| Chemical
Pesticides
Common pesticides used in homes and lawns are now being shown in medical
research to accelerate aging of the immune and nervous system resulting
in serious health problems years after exposure. Companies which use these
chemicals include TruGreen - ChemLawn - Orkin and others.
The majority of the public still believes these chemicals are completely
tested by the government. Unfortunately, this is not the case. Chemical
companies do their own testing and submit the results to the EPA for review
- setting up the potential for "selective" reporting. Of significant
concern, agriculture and consumer use pesticides are not currently required
to be tested for subtle neurological effects (i.e. memory, depression,
behavior) - child learning disorders - pregnancy developmental studies
and immune system effects (i.e. lower white blood counts - increased infection
rates and autoimmunity).
Health Effects Research
The Chemical Pesticide 2,4-D
2,4-D is a herbicide poison with reproductive and endocrine-disrupting
effects and is associated with a whole host of diseases, including cancer
of the kidney, testicles, stomach, colon, prostrate and liver; also known
to cause adverse psychological effects, immune system disorders, gastrointestinal
ulcers and altered liquid metabolism.
Trade and Other Names:2,4-D is used in many commercial products and weedkiller
mixes. Commercial names for products containing 2,4-D include Aqua-Kleen,
Barrage, Lawn-Keep, Malerbane, Planotox, Plantgard, Savage, Salvo, Trimec,
Weedone, and Weedtrine-II.
Regulatory Status: 2,4-D is a General Use Pesticide (GUP) in the U.S.
The diethylamine salt is toxicity class III- slightly toxic orally, but
toxicity class I- highly toxic by eye exposure. It bears the Signal Word
DANGER - POISON because 2,4-D has produced serious eye and skin irritation
among agricultural workers.
Chemical Class: phenoxy compound
Introduction: There are many forms or derivatives of 2,4-D including esters,
amines, and salts. Unless otherwise specified, this document will refer
to the acid form of 2,4-D. 2,4-D, a chlorinated phenoxy compound, functions
as a systemic herbicide and is used to control many types of broadleaf
weeds. It is used in cultivated agriculture, in pasture and rangeland
applications, forest management, home, garden, and to control aquatic
vegetation. It may be found in emulsion form, in aqueous solutions (salts),
and as a dry compound.
The product Agent Orange, used extensively throughout Vietnam, was about
50% 2,4-D. However, the controversies associated with the use of Agent
Orange were associated with a contaminant (dioxin) in the 2,4,5-T component
of the defoliant.
Formulation: It may be found in emulsion form, in aqueous solutions (salts),
and as a dry compound.
Toxicological Effects:
* Acute toxicity: The acid form is of slight to moderate toxicity. The
oral LD50 of 2,4-D ranges from 375 to 666 mg/kg in the rat, 370 mg/kg
in mice, and from less than 320 to 1000 mg/kg in guinea pigs. The dermal
LD50 values are 1500 mg/kg in rats and 1400 mg/kg in rabbits, respectively
[1,5,7]. In humans, prolonged breathing of 2,4-D causes coughing, burning,
dizziness, and temporary loss of muscle coordination [1]. Other symptoms
of poisoning can be fatigue and weakness with possible nausea. On rare
occasions following high levels of exposure, there can be inflammation
of the nerve endings with muscular effects [25].
* Chronic toxicity: Rats given high amounts, 50 mg/kg/day, of 2,4-D in
the diet for 2 years showed no adverse effects. Dogs fed lower amounts
in their food for 2 years died, probably because dogs do not excrete organic
acids efficiently. A human given a total of 16.3 g in 32 days therapeutically,
lapsed into a stupor and showed signs of incoordination, weak reflexes,
and loss of bladder control [1,5,7].
* Reproductive effects: High levels of 2,4-D (about 50 mg/kg/day) administered
orally to pregnant rats did not cause any adverse effects on birth weights
or litter size. Higher doses (188 mg/kg/day) resulted in fetuses with
abdominal cavity bleeding and increased mortality [1,5,7]. DNA synthesis
in the testes was significantly inhibited when mice were fed large amounts
(200 mg/kg/day) of 2,4-D [7]. The evidence suggests that if 2,4-D causes
reproductive effects in animals, this only occurs at very high doses.
Thus reproductive problems associated with 2,4-D are unlikely in humans
under normal circumstances.
* Teratogenic effects: 2,4-D may cause birth defects at high doses. Rats
fed 150 mg/kg/day on days 6 to 15 of pregnancy had offspring with increased
skeletal abnormalities, such as delayed bone development and wavy ribs
[7]. This suggests that 2,4-D exposure is unlikely to be teratogenic in
humans at expected exposure levels.
* Mutagenic effects: 2,4-D has been very extensively tested and was found
to be nonmutagenic in most systems. 2,4-D did not damage DNA in human
lung cells. However, in one study, significant effects occurred in chromosomes
in cultured human cells at low exposure levels [26]. The data suggest
that 2,4-D is not mutagenic or has low mutagenic potential.
* Carcinogenic effects: 2,4-D fed to rats for 2 years caused an increase
in malignant tumors [7]. Female mice given a single injection of 2,4-D
developed cancer (reticulum-cell sarcomas) [7]. Another study in rodents
shows a low incidence of brain tumors at moderate exposure levels (45
mg/kg/day) over a lifetime [1,7]. However, a number of questions have
been raised about the validity of this evidence and thus about the carcinogenic
potential of 2,4-D. In humans, a variety of studies give conflicting results.
Several studies suggest an association of 2,4-D exposure with cancer.
An increased occurrence of non-Hodgkin's lymphoma was found among a Kansas
and Nebraska farm population associated with the spraying of 2,4-D [25,27].
Other studies done in New Zealand, Washington, New York, Australia, and
on Vietnam veterans from the U.S. were all negative. There remains considerable
controversy about the methods used in the various studies and their results
[28]. Thus, the carcinogenic status of 2,4-D is not clear.
* Organ toxicity: Most symptoms of 2,4-D exposure disappear within a few
days, but there is a report of liver dysfunction from long-term exposure
[1,25].
* Fate in humans and animals: The absorption of 2,4-D is almost complete
in mammals after ingestion and nearly all of the dose is excreted in the
urine. The compound is readily absorbed through the skin and lungs. Men
given 5 mg/kg excreted about 82% of the dose as unchanged 2,4-D. The half-life
is between 10 and 20 hours in living organisms. There is no evidence that
2,4-D accumulates to significant level in mammals or in other organisms
[20]. Between 6 and 8 hours after doses of 1 mg/kg, peak concentrations
of 2,4-D were found in the blood, liver, kidney, lungs, and spleen of
rats. There were lower levels in muscle and brain. After 24 hours, there
were no detectable tissue residues. Only traces of the compound have been
found in the milk of lactating animals for 6 days following exposure.
2,4-D passes through the placenta in pigs and rats. In rats, about 20%
was detected in the uterus, placenta, fetus, and amniotic fluid [27].
Chickens given moderate amounts of 2,4-D in drinking water from birth
to maturity had very low levels of the compound in eggs [7].Ecological
Effects:
* Effects on birds: 2,4-D is slightly toxic to wildfowl and slightly to
moderately toxic to birds. The LD50 is 1000 mg/kg in mallards, 272 mg/kg
in pheasants, and 668 mg/kg in quail and pigeons [5-7].
* Effects on aquatic organisms: Some formulations of 2,4-D are highly
toxic to fish while others are less so. For example, the LC50 ranges between
1.0 and 100 mg/L in cutthroat trout, depending on the formulation used.
Channel catfish had less than 10% mortality when exposed to 10 mg/L for
48 hours [1,9]. Green sunfish, when exposed to 110 mg/L for 41 hours,
showed no effect on swimming response. Limited studies indicate a half-life
of less than 2 days in fish and oysters [24]. Concentrations of 10 mg/L
for 85 days did not adversely affect the survival of adult dungeness crabs.
For immature crabs, the 96-hour LC50 is greater than 10 mg/L, indicating
that 2,4-D is only slightly toxic. Brown shrimp showed a small increase
in mortality at exposures of 2 mg/L for 48 hours [7,20].
* Effects on other organisms: Moderate doses of 2,4-D severely impaired
honeybees brood production. At lower levels of exposure, exposed bees
lived significantly longer than the controls. The honeybee LD50 is 0.0115
mg/bee [6,7].Environmental Fate:
* Breakdown in soil and groundwater: 2,4-D has low soil persistence. The
half-life in soil is less than 7 days [21]. Soil microbes are primarily
responsible for its disappearance [20]. Despite its short half-life in
soil and in aquatic environments, the compound has been detected in groundwater
supplies in at least five States and in Canada [20]. Very low concentrations
have also been detected in surface waters throughout the U.S. [23].
* Breakdown in water: In aquatic environments, microorganisms readily
degrade 2,4-D. Rates of breakdown increase with increased nutrients, sediment
load, and dissolved organic carbon. Under oxygenated conditions the half-life
is 1 week to several weeks [20].
* Breakdown in vegetation: 2,4-D interferes with normal plant growth processes.
Uptake of the compound is through leaves, stems, and roots. Breakdown
in plants is by a variety of biological and chemical pathways [10]. 2,4-D
is toxic to most broad leaf crops, especially cotton, tomatoes, beets,
and fruit trees [7].Physical Properties:
* Appearance: 2,4-D is a white powder [6].
* Chemical Name: (2,4-dichlorophenoxy)acetic acid [6]
* CAS Number: 94-75-7
* Molecular Weight: 221.04
* Water Solubility: 900 mg/L @ 25 C (acid) [5]
* Solubility in Other Solvents: ethanol v.s.; diethyl ether v.s.; toluene
s.; xylene s. [6]
* Melting Point: 140.5 C [6]
* Vapor Pressure: 0.02 mPa @ 25 C (acid) [5]
* Partition Coefficient: 2.81 [20]
* Adsorption Coefficient: 20 (acid) [21]
Basic Manufacturer:
Rhone-Poulenc Ag. Co.
P.O. Box 12014
2 T.W. Alexander Dr.
Research Triangle Park, NC 27709
* Phone: 919-549-2000
* Emergency: 800-334-7577
Reference List
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W. J., Jr. and Laws, E. R., Jr., Eds. Academic Press, New York, NY, 1991.7-2
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(18) Buhler, D. R. Transport, accumulation and disappearance of pesticides.
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(19) Norris, L. A. Behavior of chemicals in the forest environment. In
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(20) Howard, P. H., Ed. Handbook of Environmental Fate and Exposure Data
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P. W. M. and Burt, J. P. SCS/ARS/CES Pesticide properties database for
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DC, 1992.7-24
(24) National Research Council Canada. Phenoxy Herbicides -- Their Effects
on Environmental Quality with Accompanying Scientific Criteria for 2,3,7,8--Tetrachlorodibenzo-p-dioxin
(TCDD). Ottawa, Canada, 1978.7-25
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Commercial Products. Williams and Wilkins, Baltimore, MD, 1984.7-26
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activity of topically applied pesticides and the herbicide 2,4-D in two
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and forestry workers. J. Nat. Cancer Inst. 76:229-234, 1986.
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Ester in the Rat in Bulletin of Environmental Contamination and Toxicology,
Vol.51, No.4. pp. 625-632.
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and Company Inc. Rahway, NJ.
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Substances. 1988. Fact Sheet No. 192: 2-(2-Methyl-4-chlorophenoxy) propionic
acid and its salts and esters. U.S. EPA. Washington, DC.
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Document #243675 and 246437. EPA. Washington, DC.
(47) Lynge, E.A. 1985. "Follow up study of cancer incidence among
workers in manufacture of phenoxy herbicides in Denmark." British
Journal of Cancer. Vol. 52. pp.259-270.
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Risk Information System (IRIS) database. HHS. Washington, DC.
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A Review. Toxicology Research Center of University of Saskatchewan. Saskatoon,
Canada.
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Is
the Grass Greener Where Cancer Danger is Greatest?
By Emily Green. Special to the Tribune. Emily
Green is a staff writer for the Los Angeles Times, a Tribune
newspaper. |
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The weapon of
choice against the dandelion is the weed killer 2,4-D, most commonly
mixed with fertilizer in "weed and feed" treatments. Each
year, Americans apply an estimated 27 million pounds of it to home
lawns, parks, cemeteries and anywhere else mown grass is found.
It is thought to be the most widely used herbicide in the world.
The appeal is that 2,4-D is selective: It kills broad-leaf plants
such as dandelions but spares grass. It overwhelms the dandelion's
hormone system, causing the weed to essentially grow itself to death.
This "uncontrolled growth," says Thomas M. Cahill, an
environmental chemist from Trent University in Ontario, Canada,
is a kind of "cancer for plants."
The question among environmentalists and medical researchers is:
Does cancer for plants also mean cancer for people?
EPA takes 2nd look
The Environmental Protection Agency, which ruled in 1997 that 2,4-D
was not classifiable as a human carcinogen, is now reviewing the
chemical's registration. Specialist committees are looking at the
issue, says Joanne Miller, product manager for EPA's pesticide registration
section. The EPA decision about registration is due in two years.
Until then, "the bottom line is: We can't make a call,"
she says. "We can't rule out, and we can't say for sure."
That uncertainty is roiling the world of American lawn care, where
the EPA estimates 20 percent of world production of 2,4-D is used.
(That name, by the way, is the chemical signature for dichlorophenoxyacetic
acid.)
Although 2,4-D has been used for decades, increasingly worried activists
at the local level are demanding warning notices when it is used,
blocking its use in city parks, and in some cases even getting it
banned.
The manufacturers contend that hundreds of studies have shown no
danger to humans.
"As long as label instructions are followed, it certainly poses
no unreasonable risk," says Don Page, executive director of
the industry's task force on 2,4-D research data. "The only
verified examples of 2,4-D poisoning in humans is in suicides. If
you drink enough of it, you can kill yourself."
By the 1980s, question marks loomed over the safety of 2,4-D, developed
in 1944 in Britain. In 1986, a study published in the Journal of
the American Medical Association suggested that Kansas crop workers
who had applied 2,4-D had a heightened rate of non-Hodgkin's lymphoma,
a cancer of the immune system. A later study also found higher than
normal levels of the disease in lawn service applicators. In 1989,
the National Academy of Sciences estimated that homeowners are likely
to use 10 times more chemicals per acre on their lawns than farmers
use on agricultural land.
Time for a review
Amid the furor sparked by the Kansas study, the EPA began its first
review of 2,4-D since the chemical's introduction in the 1940s.
In 1991, the National Cancer Institute said 2,4-D might cause a
lymphatic cancer in dogs. It also calculated that diagnoses of non-Hodgkin's
lymphoma among farm workers had been increasing 75 percent in the
past 20 years. It attributed part of the rise to better diagnoses
but also considered 2,4-D a possible contributor.
Page attacked the NCI's canvassing methods, then the interpretation
of the results, and accused the institute of scaremongering to raise
research funds.
His task force turned in the last of 270 toxicity studies in 1995.
The results showed that the amount of 2,4-D it took to harm lab
animals far exceeded anything expected to be encountered in the
environment.
But in 1996, as the cancer risk argument rolled on, University of
Minnesota pathologist Vincent Garry published a study in Environmental
Health Perspectives showing that 2,4-D might also cause birth defects.
Garry found almost twice the number of birth defects among children
of pesticide applicators than in a control population. The children
had been conceived in spraying season in a Minnesota farming region
predominantly using 2,4-D.
In 1997, with the EPA review of 2,4-D still under way, the agency's
Carcinogenicity Peer Review Committee stopped short of ranking the
chemical as a probable cause of cancer. But three years later, one
of its own statisticians and one of Garry's collaborators in the
Minnesota study linked many cancers -- of the esophagus, stomach,
rectum, throat, pancreas, larynx, prostate, kidney and brain --
to heavy wheat growing regions notable for 2,4-D use.
"We don't know what's causing it," says Dina Schreinemachers,
the EPA statistician. "It's something associated with the wheat."
Buffalo takes 1st step
By 1991, homeowners were worried. Buffalo, N.Y., was the first city
to require lawn care companies to post warning signs on chemically
treated lawns. In New York, according to Audrey Thier of the Buffalo-based
lobby Environmental Advocates, five counties have passed ordinances
that require prior notice of spraying to neighbors, and eight municipalities
have passed ordinances that phase out use of pesticides on government
property.
At last reckoning by the General Accounting Office, 23 other states
also had counties with some sort of notification requirements.
Pesticide bans are catching on
In 1991, the municipal council of Hudson, Quebec, banned the cosmetic
use of pesticides for lawn care altogether. A coalition of lawn-care
companies, including ChemLawn, sued to overturn the ban. Last June,
the Supreme Court of Canada upheld the Hudson ban.
Since then, says Angela Rickman, deputy director of the Sierra Club
of Canada, "more than 40 different communities are looking
at pesticide restriction bylaws of one form or another" in
her country. The Club declared May 11 "Dandelion Day"
and is sponsoring "Getting Your Lawn Off Drugs" workshops
this summer at Ottawa City Hall.
-- Emily Green
"Lawn care is made out to be more difficult than it really is,"
says Tom Tiddens, plant health care supervisor at the Chicago Botanic
Garden. "We teach an integrative approach to taking care of grass
and try to get people away from chemicals."
His suggestions: Plant ground covers such as periwinkle (Vinca major),
wintercreeper (Euonymus fortunei) and Japanese spurge (Pachysandra
terminalis) in areas where grass serves little purpose. Put down a
flagstone path if there's light foot traffic.
Mow high. Cutting grass too short makes for shallow roots and weaker,
more weed-prone plants.
Leaving it longer cools the soil and helps it hold moisture. It also
creates more surface for photosynthesis, resulting in sturdier grass.
Use a mulching mower with a sharp blade and leave the grass clippings
where they fall. This cuts down significantly on fertilization needs.
Aerate at least once a year. Removing thin cores of dirt helps oxygen
reach the plants' roots, makes for better drainage, and invigorates
growth.
If you need to supplement rainfall, water deeply and infrequently.
"Really soak the yard, then don't do it again for a while. Let
the grass dry out and the roots will deepen, reaching down for water.
You'll be creating a more tolerant, hardy lawn."
Copyright 2002 Chicago Tribune Company Chicago Tribune
June 18, 2002 Tuesday, NORTH SPORTS FINAL EDITION, Tempo; Pg. 6; ZONE:
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