[add: Phenoxy; Benzoic; Aryloxy Phenoxy Carboxylic Acids; Carboxylic Acids]
[add: R1 = aryl ring with halogens; R2 = salt, ester]
The basis of their differences structurally is based on how the carboxyl (-COOH) group is
attached to the phenyl ring structure, directly or through an ether (-O-) bridge; the
number of carboxyl groups in the molecule; and, the number of phenyl moieties in the
individual herbicide molecule.
Advanced Topics: Phenoxyacetic Acids
Chemistry
There are many other herbicides in this subfamily besides 2,4-D: 2,4-DB; 2,4-DEB;
2,4-DEP; 2,4,5-T; 2,4,5- TES; diclorprop; MCPA; MCPB; MCPES; mecoprop; sesone; silvex; and
erbon.
The generalized chemical structure for this family is:
[add: structure; R = Cl, CH3, etc.]
The structure for 2,4-D is:
[add: structure]
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. In general, the
acid moiety dissociates when mixed in water to the anion form. For example, the
triethanolamine salt of 2,4-D dissociates thusly:
[add: structure]
This 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.
e. 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. Examples of ester formulations are:
Isopropyl ester butoxyethyl ester
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 larger moiety of butoxyethyl ester. Volatility can
be altered with changes in ester structure, especially in the size of the aliphatic chain.
f. 2,4,5-T
1) Historical perspective
a) 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
form 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.
b) 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.
2) Chemically the synthesis, and TCDD byproduct formation, are:
TCDD
(Tetrachlorodibenzo-p-dioxin) Ultimately, a chemical that was widely and effectively used here in the U.S. for
forestry uses (pine release) was banned in a rancorous debate between the EPA and the
agrichemical industry.
The Metabolism of the Phenoxy Carboxylic Acids in Plants
Mode of Action
1. General information
a. Many mode of action studies have been done on this family. The majority of these
concern 2,4-D. These studies are good evidence of the idea in research that you find what
you went looking for when you design a research study. This is not unexpected from a
herbicide subfamily that at low concentrations has direct auxin-hormone action, and at
higher doses has a phytotoxic effect: many plant systems are affected and show effects.
b. Auxin-like compounds have in common a carboxyl (-COOH) group attached to an aromatic
ring structure in many cases (Salsbury). Often it is fruitful to compare the auxin
chemical indolacetic acid (IAA) structurally to
2,4-D to aid in understanding the herbicides hormonal role:
2,4-D IAA
2. Auxin targets are cells in the process of differentiating found near one of several
meristematic regions in plants.
a. The general response they elicit is cell elongation. This cell wall elongation is
primarily by longitudinal stretching of the cell.
b. Proposed Model: This sequence of events has not been entirely proven, but it is a good
working model.
1) Auxins probably bind to specific receptor molecules, a specific protein (Goodwin,
p279).
2) The resulting auxin-receptor complex may then switch on a gene.
3) The gene then transcribes mRNA's, which are translated into a specific protein which
facilitates the physiology of cell elongation.
4) It is at the site of the auxin receptor molecule that 2,4-D may have its primary
effects. The herbicide may bind to the receptor protein and initiate many physiological
effects, including the induction of cambial cell growth.
3. Primary molecular and cellular responses: The primary action of 2,4-D begins with the
stimulation of nucleic acid and protein synthesis (Kaufmann, p87-9).
a. It is proposed that 2,4-D binds to these auxin receptor sites and this herb- receptor
complex induces a gene to synthesize a "mediator" protein.
b. This protein acts in the cell nucleus to induce or activate unusually high levels of
RNA polymerase activity.
c. This increased RNA polymerase activity may be enhanced by another mechanism which
uncovers the DNA template, making it more readily available for transcription. This
uncovering mechanism may be accomplished by changes in secondary and tertiary DNA
structure.
d. In any case, these mechanisms induce transcription of hormone-specific genes. This
abnormal stimulation leads to abnormally high levels of cell growth, destroying phloem
tissue.
e. It is proposed that low rates not all the receptors are occupied by the herbicide and
endogenous auxins fill the other, unoccupied sites. This could allow for normal cell
function to continue. At these low levels, 2,4-D may act merely as an inducer of higher
rates of normal processes. At higher rates, the herbicide may occupy most, if not all of
the receptor sites and may completely block normal function.
4. Primary physiological responses
a. The primary effect of 2,4-D receptor site binding, is to activate and initiate cambial
cell growth in the phloem vascular tissue of higher plants.
b. This cellular proliferation clogs the phloem, pinches the phloem shut or collects on
the sieve plate elements of the phloem and blocks symplastic vascular translocation.
c. Plant growth stops eventually due to the inability of the plant to move
photoassimilates, sucrose mainly, from sources of synthesis to areas in need of energy
(sinks).
d. Another result of this cellular proliferation is the loss of absorptive capacity by
roots and shoots. The plants starve to death.
5. Other early and secondary physiological responses: In the process many other primary
and secondary physiological effects occur. Unfortunately for us, and the early
researchers, many of the modes of action of 2,4-D discovered are secondary. Some of these
secondary physiological processes are described below.
a. Enzymatic inhibition: 2,4-D retards activity of peroxidase, probably mediated by
inhibition of phenolic metabolism (Duke, p104). 2,4-D inhibits, and stimulates, ATPase
activity depending on the concentration of herbicide (Duke, p128). Stimulation occurs at 1
nM concentrations, while inhibition occurs at 50 nM concentrations.
b. Membrane function interference: 2,4-D increases membrane permeability causing greater
leakage of cellular solutes (Duke, p120). It inhibits mineral ion absorption into roots of
K+, PO4-3, NO3-, NH4+, and Cl- at high concentrations (up to 1 mM)(Duke, p124-5).
Stimulation of absorption occurred at low concentrations (less than uM). This herbicide
also causes several changes in membrane function: cell enlargement; changes in membrane
electrical potentials and resistance; and, changes in H+/K+ fluxes that may be involved in
important transmembrane gradients responsible for cellular function (Duke, p128- 9).
c. Plastid ultrastructural interference: 2,4-D causes altered and disorganized chloroplast
structural development (Duke, p74, 79). It also induces tumor-like growth in callus cell
culture, causing dilated endoplasmic reticulum, dilated mitochondrial cristae and other
mitochondrial ultrastructural changes (Duke, p84).
Mode of Phenoxy Carboxylic Acid Lethality
As stated previously, the primary action of this subfamily is to induce massive cell
proliferation in the vascular phloem tissue, effectively blocking transport. The mode of
lethality of these herbicides appears to be by plant starvation resulting from this
blockage.
C. Uptake and Movement of Phenoxy Carboxylic Acids in Plants.
1. 2,4-D is readily translocated in the phloem of many plant species once it has been
taken up. In other species translocation is limited.
2. Apparently cuticle thickness has no effect on the uptake of these herbicides into the
leaf (Duke, p206). The 2,4-D anion is moved passively across cellular membranes once the
symplast of the plant is reached. It is also actively transported across membranes,
against a concentration gradient, by an unidentified carrier (Duke, p199).
3. The chemical form of 2,4-D (amine, salt, ester, etc.) can influence the rapidity with
which it is taken into the plant, as discussed earlier.
4. In summary, 2,4-D readily enters the plant symplast equally well in most plant species.
D. The Basis of Selective Toxic Action of Phenoxy Carboxylic Acids.
1. The complete story of 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.
2. Metabolism
a. One primary difference between susceptible and resistant species appears to
differential metabolism (de-esterification) facilitating translocation in the plant. Both
types of species readily allow 2,4-D to enter the plant. A resistant species like sugar
cane allows almost all of the chemical taken up to remain in the leaf (Duke, p210). A
susceptible species like beans have only a minor portion of the applied herbicide
remaining in the leaf. Apparently, the susceptible species has translocated a greater
portion of the chemical to the phloem and areas of active growth (growing point). In both
species the 2,4-D in the plant underwent further metabolism.
b. To understand how this difference in translocation could result in differences in
susceptibility we need to understand the metabolism of the carboxyl group (-COOH) on the
molecule. Neither the amine salt nor ester forms of 2,4-D are absorbed or translocated
directly by plants. Amine forms dissociate in water to form the anion, which is capable of
uptake and translocation in the plant. Ester forms are deesterified on the surface of
leaves, and in the plant, by a group of esterases Duke, p210, 221). These esterases
hydrolize the ester to a free acid, which is readily translocated by the phloem. Part of
the basis of selectivity between species can be explained by the relative ability of a
plant species to deesterify 2,4-D as the basis of selectivity between species: susceptible
species have more efficient esterases, resistant species do not metabolize 2,4-D to the
free acid as readily.
3. A second primary difference in susceptibility between species involves the differences
in organization of vascular tissue in monocots and dicots Kaufman, p98). 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 in vascular tissue, the
locus of the proposed auxin receptor molecules. 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.
4. Other types of metabolism of 2,4-D occur in plants. These are most likely of secondary
importance in the basis of plant species selectivity. Possibly, they play a role in slower
detoxification of the herbicide that eventually removes the chemical from the plant. These
include oxidation reactions, amino acid and glucose conjugation metabolism and cellular
compartmentalization. Also implicated are other non-ring structure metabolic reactions:
side-chain decarboxylation and side-chain lengthening (LeBaron, p151).
a. Oxidative Metabolism. Aryl hydroxylation of 2,4-D in both grassy and dicot plant
species can occur (Duke, p218):
2,4-D 4-OH-2,5-D
(active) (inactive)
? Epoxide ?
The 2,4-D molecule is hydroxylated through an epoxide intermediate to 4-OH-2,5-D
[(2,5-dichloro-4-hydroxyphenoxy)acetic acid]. These reactions are probably catalyzed by
monooxygenases, collectively referred to as the mixed function oxidases (MFO's), with the
participation of cytochrome P450 transferases. These MFO's have been hard to characterize
biochemically, and this metabolism may actually be done by other oxidases or by
peroxidases. Aryl hydroxylation is, argueably, the most common reaction in herbicide
metabolism. In many of these herbicide metabolism oxidations the hydroxylated metabolites
do not accumulate as free phenols in plant tissues. Instead they are probably rapidly
conjugated as to glucose as glycosides.
b. A special case of oxidative metabolism that confers differential susceptibility between
species is that of 2,4-DB [(2,4-dichlorphenoxy)butyric acid]. Some differential
selectivity has been achieved between a susceptible dicot species like cocklebur and a
moderately tolerant crop, alfalfa. Although the physiology is not well characterized
apparently the following metabolism occurs in these two species:
Susceptible Cocklebur:
2,4-DB 2,4-D
(inactive) (active)
Beta Oxidation
Rapid
OTHER PLANT
METABOLISM
Tolerant alfalfa:
2,4-DB 2,4-D
(inactive) (active)
Beta Oxidation
Rapid
Apparently both perform two different metabolic steps in plants: beta- oxidation of the
butyric moiety (non-toxic) to the toxic acetic acid form by the removal of a 2-carbon
unit. Other, slower, unknown metabolic steps occur subsequent to this cleavage.
Differential tolerance is conferred by the relative rates that each of these steps occurs
at in the two species. A similar situation pertains with MCPB and MCPA. A similar
situation occurs with MCPB and MCPA.
c. Amino Acid Conjugation. Another metabolic reaction that 2,4-D can undergo is
conjugation to an amino acid (Duke, 223). This 2,4-D conjugation occurs through an
alpha-amide bond. The major conjugates found are the glutamic forms (2,4-D-Glu) and
aspartic forms (2,4-D-Asp). Minor amino acid conjugates formed are to alanine, valine,
leucine, phenylalanine and tryptophane. The conjugates remain biologically active, but it
is unknown if the still remain phytotoxic in whole plants. It is hard to assess the
importance of this metabolism in whole plants. It has only been studied in cell culture.
d. Cellular Compartmentalization. Some protection to the plant may be conferred by
sequestering of these herbicides in the cell. Intra-cellular compartmentalization may
confer resistance to a plant by making it unavailable for phytotoxic action (Duke, p234).
Inactivation of 2,4-D by adsorption to cellular components has also been implicated as a
selective mechanism (LeBaron, p151).
5. 2,4-D Resistant Mutants. Of interest is recent work by Chris Summerville at Michigan
State University using mutagenic chemicals on seeds. He has successfully selected for
2,4-D resistance in Arabidopsis sp.. The phenotype is a short dwarf plant. This
work has provided support that their exists auxin receptor sites that play the key role in
cell elongation and possibly internode stem elongation. It has been hypothesized that this
herbicide acts by blocking these receptor sites in the cell, and 2,4-D resistance is
conferred in the mutant by having non-functional, or non-receptive, active auxin binding
sites. This line of research opens new possibilities that plant species may have auxin
binding sites of different conformations that form the basis of differential species 2,4-D
susceptibility.
III. 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.
A. Soil.
1. 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.
2. 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.
3. 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.
4. 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.
B. Air.
1. 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. This atmospheric movement of airborn 2,4-D
molecules is also a problem with homeowner lawn applications in the spring and autumn.
2. 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.
3. Human Toxicology. 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.
IV. 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).
A. 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.
B. Parallel venation. As leaves develop, the marginal meristems can be inhibited and the
leaf form 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.
C. 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.
D. 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.
E. 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.
Advanced Topics: Dicamba
I. Introduction
A. General Information about the Benzoic Acids
1. There are several members in this sub-family, including TBA, TIBA, chloramben and
dicamba.. They possess often very different herbicidal and chemical properties. The
generalized chemical structure for the family is:
2. Dicamba (3,6-dichloro-2-methoxybenzoic acid) was introduced in 1965 and is used for
broadleaf annual and perennial weed control primarily in maize, sorghum, cereal crops and
other monocot crops, turf and pastures. It is often used to control weed species not
easily controlled by 2,4-D, such as perennial broadleaf weeds species. It is also used to
control triazine resistant weeds. It is applied preemergence and postemergence in that
crop. Its chemical structure is:
B. Physiology and Environmental Fate of the Benzoic Acids
1. The mode of action is probably similar to that of the phenoxy carboxylic acids. Rapid,
abnormal, cell growth then leads to the disruption of the phloem system and normal auxin
balance in the plant.
a. Foliar applied dicamba has been shown to increase RNA and protein content in
susceptible plants by directly affecting the removal of histone protein from the DNA
template in the nucleosomes, changes in tertiary nucleic acid structure (Ashton, p155;
kaufman, p570; goodwin, p31) This opening of the DNA nucleosome structure could be an
induction signal stimulating gene expression.
b. This molecular mechanism could also be the mechanism stimulating abnormal and rapid
cellular growth that leads to toxic reponses in the susceptible plant.
2. Mode of Lethality: As with the phenoxy carboxylic acids, these herbicides act by
stimulating abnormal cell growth in meristematic cells. This can result in the blockage of
phloem vascular tissue. Extensive destruction of cambial, phloem cells near meristems
occurs within days of treatment. The plant is killed by starvation resulting form an
inability to translocate needed energy in the phloem.
3. Uptake and Movement of Dicamba in Plants
a. Dicamba is rapidly absorbed by plant root and shoot tissue.
b. Dicamba translocates readily in the xylem and phloem.
1] Dicamba taken up by plant roots is translocated mostly in the xylem initially, but over
a longer time it moves to areas of high metabolic activity.
2] Foliar absorbed dicamba moves readily in the xylem and phloem vascular tissue.
c. It accumulates in areas of high metabolic activity.
4. Basis of Dicamba Selective Toxic Action
a. Selective dicamba toxicity amongst plant species appears to be a function of uptake,
distribution in the plant, and metabolism. In some tolerant species, translocation is
limited to the xylem.
b. Tolerant species metabolically degrade dicamba rapidly. The primary degradation pathway
is by ring hydroxylation followed by very rapid glucoside conjugation.
c. Relatively less important degradative pathways include demethoxylation followed by
conjugation to glycosides (Duke, p220).
d. The enzymes that may catalyze these reactions are uncharacterized. Decarboxylation of
dicamba has not been found to occur.
C. Fate of the Dicamba in the Environment
1. Soil.
a. Dicamba will persist in the soil for up to 3 months, or longer, in the soil.
b. Breakdown rates in the soil are primarily due to volitalization losses from the soil,
and microbial degradation in warm, moist soils. As such it is an effective soil-applied
herbicide for weed control after the spring is over.
c. Dicamba is highly mobile in soils and can leach (solubility in water 4500ppm at 25o C)
readily in the soil, especially in sandy soils. It can injure plant roots in these lighter
soils.
d. Little soil adsorption of dicamba to the soil colloidal fraction occurs. This
adsorption is a function of soil pH: adsorption increases with a decrease in soil pH,
decreased adsorption with calcareous soils.
2. Air. One of the problems encountered with the use of dicamba is volatility leading to
drift of the herbicide in the air. It is more volatile than 2,4-D and can cause injury in
more instances than that herbicide on adjacent susceptible plants. Often dicamba drift can
travel farther than 2,4-D also.
3. Toxicology. Dicamba is excreted by animals with relatively rapid uptake, with little
metabolism occuring to the parent molecule.
D. Dicamba Injury Symptomology
1. In general, dicamba injury is identitical to that caused by 2,4-D. There are some ways
to differentiate between injury caused by these two herbicides, but no symptom is
conclusive evidence of one or the other.
2. Epinasty. The most typical injury symptom of dicamba is epinasty, or curved and twisted
stems and leaves. This symptom is caused by differences in growth on different sides of an
organ.
3. Meristem Inhibition. When leaf edge meristems are inhibited by dicamba they often force
the leaf form a cup-shape. This cupping is often associated with a darker green color and
a bunched, or puckered, appearance. Injured leaves appear cupped (upward) with the upper
leaf surface the outside of the cup usually. 2,4-D can also cause leaf cupping, but
usually the cupping is with the upper leaf surface forming the inside of the cup. The
physiological basis of this difference is unknown, and may not be a consistent diagnostic
difference. Monocot plant leaves can form tightly bunched shapes,
"onion-leafing" or "buggy-whipping".
4. Abnormal Plant Part Development. Due to its auxin-like activity, dicamba can cause
growth abnormalities similar to those caused by 2,4-D. A variety of morphological
malformations can occur including leaf malformations and increased branching. Corn can
form fasciated, or fused, abnormal brace roots. Other parts of the root system can be
abnormal, with grotesque roots growth near the soil surface. Stems can become brittle and
break. They can also become weakened and form a curved, or "goose-neck", shape.
Often, dicamba can cause monocot, normally tolerant, species to lay flat for a time just
after treatment. Often, leaves can be curled or twisted in addition to the procumbent
habit of the leaves. This "relaxed" leaf position assumed by grasses treated
with dicamba often disappears hours or days after treatment.
5. Reproductive Interference. Dicamba can interfer with reproductive activities of many
species is a similar manner as does 2,4-D. Corn pollenation and seed set can be affected
by late treatments of dicamba.
6. Differences in Injury due to 2,4-D and Dicamba. It is hard, if not impossible, to
definitely differentiate between injury caused by these two similar herbicides. There are
several keys that often can be helpful though. a. Dicamba translocates more completely
throughout a plant and better control of woody and brushy species can help: these species
will be injured more by dicamba than 2,4-D.
b. Another difference is the tendency of dicamba to flatten and twist monocot leaves just
after treatment, a symptom not encountered as much with 2,4-D.
c. Dicamba can drift in the air to greater distances than does 2,4-D. d. Dicamba injury
often will develop over a longer period than 2,4-D: dicamba is slower acting.
e. 2,4-D often will cause slightly more corn stalk injury under the same conditions than
that caused by dicamba.
f. Dicamba has a longer residual effect in the soil than that from 2,4-D.
g. Dicamba costs more than 2,4-D, look for thrifty farmers using
2,4-D.
