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THIS IS ALSO TRUE OF THE DRY MESQUITE CHIPS, CHUNKS, AND FIREWOOD USED
FOR BBQ.
FROM THE EARLY 1960'S UP TO 1985 WEST TEXAS RANCHERS USED 245T TO KILL
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TO KILL THE MESQUITES.
THERE ARE THOUSANDS OF ACRES OF STANDING DEAD MESQUITE TREES IN WEST
TEXAS THAT WERE KILLED WITH 24D OR 245T.
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FIREWOOD@BITSTREET.COM
2,4,5-T: COMPOUND OF
DESTRUCTION
2,4,5-T: COMPOUND OF
DESTRUCTION
The compound 2,4,5-Trichorophenoxyacetic acid, 2,4,5-T, is a member of the
phenoxyalkanoic acid group. This compound is a herbicide and its main function is to
defoliate post-emergence growth of broadleafed, woody plants. It was first introduced in
1945 and was used primarily for foliage treatment of herbaceous plants on roadsides and
near powerlines (McEwan and Stephenson). 2,4,5-T has also been used for the control of
poison ivy, poison oak and other broadleaf weeds (Kildane et al, 1982). These phenoxy
herbcides are usually formulated as esters to be soluble in oil and amine salts to be soluble
in water. The ester form is used for foliar applications since it can penetrate easier
through the leaf's waxy cuticle (McEwan and Stephenson).
2,4,5-T is best known as a component of Agent Orange, in equal combination with its
very close relative 2,4- Dichlorophenoxyacetic acid (2,4-D). Agent orange was a
chemical used between 1961-69 in Vietnam to defoliate the jungle forests in which the
Viet Cong were hiding. At this time little was known of the effects of the chemical. Not
long after, high incidences of abortion, skin diseases and birth defects on both civilians of
Vietnam as well as US soldiers returning home, began to show up (Britannica, 1985).
These symptoms as well as the effects of the compound began to stir up a great
controversy against 2,4,5-T and related halogenated compounds. The toxicity,
biodegradation, and the long-term effects on the environment are areas of study which
are essential to understanding the problems with 2,4,5-T.
2,4,5-T shows toxic efffects on broad leaf weeds and is used as an herbicide to destroy
them. 2,4,5-T's primary mode of entry is through the foliage or leaves (through the cuticle
and stomata). Once inside, the herbicide is symplastically translocated which implies the
transport of 2,4,5-T through phloem from regions of carbohydrate synthesis (leaves) to
sugar importing tissues such as roots, buds, shoot tips and other leaves (Bovey et al,
1980). The lethal and sublethal responses of plants to 2,4,5-T have been thought to come
about as an effect of certain biochemical and metabolic changes in the plants. 2,4,5-T
causes inhibition of cell division and elongation at growing points, while abnormal division
and proliferation is stimulated in mature tissue. The actual cause of death is thought to
occur as a result of physically blocked vascular channels and the prevention of
translocation of food in the assililate stream resulting in starvation of roots and other parts
of plant parts. The cells expansion, division and callous growth plugs and crushes the
vascular tissue and is caused by the triggering of an overgrowth response (Bovey et al,
1980). Research speculates the causes of this overgrowth response.
At low concentrations, 2,4,5-T mimics the action of the natural auxin IAA, but whereas
IAA levels are probably controlled by IAA oxidase, there is little or no regulation of the
level of synthetic compounds (McFarlane, 1977). Therefore, instead of the normal
breakdown of IAA by IAA oxidase, 2,4,5-T is not degraded. Auxins are involved in
elongation of cells and organs, root formation, phototropism, geotropism, apical
dominance, parthenocarpy, abscission of leaves, initiation of flowers and activation of
cambial cells (Bovey et al, 1980). The increase in concentration of auxins can manifest
toxic effects in plants by producing growth malfunctions (Bovey et al, 1980). Since,
2,4,5-T mimics natural auxin, this has been theorized as a possible cause for the toxic and
lethal effects of 2,4,5-T in plants.
There is evidence for the existence of membrane bound auxin receptors in plants which
normally binds auxin, stimulating membrane bound ATPase actividy (McFarlane, 1977).
This may lead to injection of protons into the cell wall, lowering PH and causing a rapid
weakening of wall bonding possibly between microfibrils and xyloglycan (McFarlane,
1977). Also, the overgrowth response may be a concequence at the nuclear level. It has
been found that in areas of promoted cell division and elongation there were demonstrated
to be mafor increases in nucleic acids and protein, while in the apical growing point,
increase was prevented (McFarlane, 1977). 2,4,5-T has been proposed to increase the
enzyme responsible for messenger RNA synthesis and RNA polymerase (McFarlane,
1977). This leads to the eventual synthesis of new ribosomes and consequently stimulation
of protein biosynthesis that may cause overgrowth.
Many other modes of action such as increased ethylene production may contribute to the
toxic effects seen in the broadleaf plants. Through one of the above mecahnisms or in
combination of such mechanisms, the overgrowth lethal effects result.
Toxic effects of 2,4,5-T have been seen on some vegetative crops. 2,4,5-T has an effect
on germination and seedling behaviour of the vegetative crop S. Melongena (Jindal,
1981). This effect is less severe under dark incubation but causes abnormal expansion of
axes and and necrosis of radicle apices (Jindal, 1981). Other toxic effects have been
thought to occur in other organisms as a result of 2,4,5-T or its productions. It has been
shown that as a result of increased temperature during synthesis 2,3,7,8-TCDD is
produced (Kingman, 1982). This compound is a potential carcinogen and teratogen.
Studies on reproduction in female C57B/6 mice treated with contaminated soils from a
2,4,5-T manufacturing site displayed acute and reproductive toxicity (primarily fewer live
pups born and fewer pups surviving until weaning) (Umbreit et al, 1987). These soils
were contaminated with compunds such as halogenated dibenzodioxins, dibenzofurans,
benzene etc. as well as with 1050 mg 2,3,7,8-TCDD/kg soil (Umbreit et al, 1987).
Research also shows that serum levels of this contaminant in workers exposed before
1965 were higher than in workers exposed after 1974, when concentrations were lower
as a result of government regulations worldwide (Johnston, 1992). Therefore, the toxicity
responses due to this compound would be smaller than than before 1974.
There is great debate regarding the long term effects of 2,4,5-T use and conflicting results
in studies which investigate these effects. Movement and persistence of 2,4,5-T in the
evironment (soil, water and air) and in exposed organisms are of concern since it is a
relatively stable compound. On average, 2,4,5-T persists 2 to 4 months in soil, and up to
nine months under cold or dry conditions which slow down microbial degradation (Green,
1982). Soil at 0 to 15 cm depth showed a decrease in 2,4,5-T contamination by 90 %
during the first month following application and levels then stayed relatively constant
(Norris, 1984). The phenoxy herbicides tend to stay in the upper layers of soil which
prevents contamination of groundwater (Green, 1982). In fact, no 2,4,5-T was found
below 15 cm after 3 months exposure to fall precipitation (Norris, 1984).
In examining a forest watershed in the eastern U.S., 2,4,5-T was applied at a rate of 2.24
kg/ha. Levels of herbicide were measured for two years and those detected during
application were the highest, reaching 0.05 mg/L. No 2,4,5-T was detectable in the steam
past 13 days following application (Norris,1984). In fact, only 0.017% of the applied
herbicide was discharged into the stream from the watershed (Norris, 1984). Streams do
not show detectable contamination after heavy rain which implies that direct application is
the main source of 2,4,5-T found there (Norris, 1971).
Air does not retain the herbicide, but it tends to fall to soil, vegetation, water surfaces or is
photodegraded (Green, 1982).
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The effects of 2,4,5-T on humans is still being examined. The secretaries of Agriculture,
Interior and Health, Education and Welfare announced, on April 15, 1970, that registration
of 2,4,5-T for aquatic, home and recreational use was suspended (Van Strum, 1983).
Registration of 2,4,5-T for "all uses on food crops intended for human consumption" was
cancelled 15 days later (Van Strum, 1983). In 1979, the EPA enacted an emergency
suspension against forestry use of 2,4,5-T.
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Animal studies have shown that while 2,4,5-T can be eliminated rapidly from the body
with urinary excretion being the principal route and small amounts leaving in the feces
(Lilienfeld et al., 1989), there may be large amounts of the compound accumulated by the
kidney for prolonged periods of time (Koschier, 1979). The processes for 2,4,5-T
elimination and distribution within the body is dose-dependent (Lilienfeld et al., 1989).
Teratogenicity is a major concern with respect to 2,4,5-T. It is behaviourally teratogenic
-causing birth defects- to rats after a single dose of 6 mg/kg on the eighth day of
gestation. This level is "well below doses reported to be morphologically teratogenic, and
raises concern for human exposure" (Crampton, 1983). Strong effects have been reported
including the production of cleft palates, kidney malformations, reduced fetal weight and
fetal growth retardation in mice (Lilienfeld et al., 1989). In chickens, the addition of
2,4,5-T to eggs at low doses (7-27 mg/kg body weight) produced retarded learning,
inceased general activity and jumping (Sanderson, 1981).
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Studies determining the carcinogenicity of 2,4,5-T have linked a higher incidence of
non-Hodgkin's lymphomas in people living in areas with 2,4,5-T in soil and water (Vineis
et al., 1991). However, there was no correlation between phenoxy herbicides and
incidence of Hodgkin's disease or soft tissue sarcomas (Vineis et al., 1991).
The degradation of 2,4,5-T can be a very long process. 2,4,5-T is a halogenated aromatic
compound so is very resistant, or recalcitrant, to microbial degradation. Chlorinated
aromatic compounds, also known as organochlorides, are synthetic organic compounds in
which the hydrogens have been replaced with chlorines. Furthermore, 2,4,5-T gains
stability in its structure by having a chlorine in the meta position (position #5) This process
creates compounds which have extreme stability and could persist indefinitely. Stable
compounds such as these can result in bioaccumulation, a state where a sustance is taken
in by an organism, but is not metabolized or excreted. Also, 2,4,5-T has a low water
solubility, but high fat solubility meaning that this compound can be readily absorbed by
organisms ( Nebel, 1981). This low solubility also means that 2,4,5-T has low
bioavailability; m/o's can't easily come into contact with this compound to metabolize it.
2,4,5-T absorbs easily to other organic compounds making it less bioavailable (Racke &
Coats, 1990). So, without a method of degradation for this substance, the accumulation in
the environment would be inevitable as well as potentially hazardous.
For years it was known that 2,4,5-T was somehow degraded in soil but the organism or
chemical mechanism was not exactly known (Rosenberg & Alexander, 1980).
Fortunately a strain was discovered in 1982 that is able to use 2,4,5-T as a sole source of
carbon and energy. The microorganism (m/o) is named AC1100, but is better known as
Pseudomonas cepacia (Karns et al, 1983). This m/o can also oxidize other
chlorophenols, most importantly 2,4,5-Trichlorophenol (2,4,5-TCP), the toxic intermediate
in 2,4,5-T degradation. In fact 2,4,5-TCP is degraded very rapidly because of its toxicity
to bacteria in order to prevent accumulation of this substance during 2,4,5-T degradation.
There are a number of enzymes through which this pathway follows. 2,4,5-T oxygenase
is the first enzyme involved in degrading 2,4,5-T, it produces 2,4,5-TCP (Hill, 1995). This
enzyme is responsible for converting 2,4,5-T to 2,4,5-TCP is not inhibited by the
end-product as normal enzymes usually are. The presence of excess 2,4,5-TCP will not
slow the rate of reaction because it is immediately degraded by other enzymes (Karns et
al, 1983). The final product is usually succinyl CoA and acetyl CoA as a product of
intermediary metabolism (Hill, 1995). Succinyl CoA and acetyl CoA serve as part of the
Krebs cycle and are also precursor metabolites; they allow the cell to grow and
metabolize. So, in this way, 2,4,5-T is used as a carbon source.
In laboratory studies of P. cepacia some interesting properties of their 2,4,5-T
degradation were revealed. It was discovered that the synthesis of the enzyme
responsible for converting 2,4,5-TCP to other intermediary metabolites is repressed when
P.cepacia is grown in the presence of other carbon sources such as succinate,
glucose, and lactate. This lead to an accumulation of 2,4,5-TCP which lead to the
m/o poisoning itself and consequently discontinuing 2,4,5-T degradation (Karns et
al, 1983). This potential situation could be a factor in maintaining a population to
degrade 2,4,5-T in the field.
P. cepacia was most effective at degrading 2,4,5-T at ~ 30C, which was also the
optimum temperature for growth in a solid or liquid medium. Also, the optimal
moisture content of the soil was 25% with decreased efficiency at levels greater or
less than this value. Laboratory bred strains of P.cepacia grown under these
conditions, with no altnernate carbon source were found to degrade 2,4,5-T and
remove more than 95% of the compound from the soil in less than a week
(Chatterjee et al, 1982). However, it is unlikely that such conditions would be met
in the field.
Since 2,4,5-T degradation is a biological process, any factors that may affect
microbial activity will also affect its breakdown. This may include soil pH, soil type
(clay or sandy loam), soil organic matter, and herbicide concentration in the soil
(Racke & Coats, 1990). Another interesting factor which may affect 2,4,5-T
breakdown in soil is whether or not the soil itself has been previously treated with
the herbicide. Soils previously treated with certain herbicides, like 2,4,5-T, exhibit
an increased ability to degrade these chemicals. This increase is due to the fact that
m/o's adapted to the particular herbicide would have had a chance to proliferate
(Racke & Coats, 1990). Once a sufficiently large population has been reached,
rapid breakdownof the phenoxyactetic acid was observed. This process is known
as enhanced degradation - frequent applications of this herbicide with increase in
its breakdown (Racke & Coats,1990).
Another natural method of 2,4,5-T breakdown comes from sunlight. The maximum
range of absorption for phenoxyalkanoic acids is 280-290nm so they are able to
absorb sunlight and consequently undergo photochemical decomposition. However,
this occurs only at the soil surface and is not considered a major source of
degradation since the residues underneath a canopy layer will not be affected by
the sun's radiation (Racke&Coats, 1990).
In 1983 the only North Americn manufacturer of 2,4,5-T announced that it would
be discontinued. Today, little or no 2,4,5-T is used in North America. The only
allowable US applications are for rice fields and rangelands where it is used to kill
weeds that are toxic and teratogenic to cattle (Kruss et al,1991).
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References
Bovey, R.W., Young, A.L. The Science of 2,4,5-T and Associated Phenoxy
Herbicides. John Wiley & Sons, US. 1980. pp.217-237
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Crampton, M.A., Rogers, L.J. Low doses of 2,4,5-trichlorophenoxyacetic acid are
behaviourally teratogenic to rats. Experientia. 1983. v.39:8, pp. 891-892
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Encyclopedia Britannica. Encyclopedia Britannica INC. Chicago,IL 1985. v.1, pp.
146
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Green, K. Forests, Herbicides and People: a case study of Phenoxy Herbicides in
Western Oregon. Council on Economic Priorities. New York,NY. 1982.
pp.57-80,110-135,176-198.
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Hill B., University of Minnesota College of Biological Sciences-
Biocatalysts/Biodegradation database. ( http://dragon.labmed.umn.
edu/~lynda/2,4,5-T/2,4,5-t_map.html. ) 1995.
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Jindal, K. Effect of Three Chlorinated Phenoxy Herbicides on Germination and
Seedling Behaviour of Solanum melongena L. Acto-Ecol. 1981. v.3:1 pp. 12-23
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Johnson, D.G. et al. Current serum levels of 2,3,7,8-TCDD in Phenoxy acid
Herbicide Applicators and Characterization of Historical levels. J. of National
Cancer Inst. 1992. v.84:21. pp.1648-1653
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Karns, J.S., Kilbane, J.T., Duttagupta, S., Chakrabarty, A.M. Metabolism of
Halophenols by 2,4,5-T degrading Pseudomonas cepacia. Appl. Env. Micr. 1983.
v.46:5 pp. 1176-1181
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Kilbane, J.T., Chatterjee, D.K., Karns, J.S., Kellogg, S.T., Chakrabarty, A.M.
Biodegradation of 2,4,5-T by a pure culture of Pseudomonas cepacia. Appl. Env.
Micr. 1982. v.44:1. pp.72-78
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Kingman, G.C., Ashton, F.M., Noordhoff, L.J. Weed Science: Principles and
Practice. John Wiley & Sons, Inc. New York. 1982.
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Koschier, F.J., Hong, S.K., Berndt, W.O. Serum protein and renal tissue binding of
2,4,5-trichlorophenoxyacetic acid. Toxicology and Applied Pharmacology. 1979.
v.49:2, pp. 237-244
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Kruss, P., Demmer, M., McCaw, K. Chemicals in the Environment. Polyscience
Publications Inc. Morin Heights,PQ. 1991. pp. 92
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Lilienfeld, D.E., Gallo, M. 2,4-D, 2,4,5-T, and 2,3,7,8-TCCD: An Overview.
Epidemiologic Reviews. 1989. v.11, pp.28-58
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McEwan, F.L., Stephenson, G.R. The Use and Significance of Pesticides in the
Environment. John Wiley & Sons. New York,NY. 1979. pp.114-118
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McFarlane, N.R. Herbicides and Fungicides. The Chemical Society. Aldon Press,
London. 1977. pp.14-17
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Nebel, B.J. Environmental Science: the Way the World Works. Prentice-Hall Inc.
Engelwood Cliffs,NJ. 1981. pp. 342
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Norris, L.A. The behaviour of chemicals in the forest: in pesticides, pest control and
safety on forest range lands. Proceeding Short Course for Pesticide Applicators.
1971. pp. 90-115
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Norris, L.A., Montgomery, M.L., Loper, B.R. Movement and persistence of
2,4,5-trichlorophenoxyacetic acid in a forest watershed in the eastern United
States. Environmental Toxicology and Chemistry. 1984. v.3:4, pp.537-549
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Racke, K.D., Coats, J.R. Enhanced Biodegration of Pesticides in the Environment.
American Chemical Society, Washington,DC. 1990. pp.14-19, 137
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Rosenberg, A., Alexander, M. Microbial Metabolism of 2,4,5-T in Soil, Soil
suspensions and Axenic Culture. J. Agr.& Food Chem. 1980. v.28:2. pp.297-302
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Sanderson, C.A., Rogers, L.J. 2,4,5-Trichlorophenoxyacetic acid causes
behavioural effects in chickens at environmentally relevant doses. Science. 1981.
v.21:4482, pp.593-595
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Umbreit, T.H. et al. Chemical Exposure in Manufacture of Phenoxy Herbicides.
Arch. Environ. Toxicol. 1987. v.16:4, pp. 261-266
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Vineis, P., Faggiano, F., Tedeschi, M., Coccone, G. Incidence Rates of Lymphomas
and Soft-Tissue Sarcomas and Environmental Measurements of Phenoxy
Herbicides. Journal of the National Cancer Institute. 1991. v.83:5, pp. 362-363
