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Aromatic Carboxylic Acids
Phenoxyacetic Acids
History of 2,4-D
| General Information
| Chemistry
Metabolism in Plants | Environmental
Fate | Injury Symptomology
Advanced Topics
History of 2,4-D
It is hard for us at the end of this century to put ourselves in the position farmers were
in in the middle part of this century, especially before WWII. Individual farm size was
inherently limited, largely due to the ability of a grower to control weeds without
herbicides.
The War Years.
2,4-D (and 2,4,5-T) was first synthesized in 1940, and first proposed as a herbicide in
1941. Soon thereafter all research on 2,4-D was classified TOP SECRET by the US military
and its development was slowed. A secret Biological Warfare research unit was established
at Camp Detrick, Frederick, Maryland. All research there was kept secret until after WWII
was over, at which time its research was published.
Ms. J.W. Mitchell, a researcher in the USDA in Beltsville, Maryland in 1944, just before
the end of WWII. She is credited with being the first one to test 2,4-D on dandelions in a
turfgrass and discover its selective properties (dead dandelion, alive turf grasses) in
the field. The mother of chemical weed control tactics.
After WWII, commercialization of 2,4-D as a selective herbicide proceeded rapidly and soon
broadleaf weeds were being killed in agricultural fields across the country. The first
great weed population shift from broadleaves to grasses was underway.
General information
2,4-D: Many 1st's:
As indicated earlier, 2,4-D was the first selective herbicide. 2,4-D also was a first for
several other qualities. It was the first growth-regulator type herbicide with hormone
(auxin) like activity. It was the first low rate (1 kg ai/ha or less), high specific
activity, herbicide for agriculture.
It is hard to appreciate the impact that 2,4-D had on agriculture when it was first
introduced. Suddenly, it was possible to control dicot weed species in cereal and maize
crops easily, quickly and inexpensively. No more tillage! It also had the profound impact
of showing the chemical industry a totally new market. The path was open if more
herbicides could be discovered.
2,4-D is used primarily as a postemergence chemical: applied to foliage of emerged plants.
Although it is rapidly degraded in the soil, it is used as a soil-applied herbicide in
some situations. I saw this practice used in soybeans as a soil treatment about 2 weeks
before planting soybeans in Manchuria, northern China, in 1982.
Chemistry
Amine and Ester Formulations:
2,4-D is commercially available in many formulations. They are marketed with different
solubilities in water, and different volatilities, depending on how they will be used.
Formulations include 2,4-D in acid, amine, salt and ester chemical forms.
The acid formulation has important chemical properties needed for most agricultural uses.
Acid forms are ionic, polar, water soluable, insoluable in oils and nonvolatile. These
properties make it ideal for agricultural use which requires low drift to adjacent,
susceptible, crops like soybeans. Acids forms are readily root absorbed, as less readily
absorbed by foliage. For this reason they are not quite as effective as ester forms for
weed control.
The ester formulation is used more frequently for brush control, and for harder to kill
plant species. It usually takes a lower rate of the ester form to kill a plant than with
the acid forms. Ester forms are nonionic, nonpolar, lipid soluable, relatively insoluable
in water and volatile. They are more readily absorbed by plant foliage than by roots and
penetrate leaf cuticles more easily than salt forms. Ester forms of 2,4-D are synthesized
in several forms which confer different volatilities. A high volatility ester form is the
isopropyl ester. A low volatile ester form is the butoxyethyl ester.
2,4,5-T.
Many lay citizens are familiar with this subfamily by its most notorious member, 2,4,5-T.
The reason for this is that during the Vietnam War, 2,4-D and 2,4,5-T were mixed together
into a concoction called "Agent Orange". Agent Orange was used to defoliate
large parts of the jungle between Vietnam, Laos and Cambodia. During the American phase of
that protracted conflict, North Vietnamese regulars, and others supplying the southern
Vietnamese fighters (the Vietcong; "Charlie") travelled from North Vietnam to
South Vietnam along the border region described above. This route became known as the
"Ho Chi Minh Trail" and was a major supply route for the fighting going on in
the south. The U.S. Army needed to cut off this supply route so it was decided to
defoliate the jungle and expose the traffic on this supply artery. Ultimately, this
approach did not work militarily. It is too hard to defoliate such large areas when the
travellers just shifted in response to Agent Orange use.
When the U.S. policy was first conceived, they needed a lot of the herbicide mix very
fast. Greed for big sales got in the way of many chemical companies good, and safe, sense
and they rushed to supply these chemicals to the army. As a consequence, many of the
batches made early contained unacceptably high levels of a byproduct of 2,4,5-T synthesis:
TCDD (tetrachlorodibenzo-p-dioxin). Of the many lots of this chemical made, there were
highly varied amounts of this contaminate present. Because few good records exist, the
effects of Agent Orange, and its long-term toxicological effects, remain shrouded in
mystery and confusion; a ripe setting for controversy.
The Metabolism of the Phenoxy Carboxylic
Acids in Plants
Mode of Action and Lethality
The primary effect of 2,4-D is to stimulate cell growth in the phloem vascular tissue
of higher plants. This clogs the phloem, pinches the phloem shut and blocks translocation.
The mode of lethality of these herbicides appears to be by plant starvation resulting from
this blockage.
Uptake and Movement in Plants
2,4-D is readily translocated in the phloem of many plant species once it has been
taken up.
Selectivity between Susceptible and Resistant Plant Species
Why these herbicides inhibit dicot plant species, and have a lesser effect on grassy
species, is not entirely known. The two most important mechanisms of differential
susceptibility are differences in the ability of a species to translocate the herbicide,
and differences in the vascular structure of monocot and dicot species.
Translocation Differences.
Part of the basis of selectivity between species can be explained by the relative ability
of a plant species to metabolize and activate (deesterify) 2,4-D: susceptible species have
more efficient esterases, resistant species do not metabolize 2,4-D to the free acid
active form.
Vascular Differences.
A second primary difference in susceptibility between species involves the differences in
organization of vascular tissue in monocots and dicots. In monocots, the phloem is
scattered in bundles, each surrounded by protective schlerenchyma tissue. Also in monots
there is an absence of cambial and pericycle tissue, the probable target of these
herbicides. Another resistance factor may be the intercalary meristem in stems and leaves
of young monocot plants acting as a barrier to 2,4-D movement.
2,4-DB
Some differential selectivity has been achieved between a susceptible dicot species like
cocklebur and a moderately tolerant crop, alfalfa. Susceptible species (cocklebur sort of)
metabolize (beta oxidation) this herbicide into and active form more rapidly than a
resistant species (alfalfa sort of).
Environmental Fate of the Phenoxy
Carboxylic Acids
There exists a range of persistence of the herbicides in this subfamily in the
environment. The two most important aspects of them are their persistence in the soil and
in the air.
Soil.
2,4-D degrades in the soil fairly rapidly. Most residues capable of causing injury to a
susceptible species are gone in 1-4 weeks in warm, moist soil.
Ester forms of 2,4-D in principle do not leach through the soil as well as salt forms do
due to the ester's relative water insoluability compared to the salt. The ester form is
probably hydrolyzed rapidly by soil-born esterases to an acid. The acid anion is very
water soluable and can leach in the soil readily.
The net effect of all these factors, though, is that microbial degradation removes most of
the 2,4-D fairly quickly in the soil environment.
An interesting phenomenon with soil-applied 2,4-D has been observed. Apparently,
subsequent applications of this herbicide break down more rapidly than the initial
application. Most of the science for this soil degradation mechanism has been done in
relation to the thiocarbamate herbicides: "history soils". Soil microbe
populations appear to adapt rapidly to 2,4-D as a soil substrate, the degradative enzymes
actually shift to more efficient forms. In second, and subsequent, years of application to
the soil the herbicide is broken down at even faster rates due to the change in microflora
populations.
Air.
Drift: 2,4-D is volatile, even amine and salt forms, and can move in the air as herbicide
"drift". Often this can cause damage to non-target organisms, the most notable
in Iowa agroecosystems being soybeans.
The less notable, but the one that really really bugs me personally is its affect on
grapes. Iowa used to have a thriving and large table grape industry before WWII. With the
introduction of 2,4-D this industry was destroyed due to drift and grape fruit flower
abortion. As a consequence, the grapes (and fine wine making) in my backyard are at risk
every year. This atmospheric movement of airborn 2,4-D molecules is also a problem with
homeowner lawn applications in the spring and autumn.
Human Toxicology.
2,4-D is absorbed by exposed skin and can be breathed if in the air. It passes rapidly
through the body, kidneys and is excreted primarily in the urine in an unmetabolized form.
Much controversy has surrounded the toxicology and health hazard of 2,4-D. In its
synthesis, dioxins are formed to some extent but their toxicity is far less than that of
TCDD mentioned previously in this chapter. It has been scrutinized closely due to its
similarity to 2,4,5-T and its use in the Agent Orange mixture. A large study was conducted
in Kansas on longtime farm users and a significant coorelation with its use and higher
rates of cancer was found. Hopefully, more studies as this will be conducted to better
assess the health hazards of this widely used herbicide.
Symptomology of Phenoxy Carboxylic Injury
on Plants
The symptomology of 2,4-D injury in susceptible plants is often the rapid appearance of
epinastic effects followed by a slow yellowing and dieback over a longer period (days to
weeks).
Epinasty.
Stems, leaves and underground plant parts can form characteristic curving and twisting
forms. Often new growth will form "buggy-whipping" or "onion-rolling"
symptoms of tight curling of leafs into a tight longitudinal bunch.
Puckered Leaves & Parallel venation.
As leaves develop, the marginal meristems can be inhibited. Lower levels of injury result
in leaves that appear puckered, often forming a downward pointing cup-shaped leaf. Higher
levels of injury result in the leaf forming a narrow shape in which the veins are close
together due to lack of leaf expansion: "strap-shaped" leaves. Often interveinal
areas are puckered and dark-green in color due to lack of leaf growth and expansion: a
concentration of chlorophyll and cells into a limited area.
The top row below shows increasing soybean injury from left to right:
Swollen tissue.
As the vascular tissue becomes clogged and choked with cell proliferation, stems and other
organs can become swollen, sometimes resulting in stem splitting. Rapid, abnormal growth
can also cause abnormal tissue development. Examples include the abnormal root tissue
proliferation sometimes seen in corn, or the stalk swelling at the soil surface in corn,
some time after application. Stalk abnormalities often are expressed in curved plant
stems, e.g. "goosenecked" corn stalks.
Reproductive interference.
Several types of reproductive interference can occur with 2,4-D. Tomato flowers will abort
very easily with low levels (as low as parts per billion) of 2,4-D in the air. Often fruit
set is delayed for a long time. 2,4-D use in corn during pollenation can abort maize seed
set. Use of the herbicide in cereals can have affects also. Applied in the fall to winter
cereals when flower primordia are forming in the plant, the herbicide can cause seed head
abnormalities not observed until the following spring when grain is visible outside the
plant. Sometimes the auxin-like activity of 2,4-D can create an artificial apical
dominance in plant parts, inhibiting new bud development.
Chlorosis.
Often the slow starvation of a susceptible plant will induce slow chlorosis, or green leaf
yellowing, over an extended period of time. This can be followed by necrosis and plant
death. Sometimes these and other symptoms only appear on tissue initially exposed, and new
growth is unaffected.
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