A review of epidemiological studies on the health

effects of exposure to phenoxy herbicides suggests

that exposure may be associated with an increased
incidence of cancer and unfavorable outcomes of
pregnancy. Studies on cancer have found increased
risks of 5.3, 6.8 and 3.96 for soft-tissue sarcoma, 7.7
and 6.0 for stomach cancer, 2.05 for lung cancer,
4.8 for lymphoma, 2.3 for all cancers combined, and
5.2 for liver cancer after exposure to 2,4,5-T or
dioxin contaminants. Several studies have
suggested a possible increase in birth defects after
paternal exposure. An increased risk of hydatidiform
mole is suggested by Vietnamese studies on the
effects of maternal exposure.
Rachel Carson, author of Silent Spring, talked about the appropriate use of
herbicides to manage roadside vegetation. She was referring to 2,4-D. This
may seem surprising, because she was painted by others as such a radical.
Visionary yes, but extremist, no. The majority of her book was about the
harmful misuse of chemicals in the environment. I agree that if we're
reasonably sure something is harming wildlife, we should should stop it. But
here was a book that also talked about the judicious and beneficial use of 2,4-
D in the environment.

2,4-D in its pure form has low mammalian toxicity, and used responsibly is a
valuable management tool, especially for the protection of grass from
competition by most herbaceous dicots or broadleaf plants. Unfortunately, it
has been recognized to be rather harsh on St. Augustinegrass. In the early
1950s, Florida St. Augustinegrass sod producers started evaluating 2,4-D on
their fields, and they found that it made the stolons of the grass brittle. 2,4-D is
even worse on selected families of broadleaf plants, such as tomato and
cotton. Drift from the older formulations of 2,4-D has been known to kill crops a
couple counties downwind. But those serious problems you might expect,
because they have occurred from aerial spraying. The new amine and other
formulations of 2,4-D have much less volatility and are much less likely to
move away from their target. As with any pesticide (and weed killers, that is
herbicides, are a kind of pesticide) one must use the formulations of 2,4-D
responsibly according to the label. Reports in the 1980s of lawn damage in
Florida from 2,4-D and related chemicals eventually caused some of the
formulators to label their products, "not to be used on Floratam St.
Augustinegrass in Florida." It was not clearly determined whether these were
instances of overapplication, sensitivity of Floratam, or formulation. Most weed
killers are distributed only to professional applicators, who know how to use the
products, and are specially trained and licensed to do residential pest control.

2,4-D is normally formulated in combinations with three or four other related

chemicals, including MCPA, MCPP, and dicamba. Unfortunately, it's difficult to
tell the individual effects of each chemical, least of all their combined effects in
a mixture. What I am discovering is that some combinations containing MCPA
are almost as harmful to St. Augustinegrass, whereas those which are primarily
2,4-D have the greatest impact on removing Wedelia, and also are safest to St.
Augustinegrass. I am continuing to evaluate these chemicals in typical
condominium settings, because that's the most accurate way of determining
their potential usefulness. These are old chemicals that may have a new life
some day. The only other broadleaf weed killer for St. Augustinegrass,
atrazine, has been found in well water in the corn belt United States, and some
wonder how long its going to be available for use in lawns.
2,4-D fact sheet
The herbicide 2,4-D was first identified in 1942 and marketed in 1944. Despite its
decades of usage, there are still data gaps concerning 2,4-D's effects on human health
and environment risk.

What is 2,4-D?
This highly selective herbicide is toxic to broad leafed plants but less harmful to grasses(1). One of the
hormone weedkillers, 2,4-D (2,4-dichlorophenoxy acetic acid) is an aryloxyalkanoic acid known also as a
'phenoxy herbicide', which includes MCPA, mecoprop, triclopyr and 2,4,5-T. These chemicals have
complex mechanisms of action against weeds, resembling those of auxins (growth hormones). Once
absorbed 2,4-D is translocated within the plant and accumulates at the growing points of roots and shoots
where it inhibits growth.

Production
Introduced in 1942, 2,4-D has been off patent for many years and is manufactured and sold by many
different companies around the world.

The global market is estimated to be over US$300 million and the main producers are Agrolinz, Atanor,
Dow, AH Marks (UK), Nufarm (Australia), Polikemia, Rhône-Poulenc, Sanachem, Sinochem (China) and
Ufa, together with four other producers in Turkey(2) .

Ufa (Russia) produced about 49,000 tonnes of different formulations until production was discontinued
some years ago due to 'environmental problems'. Production has resumed at lower levels. Dow (US) is now
the largest producer with a capacity of 20,000 tonnes. Rhône-Poulenc is the largest European producer
(7,000 tonnes pa), followed by Agrolinz (4,000 tonnes).

Use
The principal use is for the control of broad leaf weeds in cereal crops-including wheat, maize, rice and
sorghum-and grassland and turf areas. It is also widely used in mixtures with other herbicides to provide
weed control in forestry, orchards and non-crop areas, and for the control of aquatic weeds.

The phenoxy acid group of herbicides are probably one of the widest used herbicide chemcial classes. The
US, South America, Europe and the former Soviet Union are major markets for 2,4-D-weed control on US
wheat relies on little else-and global use is predicted to grow over the next decade(3). In the US where it
was the third most used pesticide in the early to mid 1990s, over 31,000 tonnes of 2,4-D was used
annually(4). In the UK it is among the top six herbicides used by UK local authorities, and it ranked seventh
among herbicides used on grassland and fodder crops and twentieth among herbicides used in orchards in
1992(5,6). Overall the area of land treated with 2,4-D in UK agriculture (excluding amenity use) declined by
83% during the period 1984-1994(7). 2,4-D is also used widely in developing countries: India, for
example, used 1,300 tonnes in 1994-5(8).

Acute toxicity
2,4-D is a WHO Class II 'moderately hazardous' pesticide. This places it in the same class as endosulfan,
lindane, paraquat and toxaphene. It has an LD50 of 375 mg/kg in the rat with evidence suggesting a similar
level of toxicity in humans(9).
Occupational exposure to 2,4-D has produced serious eye and skin irritation. Other symptoms of 2,4-D
poisoning include nausea, weakness and fatigue, and in some cases neurotoxic effects including
inflammation of nerve endings(10). Some medical reports from practitioners who have treated victims of
acute exposure to 2,4-D mention severe and sometimes long lasting or even permanent symptoms. These
include, as well as those listed above, diarrhoea, temporary loss of vision, respiratory tract irritation,
confusion, numbness and tingling, bleeding and chemical hypersensitivity(11).

A recent review of 2,4-D by the UK Advisory Committee on Pesticides (ACP) noted that "Approval
holders must generate a number of toxicology/operator exposure studies to allow a full risk assessment to
be made."(12)

Chronic effects
It seems that long term exposure to 2,4-D can affect different animals in a wide variety of ways. Rats for
example were found to be largely unaffected when fed moderately large amounts in their diet over long
periods, although signs of kidney pathology were demonstrated. Dogs however died when fed smaller
amounts over shorter periods. A human fed 16.3 grammes over 32 days showed severe symptoms of
intoxication(13).

It also seems that the various chemical forms of 2,4-D can have different toxic effects. Acid, salt and
various esters differ in all their measured toxic effects to some extent, but the majority of toxicity data
relates only to the acid.

Cancer
Phenoxy acid herbicides have been linked with soft tissue sarcomas, but the UK ACP has concluded that
'the data do not suggest a positive link with 2,4-D'14 as have the Canadian authorities(15). However, the
International Agency for Research on Cancer (IARC) has classified 2,4-D among the phenoxy acid
herbicides MCPA and 2,4,5-T as a class 2B carcinogen-possibly carcinogenic to humans(16) (concluding
that there was limited evidence in humans, inadequate evidence in animals).

The US authorities have also been reluctant to declare 2,4-D as a potential human carcinogen, but the US
courts decided that a forestry worker contracted cancer and died as a direct result of his exposure to 2,4-D
during the course of his work(17).

One concern about 2,4-D has related to dioxin contamination. 2,4-D was in the past frequently co-
formulated with the herbicide 2,4,5-T. Production of 2,4,5-T was contaminated with the carcinogenic
dioxin TCDD. Those who were exposed to the mixed formulations might therefore have been exposed to
TCDD. The most notorious mixed formulation was Agent Orange, used first by the UK military in
Malaysia and later extensively by the US military to defoliate jungle regions in Vietnam. In the UK, 2,4-D
+ 2,4,5-T formulations were in use until 1994(18). 2,4-D has been produced with contaminant dioxins, but
not the harmful TCDD(19).

Reproductive effects
Abnormal foetal skeletal development, increased foetal mortality and other reproductive effects are fairly
conclusively associated with exposure to phenoxy-acid herbicide and their dioxin contaminants(20).

2,4-D has also been classified as an endocrine disrupter(21), and significant chromosomal damage occurred
in human cells cultured in the presence of 2,4-D. At the same time no evidence for mutagenicity has been
found and 2,4-D did not damage DNA in human lung cells(22).

Fate in the environment

2,4-D has low soil sorbtion and a high potential for leachability(23). Indeed 2,4-D residues have been
recorded many times both in water company monitoring programmes and by the UK Department of the
Environment(24,25). It has also been detected in groundwater supplies in a number of US States and in
Canada(26). In 1994, 3% of groundwater samples, and in 1995, 4% of surface water samples in England
and Wales exceeded the EU standard(27).

Its high potential for water contamination has led to the inclusion of 2,4-D in the EC Priority Candidate List
of chemicals to be considered for inclusion among the chemicals most tightly controlled to prevent water
pollution. 2,4-D is also a priority candidate for inclusion in the UK Department of the Environment Red
List which has a similar function.

Wildlife
Some formulations of 2,4-D are highly toxic to fish while others are less so. Aquatic invertebrates do not in
general seem to be very sensitive to 2,4-D. Moderate exposure of honey bees to 2,4-D severely impaired
reproduction. Toxicity to birds is low to moderate(28). However, the ACP noted "Insufficient data are
available to fully assess the safety of in or near water uses to aquatic life" and "Approval holders must
generate a number of studies using 2,4-D and its derivatives in order to allow a full assessment of the risk
to wildlife to be made."

Conclusions
2,4-D is a pesticide that has been heavily used in agriculture all over the world for some fifty years or more.
Alarmingly the ACP Evaluation has highlighted a large number of major data gaps-covering human health
effects, aquatic and wider environmental risk. In addition to the number and the range of these data gaps,
there continue to be concerns about long term adverse effects of 2,4-D on human health and water
pollution.

References
1. The Pesticide Manual 10th Edition, British Crop Protection Council/Royal Society of
Chemistry, 1994.
2. Generic Pesticides-the markets. Agrow report DS100, PJB Publications, Richmond, UK, 1994.
3. Post-emergence herbicides, Agrow report, PJB Publications Ltd, Richmond, UK, 1995.
4. Chemical Regulation Reporter, p 44, Bureau of National Affairs, US, 4 September 1993.
5. Produce Studies, Non agricultural use of pesticides in England and Wales, DoE, November
1996.
6. Pesticide usage survey report 119: Grassland and fodder crops in Great Britain 1993; and
Pesticide usage survey report 115: Orchards and fruit stores in Great Britain 1992, MAFF, 1994.
7. Pesticide usage survey report 100: Review of usage of pesticides in agriculture and horticulture
throughout Great Britain 1984-94, MAFF, 1997.
8. Op cit. 3.
9. International Programme on Chemical Safety, The WHO recommended classification of
pesticide by hazard and guidelines to classification 1996-97.
10. Extoxnet data sheet on 2,4-D, Pesticide Mange-ment Programme, Cornell University, US,
1994.
11. Shearer, Ruth W, Health effects of 2,4-D herbicide, in 2,4-D Information Packet, North West
Coalition for Alternatives to Pesticides, January 1990.
12. Evaluation on 2,4-dichlorophenoxyacetic acid salts and esters, MAFF, March 1993.
13. Op. cit. 10.
14. Op. cit. 12.
15. Interdepartmental Executive Committee on Pest Management, 2,4-D Re-evaluation update
and label improvement program, Plant Industry Directorate, Canada, 23 November, 1994.
16. IARC monographs on the evaluation of carcinogenic risks to humans: An updating of IARC
Monographs volumes 1 to 42. Supplement 7, WHO, Lyon, France 1987.
17. O'Brien, Mary, Jury Charges Dow $1.5 million for 2,4-D caused death of forest worker,
Journal of Pesticide Reform, 1987, 7: 4(30).
18. Veterans and Agent Orange-Update 1996, National Academy Press, US, 1996.
19. Ibid, pp35-87.
 20. Environmental Health Criteria 29, 2,4-Dichlorophenoxyacetic acid (2,4-D), IPCS, Geneva,
1984.
21. Colborn, T, et al. Developmental effects of endocrine disrupting chemicals in wildlife and
humans, Env. Health Perspectives 101:378-384, 1993.
22. Op. cit. 10.
23. Montgomery, John H, Agrochemicals desk reference, Lewis Publishers, 1993.
24. Pesticides in water: Report of the working party on the incidence of pesticides in water,
HMSO, May 1996.
25. Drinking Water Inspectorate, Drinking water 1953: A report of the Chief Inspector, HMSO,
1996.
26. Op. cit. 10.
27. Pesticides in the Aquatic Environment, 1995, Environment Agency, March 1997.
28. Op. cit. 10.

In this study we investigated the potential of phenoxy resins as compatibilizers in the blending of two high-

volume engineering thermoplastics—polyamide 6 (PA6) and polybutylene terephthalate (PBT), in an effort to

establish the usefulness of blending as a method of recycling of mixed plastic wastes. It was found that

phenoxy resins formed miscible blends with PBT, formed grafted copolymers with PBT through ester

exchange reactions, and—though formed immiscible blends with PA6—produced energetic interactions in

the form of hydrogen bonding with PA6. The ternary blend systems of 70 parts PA6, 30 parts PBT, and

respectively 5, 10, and 30 parts phenoxy resins, all by weight, revealed at two-phase nature—PA6 as the

continuous phase and miscible blends of PBT and phenoxy resins as the dispersed phase—and were found

to be stable to phase coarsening by annealing with mechanical properties at least as good as those of the

component polymers.

I-Chemicals-J-Phenoxy Herbicides-1
THE PRODUCTION OF PHENOXY HERBICIDES
Phenoxy herbicides are of great significance in New Zealand because of their strength
and
selectivity. They include a group of herbicides consisting of a benzyl ether, of which the
best known are 2,4,5-T and 2,4-D. This article focuses on 2,4-D and the herbicide
formulations made from it.
2,4-D is manufactured from 2,4-dichlorophenol in a four step process:
Step 1 - Phenol neutralisation
The (acidic) phenol is neurtralised with caustic soda.
2,4-dicholorophenol + NaOH → sodium dichlorophenate (NaDCP) + H2O + heat
Step 2 - NaMCA production
Sodium monochloroacetate is produced in another exothermic reaction.
monochloroacetic acid (MCAA) + NaOH → sodium monochloroacetate (NaMCA) +
H2O
Step 3 - Condensation
The NaDCP is condensed with NaMCA to produce Na 2,4-D - the sodium salt of 2,4-D.
NaDCP + NaMCA → sodium 2,4-dichlorophenoxyacetate + NaCl
Step 4 - Final ageing
The Na 2,4-D is aged by the slow addition of NaOH to ensure that the phenol content is
less than 0.5 w/w%.
This Na 2,4-D is then converted to its ethyl hexyl ester, emulsified and sold as a
herbicide.
INTRODUCTION
Phenoxy herbicides, such as those shown below, and have been in use since 1944. 2,4,5-
T
and 2,4-D were synthesised by Pokorny in 1942, and 2,4-D has been manufactured in
New
Zealand since 1962. It is currently the most significant phenoxy herbicide in New
Zealand.
2,4,5-T was made by Dow AgroSciences in New Zealand until November 1987 and sold
until
December 1988, but it is no longer sold here due to its environmentally hazardous
properties.
OCH2COH
Cl
Cl
Cl
O
OCH2COH
CH3
Cl
O
OCH2COH
Cl
Cl
O
2,4,5-T MCPA 2,4-D
I-Chemicals-J-Phenoxy Herbicides-2
Uses of 2,4-D
2,4-D is a highly selective herbicide, affecting broad-leaved weeds (e.g. clover) and
woody
vegetation, while being harmless toward cereals. Table 1 lists the herbicides made by
Dow
AgroSciences that contain 2,4-D and their uses.
Table 1 - A selection of commercial herbicides containing phenoxy herbicides
Commercial name Phenoxy
component
Other
component(s)
Use
2,4-D Amine
amine salt of 2,4-D
.
Broadleaf weeds in cereal
areas
2,4-DB Herbicide
sodium salt of
2,4-DB
.
Broadleaf weeds in
lucerne and new pasture
Banvine
amine salt of 2,4-D
amine salt of
dicamba
Broadleaf weeds in turf
and waste areas
2,4-D Ethyl hexyl
ester
ethyle hexyl ester of
2,4-D
.
Broadleaf weeds in pasture
MCPA
potassium salt of
MCPA
.
Broadleaf weeds in
pastures and cereals
MCPB
sodium salt of
MCPB
.
Broadleaf weeds in
pastures and some crops
Tordon 50-D
amine salt of 2,4-D
amine salt of
picloram
Perennial broadleaf weeds
Reactions
2,4-D can react in esterification, acid base and amine salt forming reactions as follows:
C
CH3
HO CH3
CH3
+
OCH2COH
Cl
Cl
O
H+
OCH2COC(CH3)3
Cl
Cl
O
OCH2COH
Cl
Cl
O
+ NaOH
OCH2CONa
Cl
Cl
O
I-Chemicals-J-Phenoxy Herbicides-3
OCH2COH
Cl
Cl
O
+ NH3
OCH2CO- +NH4
Cl
Cl
O
These reactions are used to synthesise herbicides with specific properties for commercial
use.
THE MANUFACTURING PROCESS
Phenoxy herbicides were made by Dow AgroSciences in New Zealand until December
1997.
The process involved three stages. Firstly, 2,4-dichlorophenoxyacetate was produced.
This
was then converted into a variety of pure products, which in turn were formulated into
commercial herbicides.
Production of 2,4-dichlorophenoxyacetate
2,4-dichlorophenoxyacetic acid (2,4-D) is produced from its sodium salt, which is in turn
manufactured from 2,4-dichlorophenol in a four step process, and is converted into a
variety
of products. The conversion of 2,4-dichlorophenol (DCP) into sodium 2,4-
dichlorophenoxy
acetate1 (Na 2,4-D) can be broken into four steps: neutralisation; NaMCA production;
condensaton reaction; and ageing.
Step1 - Phenol neutralisation
The neutralisation step refers to the neutralisation of DCP with caustic soda. Sufficient
caustic soda is added to create alkaline conditions although not all of the DCP is
neutralised
during this step. The neutralisation is exothermic with heat removed through a cooling
jacket
on the reactor. The product from this neutralisation is sodium dichlorophenol (NaDCP).
Cl
Cl
OH
+ NaOH Cl
Cl
ONa
+ H2O + heat
2,4-dichlorophenol caustic sodium dichlorophenate
(DCP) soda (NaDCP)
Step 2 - NaMCA production
NaMCA is produced by the neutralisation of monochloroacetic acid (MCAA) with
caustic
soda, which is an exothermic reaction. The heat of reaction is removed by reacting these
two
chemicals in a heat exchanger prior to adding the NaMCA to the reactor.
1Noteon nomenclature: sodium phenolate and sodium phenate are the same species (a benzene ring with
an ONa substituent) whereas phenoxide is the anion (a benzene ring with an O- substituent).
I-Chemicals-J-Phenoxy Herbicides-4
ClCH2COH
O
+ NaOH ClCH2CO- +Na
O
+ H2O + heat
monochloroacetic sodium monochloro
acid (MCAA) acetate (NaMCA)
Step 3 - Condensation
The NaMCA then condenses the NaDCP to produce Na 2,4-D. This reaction is highly
exothermic with the heat of reaction removed through a cooling jacket on the reactor.
ONa
Cl
Cl
+ ClCH2CO- +Na
O
OCH2CONa
Cl
Cl
O
+ NaCl
sodium sodium monochloro sodium 2,4-dichloro
dichlorophenate acetate (NaMCA) phenoxy acetate
(NaDCP)
Unwanted side reactions do occur but are kept to a minimum through the choice of
optimum
operating conditions. NaMCA and water undergo a reaction that produces sodium
glycollate
and hydrochloric acid.
HOCH2CO- +Na
O
ClCH2CO- +Na + H2O
O
+ HCl
sodium monochloro sodium glycollate
acetate (NaMCA)
Due to the alkaline nature of the reaction mixture, any HCl formed is immediately
neutralised
with caustic soda to sodium chloride and water. NaMCA also reacts with caustic soda to
produce sodium glycollate and water. For this reason the stoichiometric ratio of MCAA
and
caustic soda is strictly controlled to avoid build-up of excess caustic soda.
HOCH2CO- +Na
O
ClCH2CO- +Na + NaOH
O
+ NaCl
sodium monochloro sodium glycollate
acetate (NaMCA)
Step 4 - Final ageing
As the raw materials are used up, the speed of reaction slows because the unreacted
material
is at a low concentration in the reaction mass. An ageing period is required to ensure the
phenol content of the Na 2,4-D is below 0.5 w/w %. During the ageing step, caustic soda
is
slowly added to the reaction mass to react with any remaining phenol. The addition rate is
controlled so that alkaline conditions are maintained in the reactor.
I-Chemicals-J-Phenoxy Herbicides-5
Conversion to active species
The production of 2,4-D is the first step in the production of the following actives:
DMA 6 sequestered (i.e. it will not form complexes with hard water)
2,4-D amine technical
2,4-D ethyl hexyl ester
2,4-D concentrate
2,4-D wet acid
These actives are then used as the base for several herbicides that are formulated on site.
Different processes are used to convert 2,4-D into the various actives. The process of
converting 2,4-D into 2,4-D ethyl hexyl ester is described below as an example. In
producing
all of the actives listed above, 2,4-D undergoes an acidification, and then either a
neutralisation or an esterification depending on which active is desired.
Production of 2,4-dichlorophenoxy ethyl hexyl ester
The conversion of 2,4-D into 2,4-D ethyl hexyl ester involves two stages; an acidification
stage, and an esterification stage.
Step1: acidification
The purpose of the acidification process in the production of 2,4-D ethyl hexyl ester is
firstly
to provide the means to separate the product of the reaction step from undesirable
components, such as sodium glycollate and sodium chloride; and secondly to transform
the
reaction mass to the acidic state from which the esterification can take place.
The four steps in the acidification and their function are:
· Acidification / Separation - involves acidifying the reaction mass, and mixing, settling
and
separating the aqueous layers that form.
· First water wash - removing undesireable components from the product.
· Second water wash - removing further undesireable components from the product.
· Xylene wash - product which is miscible in the separation and wash waters is removed
with
xylene.
The acidification step involves adding water, sulphuric acid, 2-ethyl hexanol and xylene
to
the 2,4-D reaction mass. During the acidification step the 2,4-D is converted to 2,4-D
acid.
Separation of the product from the undesirable side components is achieved by exploiting
the
differing solubility’s of the components in water and xylene. The undesirable components
are
all very soluble in water, but insoluble in xylene; whilst the 2,4-D acid is soluble in
xylene
but only slightly soluble in water. The mixture is agitated for a period and when the
agitator
is stopped, two distinct layers form - a water layer, which contains most of the
undesirable
components, and a product layer that contains the 2,4-D acid and only a small amount of
the
undesirable components.
I-Chemicals-J-Phenoxy Herbicides-6
O.CH2.C.ONa
O
Cl
Cl + ½H2SO4
O.CH2.C.OH
O
Cl
Cl + ½Na2SO4
sodium 2,4-dichloro sulphuric 2,4-dichlorophenoxy
phenoxy acetate acid acetic acid
The small amount of undesirable components that remain in the xylene layer after the
acidification are removed with two water washes.
To ensure that all of the 2,4-D acid is collected, the water layers from the acidification
and
wash stages are treated with xylene to remove any 2,4-D acid that may have been soluble
in
the water.
Step2: esterification
The esterification of 2,4-D acid is the final step in the production of the herbicide active
2,4-
D ethyl hexyl ester. During this stage 2-ethyl hexanol is added to the 2,4-D acid together
with the xylene from the xylene wash. A catalyst is also added to aid the esterification.
The
esterification reaction is carried out at a high temperature, which is achieved by applying
steam to the vessel jacket.
OCH2COH
Cl
Cl
O
CH3(CH2)3CHCH2OH
CH2CH3
+
OCH2COCH2CH(CH2)3CH3
Cl
Cl
O CH2CH3
+ H2O
2,4-dichlorophenoxy 2-ethyl hexanol 2,4-D ethyl hexyl ester
acetic acid
In common with esterification reactions generally, this reaction is reversible - that is
water
reacts with the ester to give acid plus alcohol - this reverse reaction is known as
hydrolysis.
It is important to remove the water that is formed to prevent the hydrolysis step from
occurring. Water is removed with the aid of xylene. Water, xylene and 2-ethyl hexanol
form
an azeotrope which is continuously distilled off and then cooled in a condenser. When
cooled, this mixture splits into two phases - a water phase that contains a small amount of
2-
ethyl hexanol, and a xylene / alcohol layer. The water layer is run off into another vessel
whilst the xylene / 2-ethyl hexanol layer is recycled to the reactor. This cycle continues
until
esterification is complete.
Once the esterification is complete, a vacuum is applied to the reactor. The reason for
applying the vacuum is that the xylene and 2-ethyl hexanol boil at a much lower
temperature
when under a vacuum, requiring less energy to be applied to the reactor to boil off the
components. The xylene and 2-ethyl hexanol that is distilled off is no longer recycled to
the
I-Chemicals-J-Phenoxy Herbicides-7
reactor but is drained into another vessel. The reactor remains under vacuum until almost
all
the xylene and 2-ethyl hexanol is driven off the reaction mixture.
Analyses of the product include estimates of:
Total ester concentration
Total free acid, which includes unreacted 2,4-D acid and phenol
Specific gravity
A gas/liquid chromatographic scan is run to check for impurities. The GLC indicates the
ester concentration and the amount of xylene that is left in the ester at the end of the
reaction.
Formulation - making a user product
2,4-D ethyl hexyl ester is largely water-insoluble, and so cannot be usefully mixed with
water
on its own. This product is marketed in an emulsifiable form - an "emulsifiable
concentrate"
or "EC".
Water is the obvious dilutant for spraying purposes, being the cheapest, most readily
available and innocuous medium. It is therefore desirable to set up the product in a form
which will emulsify readily in water.
Even if the product is an excellent quality ester, its biological efficiency, i.e. its useful
efficiency, will be seriously restricted if it is not formulated so as to emulsify freely in
water.
2,4-D ethyl hexyl ester formulations are composed of: a solvent, the ester and an
emulsifier.
The emulsifiers used are usually a blend of anionic and non-ionic agents, the mixture
being
chosen so as to achieve desirable emulsion properties in the presence of either hard or
soft
water - as would be commonly found on farms throughout the country.
The properties of a mixture which come under close scrutiny, especially when a new
formulation is being established, include:
• Specific gravity
• Clarity
• Flash point (temperature at which vapour presence becomes high enough for an
explosive mixture to be formed with air)
• Chemical stability of the EC and of the emulsion
• Physical stability of the emulsion
• Stability of the EC under normal conditions of storage with particular reference to
precipitation’s or solidification
• Spontaneity of emulsification of the EC.
Each batch of 2,4-D emulsifiable concentrate produced is tested in terms of properties
such as
these.
I-Chemicals-J-Phenoxy Herbicides-8
ENVIRONMENTAL IMPLICATIONS
The various products containing 2,4-D are used as herbicides. They have low acute
toxicity
to animals, but are toxic to fish. There should be no adverse environmental effect if used
in
accordance with label instructions. The problems associated with the related phenoxy
herbicide 2,4,5-T relate to TCDD (2,3,7,8-tetrachlorodibenzo-D-dioxin) - an impurity
that it
commonly contains which is absent in 2,4-D.
The manufacture of these products has little effect on the environment. Waste air and
aqueous streams are treated before discharge to the environment. Other wastes are
incinerated in an approved high temperature incinerator.
All rain water that falls on site is retained in ponds on site until analysis confirms that it is
safe to release it.
Original article compiled by Andrew Syme (Dow AgroSciences). Edited by Heather
Wansbrough with reference to:
• Bovey, Rodney W. and Young, Alvin L.; The Science of 2,4,5-T and Associated
Phenoxy Herbicides; John Wiley and Sons; 1980
• DowElanco; Product Guide: Products for Agriculture and Horticulture, 6th ed.;
DowElanco; 1993
• Ivon Watkins-Dow Ltd.; 2,4,5-T and 2,4-D. The Facts about Phenoxy Herbicides; Ivon
Watkins-Dow Ltd.; 1980
• Windholz, Martha (editor); The Merck Index: an Encyclopedia of Chemicals, Drugs
and Biologicals (10th edition); Merck and Co., Inc.; 1983

116
*Journal Article 3099, Oklahoma Agricultural Experiment Station.
†NSF Undergraduate Research Participant and Professor of Agronomy, respectively.
Proc. Okla. Acad. Sci. 57: 116-118 (1977)
CHEMISTRY OF TWO CLAY SYSTEMS AND THREE
PHENOXY
HERBICIDES*
Robin Cason and Lester W. Reed†
Department of Agronomy, Oklahoma State University
Organic pesticides, particularly herbicides, usually find their way into the soil. Phenoxy herbicides
when added to soil
may react with the soil clay minerals. This study concerns such reactions. Results obtained indicate
these organic molecules are
strongly sorbed by kaolinitic and montmorillonitic clay minerals to an extent of the cation-exchange-
capacity (C.E.C.) of the
clay mineral. X-ray diffraction study showed that the phenoxy herbicides were not sorbed on the
interlayer surfaces of the clay
minerals, since the basal spacings were unaltered; they were probably bound at the edges of the
particles at charged sites.
INTRODUCTION
Herbicides are applied to soils in an attempt to control undesirable plants. Although the
user intends the
herbicide to react with the plant, ultimately most of the chemical enters the soil. Some
herbicides react with soil
clay in a predictable manner; however, many are nonpolar or weakly polar compounds
and, therefore, do not
interact with soil clays in a straightforward manner.
Mineral soils are complex heterogeneous mixtures of inorganic silicates, silica (quartz),
water, traces of
soluble salts, organic matter, and pore space. The reactive portion of the soil, in a
chemical sense, is the clay and
soil organic matter. The clay present in the soil resembles the clay minerals often found
in quite pure geological
(mineral) deposits. These minerals may be used as experimental materials in an attempt
to approximate
conditions which may be encountered in soils (1). That is, soils which contain major
quantities of a particular
type of clay mineral may be compared to some so-called "pure clay minerals" in a general
way.
The objective of this study was to determine the mode of sorption of organic herbicides
by clay minerals.
The term "sorption" used in this report refers both to adsorption and absorption.
MATERIALS AND METHODS
The three phenoxy herbicides used in this study are 2,4,5-trichlorophenoxyacetic acid
(2,4,5-TA),2-
(2,4,5-trichlorophenoxy) - propionic acid (2,4,5-TP), and 2,4-dichlorophenoxyacetic acid
(2,4-D).
Clay minerals selected for this study were fine Georgia kaolinite <0.2 μm, coarse Georgia
kaolinite 2-0.2
μm, and fine (< 0.2 μm) Camargo bentonite from northwestern Oklahoma (1). All were
partitioned with the
supercentrifuge and saturated with Mg++ (2).
Cation exchange capacity determination.
Cation-exchange capacity (C.E.C.) was determined for each clay mineral by treating 10
ml of a clay mineral
suspension with 30 ml of 1N CaCl2 in three successive 10-ml washings. The excess salt
was removed by
washing the clays seven times with deionized water until excess CaCl2 was removed, as
indicated by a negative
AgNO3 test for chloride in the last three washings. The Ca was replaced by four washings
with 10-ml portions
of 1N NaCl. The extract solution thus produced was brought to a final volume of 100 ml
with distilled water and
its Ca content measured by Versene titration as described by Jackson (2) and as follows.
Fifty milliliters of each sample were transferred to 100 ml pyrex beakers. Ten milliliters
of a
NH4Cl-NH4OH buffer was added to bring the solution to pH 10. Five drops of
Eriochrome Black T indicator
solution were added to the solution and it was titrated with EDTA (Versene) to a blue
endpoint. The C.E.C. in
milliequivalents was calculated (3) as
meq/100g = ml Versene × N X 100/sample wt. in g.
117
Herbicide determination.
The herbicide solutions were prepared by adding 0.001 mole of each one to 95% ethanol
and bringing the
volume to 100 ml.
2,4,5-TA 0.255 g/100 ml
2,4,5-TP 0.269 g/100 ml
2,4-D 0.221 g/100 ml
Standard curves were prepared by diluting the stock solutions 1:10 with 95% ethanol and
then with more
ethanol to make further dilutions of 1:2, 1:4, 1:6, and 1:8, and measuring absorption of
samples on a
Perkin-Elmer Model 202 ultraviolet-visible spectrophotometer, with 95% ethanol as a
reference. The standard
peaks were obtained at 290 nm, 293 nm, and 291 nm for 2,4,5-TA, 2,4,5-TP, and 2,4-D,
respectively.
Enough stock solution of each herbicide was added to 10 ml of each clay suspension to
supply one, two,
and three millimoles of herbicide per milliequivalent of the previously determined C.E.C.
The mixtures were
shaken on a reciprocal shaker for eight hours and then centrifuged for twenty minutes at
10,000 RPM to give
clear supernatant solutions. The concentrations of unsorbed herbicide were determined by
taking an aliquot
from the supernatant solution and determining the herbicide with the spectrophotometer.
Clay mineral samples were mounted on ceramic slides and examined by the X-ray
diffraction technique
(1,3) to determine basal or interlayering sorption of herbicide molecules on the clay
particle.
RESULTS AND DISCUSSION
The cation exchange capacity of the clay minerals is shown in
Table 1.
Sorption of herbicides by Georgia kaolinite.
Georgia kaolinite is a nonexpanding-type clay mineral. The
organic herbicides were probably sorbed on the edges of the clay
particles rather than in the interior of the structure (4). This
sorption is probably due to the ionic charges of the clay.
The extent of sorption of the organic herbicides by Georgia
kaolinite 2-0.2 μm is shown in Table 2. As this shows, variation in
levels of organic herbicides applied had no effect on percent
sorption; in all cases the organic herbicides were sorbed in
amounts close to the C.E.C. of the clay.
The results for Georgia kaolinite <0.2 μm also showed that
organic herbicides were sorbed efficiently to the extent of close to
one millimole per milliequivalent of C.E.C. of the clay. Percent
sorption of organic herbicides by this clay sample is shown in
Table 3. Again the use of different levels had no effect on the
extent of sorption.
Sorption of herbicides by Camargo bentonite <0.2 μm.
The Camargo bentonite had a high cation exchange capacity
and a high sorptive capacity due to internal charge deficits. The
degree of sorption of 2,4,5-TA, 2,4,5-TP, and 2,4-D by this
bentonite is shown in Table 4. As this shows, the herbicides
applied were sorbed to the same extent as on the kaolinite in terms
of C.E.C.
X-Ray diffraction spacing of Georgia kaolinite.
Treatment of Georgia kaolinite 2-0.2 μm with 2,4,5-TA,
2,4,5-TP, and 2,4-D had no
118
effect on the X-ray basal spacings. Results are shown in Table 5.
This shows the d-spacing to be the same as the d-spacing of
untreated kaolinite.
Since kaolinite is a nonexpanding type of clay mineral,
organic herbicides were sorbed around the edges of the clay
particle, owing to broken-bond charges there, and did not increase
or decrease the 2θ value or the d-spacing value.
Treatment of Georgia kaolinite <0.2 μm fraction with
2,5,5-TA, 2,4,5-TP, and 2,4-D had no effect on the X-ray basal
spacing as shown in Table 6. This again shows that the d-spacing
(basal) of the untreated clay was the same as that obtained with
different amounts of organic herbicides.
X-Ray diffraction pattern of Carnargo bentonite.
The X-ray diffraction spacings of Camargo bentonite <0.2
μm are shown in Table 7. The results show that the d-spacing of
the untreated bentonite was the same as the d-spacings obtained
after treatment with different amounts of herbicides, whereas
glycerol treatment produced the known increase in spacing. The
herbicides were probably sorbed on the edges of the clay particles
rather than within the interlayer structure (6). This indicates that
practically none of the interlayer free water in the structure was
displayed by the herbicide.
REFERENCES
1. G. KIDDER and L. W. REED, Clays Clay Min. 20: 13-20 (1972).
2. M. L. JACKSON, Soil Chemical Analysis, 1st ed., Prentice-Hall, Inc., Englewood
Cliffs, N.J., 1958.
3. M. L. JACKSON, Soil Chemical Analysis-Advanced Course, published by the author,
Madison, Wis., 1956.
4. G. W. BAILEY and J. D. WHITE, J. Agr. Food Chem. 12: 324-332 (1964).
5. R. L. GRIM, Clay Mineralogy, 2nd ed., McGraw-Hill Book Co., New York, N.Y.,
1968.
6. C. I. HARRIS and G. F. WARREN, Weeds 12: 120-128 (1964).

Overview of the toxic effects of 2,4-D

January 2005
Prepared by:
412-1 Nicholas St.
Ottawa, ON
K1N 7B7
613-241-4611
Sierra Club of Canada Overview of the toxic effects of 2,4-D
January 2005 1
Introduction
2,4-D (2,4-dichlorophenoxyacetic acid) is a common herbicide used around the home and
garden,
on golf courses, ball fields, parks, in agriculture and forestry. Agricultural uses include
pasture
land, wheat, corn, soybeans, barley, rice, oats, and sugar cane. In Canada, there are
currently 205
registered products containing 2,4-D.1
Despite industry efforts claiming the safety of this chemical, there is a large body of
evidence
indicating major health effects, from cancer to immunosuppression, reproductive damage
to
neurotoxicity. Environmental contamination, particularly in wetlands has also been
demonstrated,
in direction infringement of the Fisheries Act R.S., c. F-14, s. 36.
This paper aims to provide an overview of the scientific body of evidence demonstrating
the
toxic effects of 2,4-D.
Health Effects
In mammals, 2,4-D disrupts energy production (Zychlinkski & Zolnierowicz, 1990),
depleting
the body of its primary energy molecule, ATP (adenosine triphosphate) (Palmiera et al.,
1994).
2,4-D has been shown to cause cellular mutations which can lead to cancer. This mutagen
contains dioxins, a group of chemicals known to be hazardous to huma n health and to
the
environment (Littorin, 1994).
Numerous epidemiological studies have linked 2,4-D to non-Hodgkin’s lymphoma
(NHL)
among farmers (Zahm, 1997; Fontana et al, 1998, Zahm & Blair, 1992, Morrison et al.
1992).
Multi-center studies in Canada and in Sweden of members of the general public found a
30-50%
higher odds of 2,4-D exposure among people with NHL(McDuffie et al. 2001, Hardell &
Eriksson, 1999, Sterling & Arundel, 1986).
The teratogenic, neurotoxic, immunosuppressive, cytotoxic and hepatoxic effects of 2,4-
D have
been well documented (Blakely et al., 1989; Sulik et al, 1998; Barnekow et al., 2000;
Rosso et al.,
2000; Venkov et al., 2000; Charles et al., 2001; Madrigal- Bujadar et al., 2001; Osaki et
al., 2001;
Tuschl & Schwab, 2003).
Other researchers publishing in the open scientific literature have reported oxidant effects
of 2,4-
D, indicating the potential for cytotoxicity or genotoxicity. For example, Bukowska
(2003)
reported that treatment of human erythrocytes in vitro with 2,4-D at
250 and 500 ppm resulted in decreased levels of reduced glutathione, decreased activity
of
superoxide dismutase, and increased levels of glutathione peroxidase.56 These significant
changes in antioxidant enzyme activities and evidence of oxidative stress indicate that
2,4-D
should be taken seriously as a cytotoxic and potentially genotoxic agent.
1 PMRA, Electronic Labels: Search and Evaluation (ELSE). http://eddenet.pmra-arla.gc.ca/4.0/4.01.asp.
Accessed
January 13, 2005.
Sierra Club of Canada Overview of the toxic effects of 2,4-D
January 2005 2
2,4-D causes significant suppression of thyroid hormone levels in ewes dosed with this
chemical
(Rawlings et al., 1998). Similar findings have been reported in rodents, with suppression
of
thyroid hormone levels, increases in thyroid gland weight, and decreases in weight of the
ovaries
and testes (Charles et al., 1996). The increases in thyroid gland weight are consistent with
the
suppression of thyroid hormones, since the gland generally hypertrophies in an attempt to
compensate for insufficient circulating levels of thyroid hormones. Thyroid hormone is
known to
play a critical role in the development of the brain. Slight thyroid suppression has been
shown to
adversely affect neurological development in the fetus, resulting in lasting effects on
child
learning and behavior (Haddow et al., 1999).
2,4-D causes slight decreases in testosterone release and significant increases in estrogen
release
from testicular cells (Liu et al., 1996). In rodents, this chemical also increases levels of
the
hormones progesterone and prolactin, and causes abnormalities in the estrus cycle
(Duffard et al.,
1995). Male farm sprayers exposed to 2,4-D had lower sperm counts and more spermatic
abnormalities compared to men who were not exposed to this chemical (Lerda & Rizzi,
1991). In
Minnesota, higher rates of birth defects have been observed in areas of the state with the
highest
use of 2,4-D and other herbicides of the same class. This increase in birth defects was
most
pronounced among infants who were conceived in the spring, the time of greatest
herbicide use
(Garry et al, 1996).
2,4-D also interferes with the neurotransmitters serotonin and dopamine. In young
organisms,
exposure to 2,4-D results in delays in brain development and abnormal behavior patterns,
including apathy, decreased social interactions, repetitive movements, tremor, and
immobility
(Evangelista de Duffard et al, 1995). Females are more severely affected than males.
Rodent
studies have revealed a region-specific neurotoxic effect on the basal ganglia of the brain,
resulting in an array of effects on critical neurotransmitters and adverse effects on
behavior
(Bortolozzi et al., 2001).
A peer-reviewed, developmental neurotoxicity study demonstrated severe neurotoxicity
in young
rats exposed to 2,4-D from postnatal days 12 to 25 at doses of 70 mg/kg/day. These pups
showed
decreases in GM1 level, diminution in myelin deposition and alterations in all behavioral
tests at
all doses (Rosso et al, 2000). This herbicide specifically appears to impair normal
deposition of
myelin in the developing brain (Duffard et al., 1996). The neurotoxic and anti thyroid
effects of
2,4-D make it highly likely that fetuses, infants, and children will be more susceptible to
longterm
adverse health effects from exposure to this chemical although they may appear normal at
birth.
Young animals can also be exposed to 2,4-D through maternal milk. Recent research has
revealed that 2,4-D is excreted in breast milk, thereby resulting in potentially significant
exposures to the nursling. The researchers detected 2,4-D residues in stomach content,
blood,
brain and kidney of 4-day-old neonates fed by 2,4-D exposed mothers (Sturtz et al.,
2000). When
maternal exposures stopped, the chemical continued to be excreted in maternal milk for a
week.
Thus, postnatal exposures to this chemical during the critical period for development of
the
infant brain are of serious scientific concern.
Sierra Club of Canada Overview of the toxic effects of 2,4-D
January 2005 3
Agricultural Workers
Workers applying chlorinated phenoxy herbicides frequently have nervous system
disorders, are
exposed to a higher risk of soft tissue sarcoma, and show symptoms of hormonal and
internal
organ irregularities. (Kogevinas, 1995; National Research Council of Canada, 1983). A
study of
farmers in Alberta, Saskatchewan and Manitoba linked use of 2,4-D to an increased
incidence of
prostate cancer (Morrison et al, 1993). An Italian study by Miligi et al (2003) showed that
an
associated between NHL and 2,4-D in women. Hardell & Eriksson (1999) also
demonstrated the
link between exposure of 2,4-D and NHL. Their research identified a latency period
between
exposure and diagnosis of NHL, which could be a reason why there is conflicting
research on the
issue.
The risk to farm workers is pronounced because of the use of sunscreen. Agricultural
workers are
encouraged to wear sunscreen to protect their skin from UV-related skin cancer.
However,
studies have shown that the use of sunscreen increases the rates of penetration of 2,4-D.
This has
also been shown for the insect repellant DEET (Windheuser et al, 1982). One study
demonstrated 14% palmar absorption of 2,4-D after skin application of DEET (Moody et
al.,
1992). Studies have also shown that most commercial sunscreen formulations enhance
the
penetration of 2,4-D through hairless mouse skin. One such study found that sunscreens
increase
penetration of 2,4-D by over 60 percent, from an average penetration of 54.9% to 86.9%
(Pont et
al., 2004). Another study found more than a doubling in absorption from an average
penetration
of 39.1% for the no sunscreen control to 81.0% for mice pre-treated with Neutrogena Oil
Free
Sunscreen (Brand et al., 2002). These results in the mouse appear also to be relevant to
humans
(Pont et al., 2004). In addition to penetration enhancement due to commonly-applied
topical
products, one study in rodents has demonstrated a 2.2- fold enhancement in dermal
absorption
after regular ethanol consumption over a 6 to 8 week period (Brand et al., 2004).
This scenario was not examined by the USEPA in its evaluation of 2,4-D. However, it is
a reality
of agricultural workers and must be examined. It is important to note that the reevaluation
document produced by the USEPA also did not use any form of occlusion over the
applied 2,4-D.
Therefore the effect of 2,4-D that soaks clothing, or is subsequently covered by clothing
or
gloves would not be adequately assessed. Existing research on other chemicals indicates
that
occlusion is known to significantly enhance skin absorption of dermally-applied materials
(Riviere et al., 2003). As much of the reevaluation process is harmonized between
countries, this
could be the case in the PMRA’s evaluation as well, and it is crucia l that these issues are
not
overlooked.
Children living in agricultural communities are heavily exposed to pesticides, whether or
not
they work in the fields (Lu et al., 2000; Fenske, 1997). Farm children come in contact
with
pesticides through residues from their parents’ clothing, dust tracked into their homes,
contaminated soil in areas where they play, food eaten directly from the fields, drift from
aerial
spraying, contaminated well water, and breast milk. Furthermore, farm children often
accompany
their parents to work in the fields, raising their pesticide exposures even higher.
Household Use
Sierra Club of Canada Overview of the toxic effects of 2,4-D
January 2005 4
Perhaps the most documented effect of household use of 2,4-D is its association of
exposure with
cancer in canines. Particularly the study by Hayes et al (1991) has implicated 2,4-D with
an odds
ratio of 1.32 linking malignant lymphoma and 2,4-D exposure. This study was reviewed
by a
number of industry sponsored initiatives, and the authors of the original study released
their
response in 1995 which demonstrated that their scientific methods were sound and that
the study
had indeed demonstrated this increased risk of malignant lymphoma.
These risks are elevated when one discovers that homeowners using 2,4-D are likely to
track the
pesticide into their home where it is expected to persist for up to one year (Nishioka et al.
1999).
This persistence is seen after a single turf application at a concentration of approximately
0.5μg/g (Nishioka, 1996).
Surrounding and in the home is also where most exposure to children will occur. The
levels of
exposure to small children are pronounced for dermal exposure and have not been studied
for
dermal penetration of 2,4-D. We do know that the skin surface area of an infant per unit
of body
weight is double that of an adult and that all studies which have investigated dermal
exposures to
pesticides in children have found that this is a major route of exposure. Also, hands moist
with
saliva collect about 100 times more pesticide residue than dry hands, and children’s
hands are
much more likely to be moist. A study of rats perinatal exposure of 2,4-D did not express
effects
of exposure until adulthood (Garcia et al., 2001). This demonstrates the insidious nature
of the
compound, and the enormous threat it poses to children.
Given that the “PMRA considers the unique biological characteristics and exposure
patterns of
children in its risk assessments,” we trust that the studies such as those by Nishioka et al.
(1996,
1999) and that of Lu et al., (2000) and Fenske (2003) will be included in the assessment
process.
Environmental Effects
2,4-D is a moderately persistent chemical with a half- life between 20 and 200 days.
Unfortunately, the herbicide does not affect target weeds alone. It can cause low growth
rates,
reproductive problems, changes in appearance or behaviour, or death in non-target
species.
Due to the widespread use of 2,4-D on agricultural land, the environmental effects of this
use are
emerging in scientific studies. Donald et al. (1999) found agricultural pesticides in
wetlands, and
2,4-D was the most commonly detected pesticide. Although its concentrations in
wetlands
exceeded the guidelines in less than 1% of the wetlands, these guidelines are created in
isolation,
not accounting for the synergistic effects of pesticides. For example, Forsyth et al. (1997)
found
synergistic effects of picloram and 2,4-D on macrophytes. The chemical will also be
carried by
run-off into the local river systems. This has been demonstrated here in Ottawa, where a
city
report on pesticide monitoring of local tributaries showed that 60% of all samples
contaminated
with phenoxy herbicides. Due to the numerous acceptable uses of 2,4-D, it is likely that
the
majority of watersheds in rural and urban Canada are contaminated.
Wildlife
Sierra Club of Canada Overview of the toxic effects of 2,4-D
January 2005 5
2,4-D has been shown to have negative impacts on a number of groups of animals. In
birds, 2,4-
D exposure reduced hatching success and caused birth defects (Duffard et al., 1981). It is
also
indirectly affects birds by destroying their habitat and food source. The toxicity of 2,4-D
to fish
is variable, with the ester form of 2,4-D expressing greater toxicity than other forms. 2,4-
D has
also been demonstrated to bio-accumulate in fish (Wang et al., 1994). A product of the
breakdown process of 2,4-D is 2,4-dicholorophenol. This chemical is extremely toxic to
earthworms, 15 times more toxic than 2,4-D itself (Roberts & Dorough, 1984). Beneficial
insects
have reduced fecundity when exposed to 2,4-D.
The use of 2,4-D has had drastic affects for both agricultural and wildlife animals
including, the
deaths of cattle and horses grazing of treated plants, and the destruction of plant food
sources of
moose, gopher and voles.
Conclusion
Given the effects outlined above, Sierra Club of Canada insists that use of this chemical
discontinued. Perhaps the most promising outcoming of this proposed action would be a
decline
in cancer, which we have seen in Sweden after the banning of phenoxy herbicides
(Hardell and
Eriksson, 2003). Cancer prevention could start with this step.
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