and I shall refer to it here simply as "dioxin". Dioxin is produced as an undesired contaminant during the manufacture of 2,4,5-T. Tests show that it is a potent teratogen for some laboratory animals; that is, exposure of pregnant females to exceedingly small amounts of dioxin causes malformed offspring. Some investigators believe that the rate of birth defects in Vietnamese women was increased in the sprayed areas.

The most clearly established health effect of dioxin in humans is a skin eruption called chloracne. An explosion in a chemical factory in Seveso, Italy in 1976 contaminated the vicinity with dioxin and caused many cases of chloracne.


Many Vietnam veterans believe that exposure to dioxin while they served in Vietnam later caused them to father babies with birth defects. However, careful study of several thousand families in the area of Atlanta, Georgia revealed that the % of babies born with birth defects to fathers who had served in Vietnam (2-3%) was the same as for fathers who had served elsewhere in the military and the same for fathers who had never had military service at all.


A study in 1987 of Vietnam ground troops who served in sprayed areas revealed that they averaged 4 parts per trillion (ppt) of dioxin in their blood. The half-life of dioxin in the body is 6-10 years so assuming that these men got all their dioxin exposure in Vietnam, they would have had some 20 ppt (the maximum permissible amount in U.S. civilians) at that time. But this assumption is certainly false. Dioxins are produced whenever organic matter is burned (backyard barbecues, municipal incinerators, wood-burning stoves). Furthermore, 4 ppt of dioxin was also found in the blood of an otherwise matched group of veterans who did not serve in Vietnam. U.S. civilians with no known exposure to TCDD should not have serum levels of TCDD exceeding 20 ppt. The highest level found in persons living near Seveso was 1,800 ppt.


 The health of Vietnam veterans is still being monitored. Those that were directly involved in the spraying itself (called "Operation Ranch Hand") are now developing diabetes at a significantly higher rate than the oth




Name given any member of a family of closely-related chemicals. The term is often used for one of these: 2,3,7,8-tetrachlorodibenzo-p-dioxin or TCDD. This substance was present as a contaminant in the herbicide agent orange, which was so widely used during the Vietnam war.


When ingested or injected, dioxin is extremely poisonous to laboratory animals. At sub-lethal concentrations, it causes cancer and birth defects in them.


Exposure to high levels of dioxin causes a severe skin disease (chloracne) in humans as well as damage to the liver and nervous system. While the evidence is still hotly debated, the U.S. Environmental Protection Agency (EPA) is now (June 2000) convinced that dioxin causes cancer in humans. They base this conclusion on

extrapolating from dose-response studies done in animals (rats) [Link to discussion of how such estimates are made.

following the health of industrial workers who were exposed to dioxin in the U.S., Germany, and Holland.

Thanks to the development of delicate analytical techniques, it is possible to detect trace amounts in everyone's blood. Most of us have a few parts per trillion (ppt) of TCDD in our serum.


TCDD (and other dioxins) are produced when organic matter is burned. Measurable levels are found in soot from wood-burning stoves and the ash of municipal incinerators. However, the amounts to which we are exposed have dropped some threefold since the mid-80s, and the cancer risk dioxin poses for most of us is probably close to zero.


 Synthetic auxins as weed killers

Some of the most widely-used weed killers are synthetic auxins. These include 2,4-dichlorophenoxy acetic acid (2,4-D) and 2,4,5-trichlorophenoxy acetic acid (2,4,5-


 As the formulas show, 2,4,5-T is 2,4-D with a third chlorine atom, instead of a hydrogen atom, at the #5 position in the benzene ring (blue circles).


2,4-D and its many variants are popular because they are selective herbicides, killing broad-leaved plants but not grasses (no one knows the basis of this selectivity).


Why should a synthetic auxin kill the plant? Auxin (IAA) is actively transported into cells by a transmembrane transporter and leaves the cells by facilitated diffusion through a different transporter. It turns out that the importer works fine for 2,4-D but that 2,4-D cannot leave the cell through the exporter. Perhaps it is the resulting accumulation of 2,4-D within the cell that kills it.


A mixture of 2,4,-D and 2,4,5-T was the "agent orange" used by the U.S. military to defoliate the forest in parts of South Vietnam


Abscisic acid (ABA)


Unlike animals, plants cannot flee from potentially harmful conditions like

drought the approach of winter

They must adapt or die.

The plant hormone abscisic acid (ABA) is the major player in mediating the adaptation of the plant to stress.

Here are a few examples.

1. Bud dormancy

ABA mediates the conversion of the apical meristem into a dormant bud. The newly developing leaves growing above the meristem become converted into stiff bud scales that wrap the meristem closely and will protect it from mechanical damage and drying out during the winter.


ABA in the bud also acts to enforce dormancy so if an unseasonably warm spell occurs before winter is over, the buds will not sprout prematurely. Only after a prolonged period of cold or the lengthening days of spring photoperiodism will bud dormancy be lifted.


2. Seed maturation and dormancy

Seeds are not only important agents of reproduction and dispersal, but they are also essential to the survival of annual and biennial plants. These angiosperms die after flowering and seed formation is complete. ABA plays a role in seed maturation, at least in some species, and also enforces a period of seed dormancy. As we saw for buds, it is important the seeds not germinate prematurely during unseasonably mild conditions prior to the onset of winter or a dry season. ABA in the seed enforces this dormancy. Not until the seed has been exposed to a prolonged cold spell and/or sufficient water to support germination is dormancy lifted.


3. Abscission

ABA also promotes abscission of leaves and fruits (in contrast to auxin, which inhibits abscission). It is, in fact, this action that gave rise to the name abscisic acid.


The dropping of leaves in the autumn is a vital response to the onset of winter when ground water is frozen - and thus cannot support transpiration - and snow load would threaten to break any branches still in leaf.


Most nondeciduous species in cold climates (e.g., pines) have "needles" for leaves. These are very narrow and have a heavy waterproof cuticle. The shape aids in shedding snow, and the cuticle cuts down on water loss.


4. Closing of stomata

Some 90% of the water taken up by a plant is lost in transpiration. Most of this leaves the plant through the pores - called stomata - in the leaf. Each stoma is flanked by a pair of guard cells. When the guard cells are turgid, the stoma is open. When turgor is lost, the stoma closes. Discussion of gas exchange in the leaf.


ABA is the hormone that triggers closing of the stomata when soil water is insufficient to keep up with transpiration.


The mechanism:

ABA binds to receptors at the surface of the plasma membrane of the guard cells.

The receptors activate several interconecting pathways which converge to produce

a rise in pH in the cytosol

transfer of Ca2+ from the vacuole to the cytosol

The increased Ca2+ in the cytosol blocks the uptake of K+ into the guard cell while

the increased pH stimulates the loss of Cl- and organic ions (e.g., malate2-) from the cell.

The loss of these solutes in the cytosol reduces the osmotic pressure of the cell and thus turgor.


     Corn fields, representing a fundamental staple of the peasant         economy, have been completely destroyed by fumigation. 

           Corn withers and dies within 8 days of being fumigated




 Basic staples and alternative cash crops such as banana and papaya may be       fumigated even in areas where there is no nearby coca.