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Pesticide Info

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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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.

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


Mow High and Water Deep

"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: C

©2002 Sustain